Named conditions using ICD-9 categories for 10 year old children in 1980 (n=13201).
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Barely three months into the new year and we are happy to announce a monumental milestone reached - 150 million downloads.
\n\nThis achievement solidifies IntechOpen’s place as a pioneer in Open Access publishing and the home to some of the most relevant scientific research available through Open Access.
\n\nWe are so proud to have worked with so many bright minds throughout the years who have helped us spread knowledge through the power of Open Access and we look forward to continuing to support some of the greatest thinkers of our day.
\n\nThank you for making IntechOpen your place of learning, sharing, and discovery, and here’s to 150 million more!
\n\n\n\n\n'}],latestNews:[{slug:"intechopen-supports-asapbio-s-new-initiative-publish-your-reviews-20220729",title:"IntechOpen Supports ASAPbio’s New Initiative Publish Your Reviews"},{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"}]},book:{item:{type:"book",id:"468",leadTitle:null,fullTitle:"Electronic Properties of Carbon Nanotubes",title:"Electronic Properties of Carbon Nanotubes",subtitle:null,reviewType:"peer-reviewed",abstract:"Carbon nanotubes (CNTs), discovered in 1991, have been a subject of intensive research for a wide range of applications. These one-dimensional (1D) graphene sheets rolled into a tubular form have been the target of many researchers around the world. This book concentrates on the semiconductor physics of carbon nanotubes, it brings unique insight into the phenomena encountered in the electronic structure when operating with carbon nanotubes. This book also presents to reader useful information on the fabrication and applications of these outstanding materials. The main objective of this book is to give in-depth understanding of the physics and electronic structure of carbon nanotubes. \nReaders of this book should have a strong background on physical electronics and semiconductor device physics. This book first discusses fabrication techniques followed by an analysis on the physical properties of carbon nanotubes, including density of states and electronic structures. Ultimately, the book pursues a significant amount of work in the industry applications of carbon nanotubes.",isbn:null,printIsbn:"978-953-307-499-3",pdfIsbn:"978-953-51-4483-0",doi:"10.5772/980",price:159,priceEur:175,priceUsd:205,slug:"electronic-properties-of-carbon-nanotubes",numberOfPages:698,isOpenForSubmission:!1,isInWos:1,isInBkci:!0,hash:null,bookSignature:"Jose Mauricio Marulanda",publishedDate:"July 27th 2011",coverURL:"https://cdn.intechopen.com/books/images_new/468.jpg",numberOfDownloads:117258,numberOfWosCitations:134,numberOfCrossrefCitations:46,numberOfCrossrefCitationsByBook:6,numberOfDimensionsCitations:110,numberOfDimensionsCitationsByBook:9,hasAltmetrics:1,numberOfTotalCitations:290,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 12th 2010",dateEndSecondStepPublish:"November 9th 2010",dateEndThirdStepPublish:"March 16th 2011",dateEndFourthStepPublish:"April 15th 2011",dateEndFifthStepPublish:"June 14th 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,7,8",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"9142",title:"Prof.",name:"Jose Mauricio",middleName:null,surname:"Marulanda",slug:"jose-mauricio-marulanda",fullName:"Jose Mauricio Marulanda",profilePictureURL:"https://mts.intechopen.com/storage/users/9142/images/1746_n.jpg",biography:"Jose Mauricio Marulanda has a Doctor of Philosophy in Electrical Engineering from Louisiana State University. 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In this chapter I review the extent to which autistic individuals can also experience a range of other difficulties, but my focus will be on the common neurodevelopmental disorders. The most common of these include dyslexia, attention deficit hyperactivity disorder (ADHD), dyspraxia, specific language impairment, and dyscalculia. There is considerable symptom overlap in particular between ADHD and dyslexia, and like autism both are described as developmental disorders by psychiatric classification systems (American Psychiatric Association, 2000; World Health Organization., 1992). Overlapping conditions are termed ‘co-morbidity’ by medical practitioners. Co-morbidity may reflect the greater difficulties experienced by children with a combination of deficits. Sometimes it is apparent that many children with a developmental disorder could be classified in several ways. Here I will firstly examine the research evidence that examines how often symptoms of dyslexia and ADHD occur in the population of autistic children, and second, review the various theories that have tried to explain why such co-occurring difficulties are so common.
‘Comorbidity’, a term used in medical literature to mean a dual diagnosis, or multiple diagnoses, can reflect an inability to supply a single diagnosis that accounts for all symptoms. Children with ASD have been shown to have higher rates of epilepsy, with 30% of cases having epilepsy comorbid (Danielsson, Gillberg, Billstedt, Gillberg, & Olsson, 2005). Other conditions that are commonly co-morbid with ASD include hearing impairment (Kielinen, Rantala, Timonen, Linna, & Moilanen, 2004) mental health and behavioural problems (Bradley, Summers, Wood, & Bryson, 2004), including anxiety, and depression (Evans, Canavera, Kleinpeter, Maccubbin, & Taga, 2005). It has also been shown that parents of autistic children are twice as likely themselves to have suffered from psychiatric illness than parents of non-autistic children (Daniels et al., 2008).
Most of these problems are distinct from those examined in this chapter: the common developmental disorders of childhood which are also found to co-occur with autism, particularly ADHD and dyslexia.
Before reviewing the evidence that suggests many children share difficulties symptomatic of these conditions, and the theories of why this may be, I will briefly describe how dyslexia and ADHD manifest themselves.
Dyslexia is conceptualized by both educational bodies and the psychiatric classification systems as a learning difficulty that primarily affects the skills involved in accurate and fluent word reading and spelling. Characteristic features of dyslexia are difficulties in phonological awareness, verbal memory and verbal processing speed. Dyslexia is developmental delay in literacy and generally slow and inaccurate reading and spelling. The definition of dyslexia has changed over time, and such changes have often been based on the research identifying a range of associated difficulties that occur with dyslexia. Estimates of the prevalence of dyslexia have been complicated because dyslexia cut-offs are contested (Coltheart & Jackson, 1998) and dyslexia manifests itself differently in various languages according to levels of phonic regularity (Miles, 2004). Research over the last 40 years has focused on phonological skills. These are the reading and de-coding skills used when breaking down language into its component sounds and reassembling the parts in order to read or to spell a word.
Like autism, dyslexic difficulties are considered to exist in a continuum throughout the general population (Fawcett, 2012). There is much interest in the association of cognitive ability with changing symptom profiles and diagnosis. The definition of dyslexia is in flux, and has been recently redefined by many national bodies, for example in the UK, the British Psychological Society, focusing on literacy learning at the \'word level\' without attainment discrepancy:
Dyslexia is evident when accurate and fluent word reading and/or spelling develops very incompletely or with great difficulty (British Psychological Society, 1999)
This definition implies that the problem is severe and persistent despite appropriate learning opportunities. This UK definition differs from the ICD-10 diagnosis of developmental dyslexia or ‘Specific Reading Disorder’, which requires a discrepancy between actual reading ability and the reading ability predicted by a child’s IQ. So an intellectual disability, (generally considered IQ below 70) can co-occur with the British Psychological Society definition of dyslexia. This new definition includes the so called ‘garden variety’ dyslexic children who have difficulties with reading and spelling as well as other generalized intellectual disabilities. The implications of including this group as dyslexic mean that more children with an intellectual disability would also be classified as ‘dyslexic’. As ASD includes a large group with intellectual disability the extension is likely to increase the number of children who may be classified as having both conditions. This is important as the clinical and education label may determine the interventions a particular child receives.
In addition to these characteristics, dyslexic children may experience visual and auditory processing difficulties, similar to hyper or hypo sensitivity often associated with ASD. Like the ‘islets of ability’ seen in many children with ASD, some dyslexic children may also have strengths in particular areas, such as design, logic, and creative skills.
ADHD is known as ‘Hyperkinetic Disorder’ in ICD-10; there are three subtypes of ADHD according the DSM. In the first, a child will primarily have problems with attention which may manifest as an inability to remain ‘on task’ for long periods, lack of response to instruction or distractibility. In the second sub-type, symptoms of hyperactivity and impulsivity dominate, which is characterized by wriggling, squirming, being unable to sit still, interrupting and finding it difficult to wait. Children may also be climbing in inappropriate situations and always on the move when free to do so. The third sub-type is simply the co-existence of both attention problems and hyperactivity, with each behavior occurring infrequently alone and symptoms starting before seven years of age.
According to ICD-10, eventually, assessment instruments should develop to the point where it is possible to take a quantitative cut-off score to assess ADHD. Like dyslexia and autism, the symptoms are behavioural in nature, and are part of a continuously distributed pattern that extends into the population at large.
The persistence of ADHD symptoms is not so marked as for autism. Around 70 to 50 percent of those individuals diagnosed in childhood do not continue to have symptoms into adulthood (Elia, Ambrosini, & Rapoport, 1999). There is evidence suggesting to some extent symptoms of ADHD are expressed in reaction to home (Mulligan et al. 2011) and other environmental contexts. Individuals with ADHD also tend to develop coping mechanisms to compensate for some or all of their impairments. ADHD is diagnosed more often in boys with the reported ratio varying from 2:1 to 4:1 (Dulcan, 1997; Kessler et al., 2005) though some studies suggest this may be partially due to referral bias where teachers are more likely to refer boys than girls (Sciutto, Nolfi, & Bluhm, 2004). Treatments for ADHD involve a combination of medication, usually methyphenidates which are well established in improving symptoms of inattention, and behavioral intervention in education and at home. The issue of girls being overlooked on identification is a common thread for research in dyslexia, ADHD and autism. Our own results suggest there is some evidence to back up the claim that boys with ASD symptoms are given the diagnosis more frequently than girls with equivalent ASD symptoms (Russell, Steer, & Golding, 2011). This may be because the disorders tend to be conceptualized as ‘male’ leading to referral bias.
Because ASD, Dyslexia and ADHD are all behaviorally defined, so ‘symptoms’ are behaviours. All three conditions are conceived as particular behaviours along a spectrum, where traits have a continuous distribution and extend into the general (non-disordered) population. An arbitrary cut off point determines who is considered to be within the various categories and who is not. The clinician giving a diagnosis will be responsible for judging where this cut off may come, guided by diagnostic criteria and standards within disciplines as well as perceived implications: the benfits versus any possible risks of assigning a diagnosis. This is perhaps best established for autism: Constantino and Todd (2003) measured autistic traits in a large community sample, and found no jump in the threshold of autistic behaviours between ‘normal’ individuals and those with an autism spectrum diagnosis, rather they found a continuous distribution. These findings concurred with those in a Scandinavian study (Posserud, Lundervold, & Gillberg, 2006). One of our own studies has likewise shown that autistic traits do extend into the ‘subclinical’ population (Figure 1). As with dyslexia and ADHD, there is not a sharp line separating severity in those with a diagnosis from less severe traits in those without (London, 2007). In both dyslexia, ADHD and the autism spectrum, some children have more severe difficulties than others, and the symptoms extend into the population of children (and adults) as a whole. For dyslexia, there are many people who may have mild dyslexic difficulties but perhaps might not qualify as ‘dyslexic’. For autism spectrum disorders, many people without an autism diagnosis do have autistic-type behaviours but the severity and frequency of those behavioural symptoms is less severe than in those deemed to qualify for a diagnosis.
The distribution of an ASD composite trait in the general population from
The imposition of a cut off between normality and abnormality is therefore ‘an arbitrary but convenient way of converting a dimension into a category’ as Goodman and Scott (1997, p. 23) point out.
Various studies have looked for ADHD or ADHD symptoms in samples of children with autism or ASD. Rates of ADHD have ranged from 28% to 78% of these samples (Ronald, Edelson, Asherson, & Saudino, 2010). Studies that look at ADHD symptoms have reported even higher numbers: for example, Sturm, Fernell, & Gillberg, (2004) looked at a sample of around 100 high functioning children with ASD and found 95% had attention problems, 75% had motor difficulties, 86% had problems with regulation of activity level, and 50% had impulsiveness. About three-quarters had symptoms compatible with mild or severe ADHD, or had deficits in attention, motor control, and perception, indicating a considerable overlap between these disorders and high-functioning ASD in children.
In an large analysis of nine hundred forty-six twins, Reierson and colleagues (2008) assigned DSM-IV ADHD diagnoses, and measured autistic traits using the Social Responsiveness Scale. The study showed that there are clinically significant elevations of autistic traits in children meeting diagnostic criteria for ADHD. These findings confirm results in earlier studies (Clark, Feehan, Tinline, & Vostanis, 1999). Santosh and Mijoovic (2004) which found children with ADHD had elevated levels of impairment in all three autistic symptom domains, namely social deficits, communication and stereotyped behaviors. Clark
In an analysis conducted with Lauren Rodgers at the Peninsula Medical School in the UK using data from the Millennium Cohort Study, a cohort of around 19,000 children who were all born between 2000 and 2002, we noted 44 children had a dual diagnosis of both ASD and ADHD (proportion of total population 0.3%) by age seven. The prevalence of children with identified ADHD in the ASD sample was 17%. Conversely, the prevalence of children with ASD in the ADHD sample was higher at 27%. Both figures indicate substantial overlap between these conditions.
Various European research groups have examined co-morbid disorders in adults with diagnosed ASD. An international team lead by Hofvander studied a group of 122 adults with normal IQ from specialist clinics in three European cities: Gothenburg, Paris and Malmö (Hofvander et al., 2009). Here the overwhelming majority had symptoms of ASD. Nonverbal communication problems were also very common, described in 89% of all their subjects. In this study over half the participants, (52%) were diagnosed with co-morbid ADHD. Interestingly, participants diagnosed with pervasive developmental disorder. ‘Not Otherwise Specified’ (PDD-NOS) diagnosis had significantly more symptoms of inattention and hyperactivity/impulsivity compared to subjects diagnosed with Asperger’s syndrome. However, the prevalence of the categorical diagnosis of ADHD did not differ significantly between the groups, nor were gender differences apparent. Although the study presents clear evidence of many cases where patients display symptoms of both ADHD and ASD, the clinical setting may have led to selection bias as patients with complex needs may be more likely to seek help.
Because behaviours associated with both conditions lie on a spectrum extending into the normal range, some studies have found a range of frequency and severity of symptoms. In Mulligan et al.’s (2009) study, for example, 75 of children with ADHD had severe autism traits, and over half showed sub-clinical autism symptoms. Kadesjö and colleagues (Kadesjö, Gillberg, & Hagberg, 1999), looked at comorbidity of ADHD in Swedish school-age children and found only 1% of children meeting the threshold for ADHD had comorbid Aspergers Syndrome (AS). The estimates of co-morbidity of ADHD symptoms with ASD symptoms vary widely because of differing methods of case ascertainment. An additional problem is that the estimate of the prevalence of ASD itself has increased so much in western countries, making ASD itself a ‘moving target’ (Figure 2).
Patricia Howlin (2000) reviewed the estimated rates of co-existing psychiatric disorders in subjects with high functioning ASD and found these estimates varied from 9% to 89% - very substantial differences. However it is possible to generalise; thirty years of research have confirmed that attention deficits and hyperactivity are relatively common in children and adults with ASD even if the exact extent of overlap is dependent on methodology and ascertainment (Hofvander et al., 2009, Sturm, Fernell, & Gillberg, 2004).
The rising prevalence of autism spectrum disorders over 50 years. (Data from ‘Autism Speaks’ and CDC, USA)
Recent trends have made categorical diagnosis an integral part of everyday clinical and research practice (Sonuga-Barke & Halperin, 2010). Christopher Gillberg (2010) points out that clinicians have become focused on dichotomous categories of disorder and that clinics have become increasingly specialized and overlook difficulties not within their immediate jurisdiction. Gillberg has argued that co-existence of disorders is the rule rather than the exception in child psychiatry and developmental medicine. He has coined the acronym ESSENCE (referring to Early Symptomatic Syndromes Eliciting
Neurodevelopmental Clinical Examinations). This describes cases where a combination of symptoms including inattention, hyperactivity, social and reading difficulties are observed. Major problems in at least one ESSENCE domain before age 5 years often signal major problems in the same or overlapping domains years later.
To summarize, although ADHD and ASD are separate and recognizable, there is good evidence that these conditions co-occur, constituting an amalgam of problems.
There is only a small literature on the overlap in symptomology between autism spectrum disorders with those of dyslexia. Officially, as for ADHD, ASD is an exclusionary criterion for diagnosis of dyslexia and vice versa, but ASD also shows overlap with dyslexia in both cognitive and behavioural features (Reiersen & Todd, 2008, Simonoff et al., 2008). A proportion of children share symptoms between dyslexia, ADHD
The number of children that do share symptoms of ASD and dyslexia is likely to be small (Wright, Conlon, Wright, & Dyck, 2011). The frequency of reading disorder in combination with disorder of written expression (i.e. dyslexia) was around 14% in a sample of adults with Asperger’s Syndrome (AS) so according to this result around one in seven individuals with AS will have co-occurring dyslexia (Hofvander et al., 2009). However the proportion of individuals with dyslexia who have co-occuring AS is likely to be low as Asperger’s Syndrome is much a rarer condition than dyslexia.
A common problem for children with dyslexia is misinterpretation of spoken language, which can also manifest itself in comprehension. This produces further overlap with pragmatic language impairment (PLI) which itself is virtually indistinguishable from communication difficulties associated with high functioning autism. Pragmatic language difficulties may involve literal interpretation so ‘run on the spot’ would have a child looking for a big black spot to run on, for example. Children with PLI will often fail to interpret the core meaning or saliency of events. This causes a penchant for routine and \'sameness\' (also seen in autism and Asperger\'s Syndrome) as PLI children struggle to generalize and take hold of the meaning of novel situations. Obvious and concrete instructions are clearly understood and carried out, whereas simple but non-literal expressions such as jokes, sarcasm and general social chatting are difficult and may be misinterpretated. PLI may therefore impact on the social abilities of the child who has difficulty interpreting jokes. Current thinking is that PLI is not a problem rooted in language skills but one of social communication and information processing. Griffiths (2007) identified difficulties of this type in dyslexic students, showed they were impaired in making inferences from a story and choosing the right punch-line for a joke. This of course can have implications for written language and examinations under stress, as well as for a range of social interactions.
It is not just that ASD is co-morbid with dyslexia and ADHD. Other studies have noted high comorbidity with other developmental disorders. Dyspraxia and dyscalculia and conditions with shared symptoms such as specific language impairment are frequently comorbid with autism. Also dyslexia and ADHD themselves co-occur Willcutt and colleagues (Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005) showed that 40% of a sample of twins with either dyslexia or ADHD was co-morbid for the other disorder. Reading difficulties were measured with both rating scale and an objective task in a study by Cheung et al. (2012) and correlations were observed among ADHD, reading difficulties and IQ. Over half, (53%-72%) of the overlapping familial influences between ADHD and reading difficulties were not shared with IQ. In a school based study Kadesjö and colleagues found 40% of children with ADHD showed reading problems and 29% writing problems (2005).
Overall, the literature suggests, there is good evidence to suggest that some children do suffer from symptoms of both dyslexia and ASD, although this is not so well established, and does not occur so frequently as co-morbidity between ADHD and ASD.
Several theories have been put forward to explain the shared symptoms of the various developmental conditions – in other words why specific learning and language and social disorders are not specific. It is likely that all the explanations below play a part in co-occurrence; the causality of co-morbidity is most probably due to a complex web of interacting factors.
One of the most persuasive explanations is that a genetic predisposition may lead to abnormal neurological development, which in turn may manifest in various different aberrant behaviors and developmental delays. As autism, ADHD and dyslexia and other developmental conditions are all highly heritable, so they all have a large genetic component, the theory seems plausible. The same genetic anomaly may lead to several disorders or psychiatric conditions. In other words one genotype may lead to several (related) phenotypes. This is known as ‘pleiotropy’. Researchers have suggested that co-occurrence of autism and ADHD (and other developmental disorders) may reflect such common genetic causes (Reierson et al, 2008). In this model, the origins of both sets of difficulties are due to common genetic anomalies that predispose children to delayed or atypical neurological development. Certainly, specific genetic anomalies have been associated with a range of psychopathologies in adulthood. However, the genetic picture is complex and exact pathways are not established. It is estimated there are more than a thousand gene variations which could disrupt brain development enough to result in social delays (Sanders et al., 2012).
Such a genetic predisposition is almost certainly complex and multi factorial. So far, over 100 candidate genes have been associated with ASD, most of which encode proteins involved in neural development, but exact mutations within the candidate genes have yet to be identified (Freitag, 2007). Furthermore, different individuals may have mutations in different sets of genes and most of the discovered gene variations are likely to have a low penetrance, thus not all carriers will develop the disorder. There may be interactions among mutations in several genes, e.g. between regulatory genes and coding regions, or between the environment and mutated genes, altering their expression. The effect of a mutation or deletion can depend on processes relating to gene expression and regulation as well as the subsequent effects on the expression of other genes.
The advent of genomics and the emphasis placed on this has led to much research to identify genetic predispositions to ASD. The field of psychiatry as a whole has been ‘geneticised’ according to some social theorists. This refers to the potential reclassification of psychiatric conditions in the light of findings from molecular biology. For example, a particular sub-category of DSM-IV schizophrenia has been linked to a substitution of a single base in the sequence of DNA of a particular gene localised to a precise place on a particular chromosome, leading to a substitution of one amino-acid for another in an enzyme involved in neurotransmission. Hedgecoe (2001) provides a discussion of the geneticisation of schizophrenia. The debate as to whether the old psychiatric systems of classification should be overhauled in the light of new genomic knowledge which illuminates genetic aetiologies is ongoing (Ericson & Doyle, 2003).
A second theory is that an environmental insult or a stressful event in the life of the fetus or in a young child’s life, may trigger a genetic predisposition to be expressed. Thus this constitutes a gene- environmental interaction theory. An example might be the high testosterone levels in the womb that have been observed in some studies. Baron-Cohen’s Cambridge group, for example, has carried out work that has suggested high levels of fetal testosterone may be linked to the development of autistic traits (Ingudomnukul, Baron-Cohen, Wheelwright, & Knickmeyer, 2007). According to the gene-environment explanation, the elevated testosterone might lead to the differential expression of genes controlling the neurological development of the child. Another example that has been quite widely publicized concerns Omega 3 fatty acids. These have been implicated by Richardson (2006), who has argued that attention-deficit/hyperactivity disorder, dyslexia, developmental coordination disorder (dyspraxia) and conditions on the autism spectrum may all share common origins triggered by problems with phospholipid (fatty acid) metabolism. However this is just one genetic / environmental explanation for co-occurrence that vies with several others, and the available evidence is subject to interpretation.
In the majority of cases, the gene-environment hypothesis seems highly plausible. It may be that autism and co-occurring developmental conditions may all be caused by a genetic predisposition which is triggered by an early environmental influence (Trottier, Srivastava, & Walker, 1999).
Many environmental factors have been implicated in ASD but the effect of each is poorly established. After the well publicized paper that linked autism to the MMR vaccination, research has repeatedly refuted a link between the MMR jab and ASD (Rutter, 2005). Deykin and MacMahon (1979) found increased risk due to exposure to, and clinical illness from, common viral illnesses in the first 18 months of life. In this study, mumps, chickenpox, fever of unknown origin, and ear infections were all significantly associated with ASD risk. Epidemiological studies have shown there is a higher rate of adverse prenatal and postnatal events in children with ASD than in the general population (Zwaigenbaum et al., 2002). Newschaffer and colleague’s (2007) review named associated obstetric conditions that included low birth weight, gestation duration, and caesarean section. It is possible that such an underlying cause partially could explain both autism and the associated conditions (Kolevzon, Gross, & Reichenberg, 2007). There is evidence to suggest adverse prenatal and perinatal events are also associated with ADHD and cognitive development. Some studies have suggested that the risk of autism may be increased with advancing maternal age (Bolton et al., 1997). Paternal age too has frequently (but not always) associated with autism. There are more mutations in the gametes of older men, and this higher rate of mutation in the genetic material from the paternal side may explain the higher levels of neurodevelopmental disabilities in their offspring. An alternative explanation is that fathers who themselves have autistic traits are less likely to have children young. Using anticonvulsants during pregnancy also appears to increase the risk of ASD (Moore et al., 2000). These drugs are used to combat epilepsy which is commonly often comorbid with ASD. Parental occupational exposure to chemicals during the preconception period has also been higher in ASD families than controls in some studies (Felicetti, 1981).
Environmental risk factors have received widespread media coverage within the last few years, perhaps because of the strong degree of public concern (Russell & Kelly, 2011). In most health and disease categories, a secondary function of diagnosis is to group together people who have a common aetiology. However, the specific effects of genetic factors and environmental risk factors that might play a part in abnormal neural development are largely unresolved. Goodman and Scott (1997) stress that current understanding of aetiology for childhood developmental conditions will probably look ridiculously simplistic or misguided in years to come. Despite, or perhaps because of, the uncertainty, there is an underlying concern among people involved with children who are diagnosed with developmental conditions that environmental influences may be partially to blame for rising incidence. Novel prenatal and perinatal medical practices, changing diet, shifting family structures and childhood social activities have all been the subject of lay theories to explain rising prevalence not just of ASD, but developmental disorders in childhood more generally, including ADHD and dyslexia (Russell & Kelly, 2011).
A third possibility is that environmental factors alone may be enough to trigger not just autistic behaviors, but also other maladaptive behaviors such as inattention. Autistic behaviors were observed in a study of abandoned Romanian children, conducted by Michael Rutter and colleagues (1999). As well as cases with known genetic causes, in some cases, underlying social factors may predispose autistic symptoms. In this study, Rutter and colleagues noted a very high instance of autism (6%) in the Romanian baby cohort, which they put down to poor early care. These children exhibited typical symptoms of autism at four years old, but unlike cases of autism without maltreatment, symptoms by age 6 were much milder. This case is an illustration of how children who share severe autistic symptoms at young ages may have differing developmental trajectories. In this study, the symptoms of autism may have been triggered primarily by the early neglect, rather than by a genetic predisposition, for if a genetic predisposition was involved it would effect 6% or more of the babies, a very high proportion.
It is not just aetiological environmental factors that seem to lead to increased risks of displaying autistic behaviours. Aetiological causes can be distinguished from proximate determinates which occur at the same time as symptoms, for example, social situations or fluorescent lights may exacerbate the expression of ASD symptoms. There are also those influences in the environment that are sometimes referred to in psychiatry as maintenance factors, including stigmatisation and labelling. Although their influence in perpetuating ASD and other developmental disorders is unclear, an influence in maintaining symptomatic behaviours of autism and co-morbid conditions can not be discounted. Biological causes and behavioural outcomes are mediated by experiential and environmental factors.
The competing psychological theories that have been put forward concerning the psychological mechanisms of ASD include weak central coherence theory, deficits in executive function and the extreme male brain theory, all were reviewed by Happé in 1994.
The extreme male brain theory as developed by Baron-Cohen (2002) suggests that autistic individuals can systematize—that is, they can develop internal rules of operation—but are less effective at empathizing and handling events that are unexpected or social. The theory was developed from the earlier ‘theory of mind’ (Baron-Cohen, Leslie, & Frith, 1985). This suggested that autistic people lack the ability to understand other peoples’ mental states, put themselves in another person’s place or imagine what they might be thinking or experiencing. This lack of mentalising is discussed by Frith and Happé in their discussion of dyslexia, autism and downstream effects of specific impairments (1998). The ‘theory of mind’ lines up with the ‘mirror neuron theory of autism’ (Iacoboni & Dapretto, 2006) which was based on the discovery that the macaque monkey brain contained ‘mirror neurons’ that fired not only when the animal is in action, but also when it observes others carrying out the same actions.
An alternative psychological theory for autism is provided by Frith whose ‘weak central coherence’ theory (Frith, 2003; Happé & Frith, 2006) describes the ability to place information in a context in order to give it meaning. Most people pull together numerous stimuli to form a coherent picture of the world, allowing them to see the ‘bigger picture’. In central coherence theory, the failure to appreciate the whole accounts for the piecemeal way in which people with ASD acquire knowledge. People with ASD may also show relative strengths in some areas, known as ‘islets of ability’; and this accounts for savant skills. Related to central coherence is the theory that autistic behaviours are due to interference in executive function (Hill, 2004). Executive functions coordinate the flow of information processing in the brain and are the mechanisms of transferring attention from one thing to another flexibly and easily. They allow people to plan strategically, solve problems and set objectives. Their absence means autistic people show an inability to plan and attain overarching goals. This manifests as easily distractible behaviour and reliance on routines. Such psychological theories of ASD are useful models but have also been subject to criticism. Bailey and Parr (2003) describe such theories of psychological mechanisms as ‘narrow cognitive conceptualisations’ (p. 27), because they cannot accommodate the presence of sub-clinical autistic traits in the general population.
These theories seem very distinct from some psychological theories that explain dyslexic type and attention and hyperactive difficulties. The exception to this is that, deficits in executive function have been suggested as causal for ADHD, as they affect both cognitive and motivational systems (Willcutt et al., 2005). Frith and Happé (1998) focusing on dyslexia and autism, argue that psychological mechanisms could act as ‘gateways’ to impairment in other domains. These downstream developmental effects have not yet been fully considered, they suggest. Although they focus on autism and dyslexia, ADHD and other developmental disorders could easily be included in their model. As they point out, both dyslexia and autism have genetic origins, an anatomical basis and extremely variable behavioral manifestations. Their idea is that in addition to the genetic and anatomical origins, an additional developmental pathway may contribute to later difficulties. They argue that specific impairments seen in dyslexia or autism (such as dyslexic phonological or autistic mentalising difficulties) may have a ‘gatekeeping’ function and subsequently lead to difficulties in other areas. Thus impairments in domain-specific functions may have wide ranging developmental effects.
The idea put simply is that during development, one behavior exacerbates problems in other domains. It is perhaps easier to understand given a few concrete examples. Frith and Happé suggest that the core autistic difficulty of social engagement may lead to missed opportunities for learning, including learning vocabulary. This may effect language acquisition and in turn the development of language based skills evident in dyslexia. An easier pathway to understand might be via gatekeeping function of inattention. If a child is inattentive (a core symptom of ADHD) then the likelihood is they may struggle to focus on learning to read. Hence difficulties symptomatic of dyslexia may be expected. Conversely perhaps reading difficulties are primary, in which case inattention might come from frustration and inability to deal with task demands. This direction of causality seems likely in the sub-group of ADHD children whose problems only appear at school, and who are more likely than other groups to show reading problems according to Taylor (2011). Furthermore, an inattentive child may find it difficult to socialize normally, and may have difficulties following instruction. This may lead to the impairment in social skills symptomatic of autism.
In a similar way, it is possible to theorize that each domain of behavioural impairment in the triad for autism might lead to another. In a review of evidence for single genetic or cognitive causes for autism, Happé, Ronald, and Plomin (2006) note that twin studies suggest combinations of largely non-overlapping genes act on each area of impairment. Their own study found only modest correlations between the three domains of behavioural traits in the triad (namely deficits in social skills and communication and stereotyped behaviour or restricted interests). In the general population, correlations ranged from 0.1- 0.4 for the relationship of each domain to the other. This evidence shows that the three types of autistic traits may be clustered or linked or co-inherited, but with a weak association. These low correlations could be attributed to developmental pathways factors as well as genetic links. Such residual downstream developmental effects are easy to conceptualise. If a young boy is very asocial for example, then his communication skills will not be practised with peers, so he is unlikely to develop as quickly in measures of communication as a more sociable child. The weak correlation between repetitive behaviours is harder to explain. Speculation is possible: repetitive behaviours have been shown to have both self-stimulatory as well as calming functions (Turner, 1999). Repetitive behaviours can therefore be interpreted as responses to unwanted stimuli, e.g. social stimuli with which autistic people have difficulty. Williams (1994) has given a first person account of use of repetitive behaviours to ameliorate the stress of social situations. Conversely, the need for stimulatory repetitive behaviours, concentrating on drawing lines or circles for example, may interfere with social opportunities. Weak associations do not confirm or deny genetic co-inheritance. Developmental pathways where one type of behaviour leads to another may also provide a partial explanation.
In a different but related developmental scenario, Cheslack-Postava and Jordan –Young (2012) suggest that a child’s upbringing is highly gendered, and proposed a gendered embodiment model for autism. They cite numerous studies illustrating that the nature of parenting in particular depends on the gender of the child. This they use to describe a gendered theory of development of autism, although the model could also explain the large predominance of boys with other developmental disorders. Cooper (2001) suggests boys are socialized to encourage competition and activity thus a conflict between passivity required at western schools and masculine identity is generated. Some behaviours associated with ADHD when used excessively in school environments, climbing trees for example, are encouraged more often in boys than girls. Cheslack-Postava and Jordan –Young suggest such gendered social processes interact with biology to promote certain ‘disordered’ behaviours. This they call the ‘pervasive developmental environment’.
As well as downstream developmental models, some theorists have suggested one cognitive deficit may underlie several symptomatic behaviours. Although the cognitive/psychological theories of dyslexia and autism seem quite distinct, some research does suggest children with both ADHD and dyslexic difficulties show a distinctive deficit in rapid naming speed, so it may that processing speed underlies the link (Bental & Tirosh, 2007).
A second example is provided by executive function which is impaired in both autism and ADHD (Willcutt et al, 2005). According to some models, an underlying impairment in executive function prevents children from coordinating information processing in the brain, and prevents the transfer attention from one thing to another. It is easy to understand how this absence may translate into symptoms of either autism, due to inability to plan with strategic overarching vision, and hence reliance on routines, or as inattention and distractibility symptomatic of ADHD. Executive functions are neuropsychological processes needed to sustain problem-solving toward a goal. Executive functions allow a resolution of conflict when two responses are simultaneously called for by stimuli. In the laboratory, the Stroop task is an example. The conflicting combination of a word like
Russell Barkley (2012) conceptualizes executive control as the methods of self-regulation. He writes entertainingly on how a person might use executive functions to resist the temptation to buy a tempting pastry from a shop:
…avert your eyes from the counter, walk to a different section of the shop away from the tempting goodies, engage yourself in mental conversation about why you need to not buy those products, and even visualize an image of the new slenderer version of yourself you expect to achieve in the near future. All of these are self-directed actions you are using to try and alter the likelihood of giving into temptation and therefore increase your chances of meeting your goal of weight loss this month. This situation calls upon a number of distinct yet interacting mental abilities to successfully negotiate the situation. You have to be aware that a dilemma has arisen when you walked into the shop (self-awareness), you have to restrain your urge to order the pastry to go with the coffee you have ordered (inhibition), you re-directed your attention away from the tempting objects (executive attention or attentional management), you spoke to yourself using your mind’s voice (verbal self-instruction or working memory), and you visualized an image of your goal and what you would look like when you successfully attain it (nonverbal working memory, or visual imagery). You may also have found yourself thinking about various other ways you could have coped effectively with these temptations (problem-solving), and may have even used words of encouragement toward yourself to enhance the likelihood that you would follow your plan (self-motivation).
Barkley explains that these and other mental activities are usually included in the understanding of human self-regulation, and it is difficulties in these areas (which are processes in executive function) that may lead to ADHD. Children with ADHD are distractible and self-regulation, the ability to override incoming stimuli, to see the bigger picture and lack the ability to see the consequences of their future actions. Children with ASD have difficulties transferring attention from one thing to another because they also lack overview (and implications of their actions in the future).
Gooch, Snowling and Hulme (2011) note that deficits in time perception (the ability to judge the length of time intervals) have been found in children with both dyslexia and ADHD. These researchers found children with comorbid dyslexia and attention problems performed poorly on measures of executive function as well as on phonological tasks. However, their results were interpreted as the effect of independent underlying cognitive causes. Although deficits in duration discrimination were associated with both dyslexia and attention problems, they concluded the results supported the claim that the two disorders are products of different cognitive defects originating from shared genes with pleiotropic effects.
Developmental models explain comorbidity of developmental disorders by shared cognitive deficits, either as ‘gateways’ as in Frith and Happés (1998) model, where one difficulty leads to another later in life, or as underlying shared deficits, for example impaired executive function causing both autism and ADHD. The alternative model suggests that cognitive difficulties associated with each disorder are distinct, but multiple cognitive deficits arise from similar genetic/environmental origins. All these theories have some empirical support.
When symptoms of two or more conditions are shared, whatever the psychological mechanisms (whether or not there are shared underlying cognitive deficits, and /or genetic and neurological differences) then the area of functioning that is highlighted as a problem may depend on which tests are administered. In our recent research we followed a six year old child who was assessed by three educational psychologists and one multidisciplinary team, each blind to the findings of the others. One concluded that the child had dyspraxia, two that the child had dyslexic difficulties, and a third that borderline AS was likely. We interpreted these differences in the use of diagnostic labels as dependent on settings that varied during assessments, and assessment methods that exposed different types of behaviour (Russell, Norwich, & Gwernan-Jones, 2012). This work suggests that which diagnosis is assigned depends to some extent on social and cultural factors as well as actual symptoms. If a child has symptoms of several disorders, then one context or test may draw out symptoms associated with one disorder, whereas another setting may expose symptoms of another. Thus for co-occurring symptoms it is difficult to differentiate between disorders and the likelihood that a co-morbid disorder will be missed is increased. This emphasizes the need for assessment in multiple settings and reassessment over time.
One of the most compelling cross cultural descriptions of how autism is regarded across various cultures was the book
Our own work suggests that since the 1980s, the recorded prevalence of both ASD and ADHD in the UK has increased dramatically. We examined data from both the Millennium Cohort Study, (the large cohort of around 19,000 children who have been followed from their birth through to seven years old and beyond), and another cohort, called the British Cohort Study, where children were born thirty years previously. Both cohorts were representative of the UK as a whole, and medical reports of both ASD and ADHD were given when children were age seven for in 2007-9 and ten in 1980. The results from 2007 contrasted with the 1980 sample at age 10. Only 11 children in the 1970 British Cohort Study were reported as having ADHD in their medical exam, giving an estimated prevalence of 0.083%. The autism diagnosis was rarely used with just 3 children assigned the label; 0.023% of children. A number of other child psychiatric diagnoses were available and many of these were diagnosed during the medical exams. Details of these alternative labels are given in Table 1.
\n\t\t\t\t | \n\t\t\t\n\t\t\t\t | \n\t\t\t\n\t\t\t\t | \n\t\t
Autism (299.0/1/8/9) | \n\t\t\t3 | \n\t\t\t0.023 | \n\t\t
ADHD (314.00/01, 314.9) | \n\t\t\t11 | \n\t\t\t0.083 | \n\t\t
Disturbance in emotions (313) | \n\t\t\t7 | \n\t\t\t0.053 | \n\t\t
Delays in development: Reading (315.0) | \n\t\t\t13 | \n\t\t\t0.098 | \n\t\t
Delays in learning & development (315.2/8/9/5) | \n\t\t\t81 | \n\t\t\t0.614 | \n\t\t
Delays in language (315.3) | \n\t\t\t62 (1 autism co-morbid) | \n\t\t\t0.462 | \n\t\t
Impulse control (312.3/9) | \n\t\t\t1 | \n\t\t\t0.007 | \n\t\t
Mild mental retardation (317) | \n\t\t\t34 (1 ADHD co-morbid) | \n\t\t\t0.258 | \n\t\t
Other specified delays in development (318) | \n\t\t\t22 (1 ADHD co-morbid) | \n\t\t\t0.166 | \n\t\t
Unspecified delays in development (319) | \n\t\t\t25 (1 ADHD co-morbid) | \n\t\t\t0.379 | \n\t\t
Total | \n\t\t\t259 | \n\t\t\t1.961 | \n\t\t
Named conditions using ICD-9 categories for 10 year old children in 1980 (n=13201).
Among the 14,043 children in the 2007 cohort, 209 (1.49%) were reported to have ASD, and 180 (1.28%) were reported having been given an ADHD diagnosis by a clinician (unweighted figures). There was disproportional stratification in the Millennium Cohort, meaning that all analyses were weighted to account for the clustering and over-inclusion of participants from disadvantaged areas. After weighting, 1.7 % of children were reported as having an ASD (95% CI, 1.4-1.99). 1.3% of these were boys, and 0.25% girls, giving boy girl ratio of approx 5:1 for ASD. Surprisingly, the figure for ADHD was lower. After weighting, 1.4% of the population were reported as having ADHD (95% CI, 1.2-1.7). Of these, 2.3% were boys and 0.25% girls, giving a gender ratio of approximately of 1 girl to every 4 boys with ADHD.
One interpretation of the historical shift is that diagnostic substitution has occurred: children with similar symptoms in 1980 may have been more likely to receive generalised labels of ‘delays in learning & development’ than ASD or ADHD. So changing diagnostic practice, cultural factors and context may do much to explain both co-morbidity and rising prevalence. The steep rise in children assigned these diagnoses cannot be totally explained by the substitution mechanism- twice as many children were given either ASD or ADHD diagnoses in 2009 as the total number diagnosed with any type of developmental disorder in 1980.
Context also has a big part to play in the identification of difficulties, in terms of what is considered to be ‘disordered’. Social constructionists have also pointed out that the conceptualization of difficulties associated with both dyslexia and ASD as ‘disorders’ is itself a product of social and cultural standards, and of course the definition of each disorder has changed over time. This has prompted calls for the term autism spectrum ‘conditions’ to replace autism spectrum ‘disorders’ (2009). Our own analysis of the Millennium Cohort has shown a strong association between ADHD and poverty, reflecting findings from US studies which have also found differing levels of ADHD amongst various ethnic groups- Hispanic children were more likely to be identified with ADHD in a study by Akinbami et al. (2011). It is unclear whether this is entirely due to greater awareness and access to health care in some groups, differential reporting about the same level of difficulties between ethnic groups or whether children in different groups have truly varying symptom levels (Boyle et al., 2011). A study by Cuccaro et al. (1996) showed the nature of diagnosis of developmental disorders varied according to the socio-economic status of the child’s family; autism was more likely to be identified in children of higher income families, although no biases of SES were found for identification with ADHD. Cooper (2001) points out that the behaviour symptomatic of ADHD becomes problematic where high value is placed on ability to remain sedentary and sustain attention on tasks, in other words, in schools. Hulme and Snowling (2009) describe how differences of this nature must therefore be thought of as
Two conclusions can be drawn. First, co-morbidities between developmental disorders are common, and second, the causes of these overlapping difficulties are likely to be complex, multifactorial and interacting. Firstly, the high overlap between symptoms of different developmental disorders has been identified in a number of studies and there is an international consensus on this overlap. Studies from Canada, the UK, USA and Scandinavia all show how hard it is provide an unequivocal diagnosis, leading to the quote from Kaplan and her colleagues (2001)
Secondly, in considering the reasons for co-morbidities, a complex bio-psycho-social model is required that leads to symptoms that may result in diagnosis. The nature of the diagnosis itself may depend on social context as well as an individual child’s behaviour. A hint of this complexity is achieved in Figure 3, which is a schematic diagram of various potential causal pathways. It is plausible that the same underlying genetic or neurological mechanisms may underlie co-occurrence of dyslexia, ADHD and ASD. The reverse pathways are not at first so obvious. But recent advances in systems biology have shown that the environment of the cell affects gene expression and protein synthesis at molecular levels. Thus environmental influences can alter ‘core’ biology: for example Mack and Mack (1992) describe how tweaking rats’ whiskers changes gene expression in the sensory cortex. In systems theory, genetic influences are conceptualised more like a set of piano keys on which notes may be played or not played, played slowly or quickly, and there is enormous variation in the music produced even with the same basic set of keys. So the cellular environment can affect genetic expression. A simplified model underlying much behaviour genetics research envisages a direct linear relationship between individual genes and behaviours. The reality is likely to be far more complex with gene networks and multiple environmental factors impacting brain development and function, which in turn will influence behaviour (Hamer, 2002). Karmiloff-Smith (2007) emphasizes how learning and experience effects gene expression in humans. Such scholars demonstrate that the social can affect the biological as well as the more intuitive path of genetic origin leading to neurological development leading to aberrant behaviour. Diagnosis itself may influence behaviour too, through differential treatment and interventions. Thus the pervasive developmental environment is composed of many related factors, environmental stresses, and genetic predispositions, and the social contexts all of which may interact to produce developmental outcomes that themselves may contribute to predicting ongoing child development.
Schematic of interacting causal mechanisms for co-morbidity.
Snowling (2012) suggests a new dimensional classification of disorder, where deficits in different components of learning are seen as additive, impacting on the potential for remediation, rather than classing children into dichotomous ‘disorder’ categories. Taylor (2011) notes that for many children, it is better to think of changes in cognitive style, learning and motivation rather than symptoms. Both conclude that it is important to examine children for evidence of co-occurring disorders, and not simply continue to examine the areas which we expect to be impaired according to categorization. The practical application of assessing children for a range of difficulties is that children will be best helped not by any all encompassing diagnosis, but by individual analysis of their strengths and weaknesses. Future research may be wise to focus on the individual profiles of children across a broad range of areas, looking at the unique strengths, as well as the weaknesses of the individual children, so that parents and educators may adapt their support accordingly, regardless of the diagnostic label a child receives.
Chronic myeloproliferative disorders are a group of clonal diseases of the stem cell. It is a group of several diseases with some common features. They derive from a multipotential hematopoietic stem cell. A clone of neoplastic cells in all these neoplams is characterized by a lower proliferative activity than that of acute myeloproliferative diseases. In each of these diseases, leukocytosis, thrombocythemia, and polyglobulia may appear at some stage, depending on the diagnosis [1, 2].
The research on interferon has been going on since the 1950s [3]. Then, the attention was paid to its influence on the immune system. It has been noted that it can exert an antiproliferative effect by stimulating cells of the immune system [4]. In 1987, a publication by Ludwig et al. was published, which reported the effectiveness of interferon alpha in the treatment of chronic myeloproliferative disorders [5].
More and more new studies have been showing the effectiveness of interferon alpha in reducing the number of platelets, reducing the need for phlebotomies in patients with polycythemia vera and also in reducing the number of leukocytes. Moreover, interferon reduced the symptoms of myeloproliferative disorders such as redness and itching of the skin. Additionally, it turned out to be effective in reducing the size of the spleen.
Further studies on the assessment of remission using molecular-level response assessments indicate that the interferon action in chronic myeloproliferation diseases targets cells from the mutant clone with no effect on normal bone marrow cells [6].
Over the years, interferon alpha-2a and interferon alpha-2b have been introduced into the treatment of chronic myeloproliferation, followed by their pegylated forms. The introduction of pegylated forms allowed for a reduction in the number of side effects and less frequent administration of the drug to patients. In recent years, monopegylated interferon alpha-2b has been used to further increase the interval between drug administrations while maintaining its antiproliferative efficacy.
The exact mechanism of action of interferon alpha in the treatment of chronic myeloproliferative disease is still not fully understood, but it has an impact on JAK2 (Janus Kinase) signal transducers and activates the STAT signal pathway (Janus Kinase/SignalTransducer and Activator of Transcription).
Interferon alpha binds to IFNAR1 and IFNAR2c, which are type I interferon receptors. Interferon alpha has an impact on JAK2(Janus Kinase) signal transducers and activates the STAT signal pathway. The disturbances in this signaling pathway are observed in chronic myeloproliferative disorders [7].
Interferon inhibits the JAK-STAT signaling pathway by directly inhibiting the action of thrombopoietin in this pathway [8].
So far, three driver mutations have been described in the course of chronic myeloproliferative diseases that affect the functioning of the JAK-STAT pathway.
JAK2 kinase and JAK1, JAK3, and TYK2 kinases belong to the family of non-receptor tyrosine kinases. They are involved in the intracellular signal transduction of the JAK-STAT pathway. It is a system of intracellular proteins used by growth factors and cytokines to express genes that regulate cell activation, proliferation, and differentiation. The mechanism of JAK activation is based on the autophosphorylation of tyrosine residues that occurs after ligand binds to the receptor. JAK2 kinase transmits signals from the hematopoietic cytokine receptors of the myeloid lineage (erythropoietin, granulocyte-colony stimulating factor thrombopoietin, and lymphoid lineage [9].
A somatic G/T point mutation in exon 14 of the JAK2 kinase gene converts valine to phenylalanine at position 617 (V617F) in the JAK2 pseudokinase domain, which allows constitutive, ligand-independent activation of the receptor to trigger a proliferative signal [10].
Mutation of the MPL gene, which encodes the receptor for thrombopoietin, increases the sensitivity of magekaryocytes to the action of thrombopoietin, which stimulates their proliferation [11].
Malfunction of calreticulin as a result of mutation of the CARL gene leads to the activation of the MPL-JAK/STAT signaling pathway, which is independent of the ligand, as calreticulin is responsible, for the proper formation of the MPL receptor. Consequently, there is a clonal proliferation of hematopoietic stem cells [12].
Below, we provide an overview of some clinical studies on the efficacy of interferon in chronic myeloproliferative disorders.
Polycythemia vera (PV) is characterized by an increase in the number of erythrocytes in the peripheral blood.
Polycythemia vera is caused by a clonal mutation in the multipotential hematopoietic stem cell of the bone marrow. The mutation leads to an uncontrolled proliferation of the mutated cell clone, independent of erythropoietin and other regulatory factors. As the mutation takes place at an early stage of hematopoiesis, an increase of the number of erythrocytes as well as of leukocytes and platelets is observed in the peripheral blood. The cause of proliferation in PV independent from external factors is a mutation in the Janus 2 (JAK2) tyrosine kinase gene. The V617F point mutation in the JAK2 gene is responsible for about 96% mutation, and in the remaining cases the mutation arises in exon 12. Both mutations lead to constitutive activation of the JAK-STAT signaling pathway [13].
As a result of the uncontrolled proliferation, blood viscosity increases, which generates symptoms such as headaches and dizziness, visual disturbances, or erythromelalgia. As the number of all hematopoietic cells, including the granulocytes ones, increases, the difficult to control symptoms of their hyperdegranulation may appear, among which gastric ulcer or skin itching is often observed. During the disease progression, the spleen and liver become enlarged.
The most common complication of the disease is episodes of thrombosis, especially arterial one. During the course of the disease, it can also evolve into myelofibrosis or acute myeloid leukemia.
The treatment of PV is aimed at preventing thromboembolic complications, relieving the general symptoms, the appearance of hepatosplenomegaly as well as preventing its progression.
Each patient should receive an antiplatelet drug chronically, and usually acetylsalicylic acid is the choice. Most often, the treatment is started with phlebotomy in order to rapidly lower the hematocrit level. If cytoreductive therapy is necessary, the drugs of first choice are hydroxycarbamide and interferon [2].
However, the research on the mechanism of the action of interferons is still ongoing. In vitro studies with CD34+ cells from peripheral blood of patients diagnosed with polycythemia vera showed that interferon inhibits clonal changed cells selectively. It was found that interferon alpha-2b and pegylated interferon alpha-2a reduce the percentage of cells with JAK2 V617F mutation by about 40%. Pegylated interferon alpha-2a works by activating mitogen-activated protein kinase P38. It affects CD34+ cells of patients with polycythemia vera by increasing the rate of their apoptosis [6].
A case of a patient with PV with a confirmed chromosomal translocation t(6;8) treated with interferon alpha-2b, which resulted in a reduction of the clone with translocation by 50% from the baseline value, was also described [14].
In 2019, the results of a phase II multicenter study were published, which aimed at assessing the effectiveness of recombinant pegylated interferon alpha-2a in cases of refractory to previously hydroxycarbamide therapy. The study included 65 patients with essential thrombocythemia (ET) and 50 patients with polycythemia vera. All patients had previously been treated with hydroxycarbamide and showed resistance to this drug or its intolerance.
The assessment of the response was performed after 12 months of treatment. Overall response rate to interferon was higher in patients diagnosed with ET than in patients with polycythemia vera. In essential thrombocythemia, the percentage of achieved complete remissions was 43 and 26% of partial remissions. The remission rate in ET patients was higher if calreticulin CALR gene mutation was present. Patients with polycythemia vera achieved complete remission in 22% of cases and partial remission in 38% of cases.
Treatment-related side effects that follow to discontinuation of treatment were reported in almost 14% of patients [15].
The duration of response to treatment with pegylated interferon alpha-2a and the assessment of its safety in long-term use in patients with chronic myeloproliferative disorders was the goal of a phase II of the single-center study. Forty-three adult patients with polycythemia vera and 40 patients with essential thrombocythemia were enrolled in the study. The complete hematological response was defined as a decrease in hemoglobin concentration below 15.0 g/l, without phlebotomies, a resolution of splenomegaly, and no thrombotic episodes in the case of PV, and for essential thrombocythemia—a decrease platelet count below 440,000/μl and two other conditions as above. The assessment of the hematological response was performed every 3–6 months. The median follow-up was 83 months.
The hematological response was obtained in 80% of cases for the entire group. In patients with polycythemia vera, 77% of patients achieved a complete response (CR) while 7% a partial response (PR). The duration of response averaged 65 months for CR and 35 months for PR. In the group of patients diagnosed with essential thrombocythemia, CR was achieved in 73% and PR in 3%. The durance of CR was 58 months and PR was 25 months.
The molecular response for the entire group was achieved in 63% of cases.
The overall analysis showed that the duration of hematological remission and its achievement with pegylated interferon alpha-2a treatment is not affected neither by baseline disease characteristics nor JAK2 allele burden and disease molecular status. There was also no effect on age, sex, or the presence of splenomegaly.
During the course of the study, 22% of patients discontinued the treatment, because of toxicity. Toxicity was the greatest at the beginning of treatment. The starting dose was 450 μg per week and was gradually tapered off.
Thus, on the basis of the above observations, the researchers established that pegylated interferon alpha-2a may give long-term hematological and molecular remissions [16].
The assessment of pegylated interferon alpha-2a in group of patients diagnosed with polycythemia vera only was performed. The evaluation was carried out on a group of 27 patients. Interferon decreased the JAK2 V617F allele burden in 89% of cases. In three patients who were JAK2 homozygous at baseline, after the interferon alpha-2a treatment wild-type of JAK2 reappeared. The reduction of the JAK2 allele burden was estimated from 49% to an average 27%, and additional in one patient the mutant JAK2 allele was not detectable after treatment. It can therefore be postulated that the action of pegylated interferon alpha-2a is directed to cells of the polycythemia vera clone [17].
In 2005, the results of treatment by pegylated interferon alpha-2b of 21 patients diagnosed with polycythemia vera and 21 patients diagnosed with essential thrombocythemia were published. In the case of polycythemia vera in 14 patients, PRV-1 gene mutation was initially detected. In 36% of cases, PRV-1 expression normalized after treatment with pegylated interferon alpha-2b. For the entire group of 42 patients, the remission assessment showed that complete remission was achieved in 69% cases after 6 months of treatment. However, only in 19 patients remission was still maintained 2 years after the start of the study. Pegylated interferon alpha-2b was equally effective in patients with PV and ET. The use and the type of prior therapy did not affect the achievement of remission [18].
Another study with enrolled only PV patients included 136 patients. They were divided into two arms. One group received interferon alpha-2b and the other group received hydroxycarbamide. Interferon dosage was administered in 3 million units three times a week for 2 years and then 5 million units two times a week. Hydroxycarbamide was administered at a dose between 15 and 20 mg/kg/day.
In the group of patients treated with interferon, a significantly lower percentage of patients developed erythromelalgia (9.4%) and distal parasthesia (14%) compared with the group treated with hydroxycarbamide, for whom these percentages were respectively: 29 and 37.5%. Interferon alpha-2b was found to be more effective in inducing a molecular response, which was achieved in 54.7% of cases, in comparison with hydroxycarbamide—19.4% of cases, despite the fact that the percentage of achieved general hematological responses did not differ between the groups and amounted about 70%. The 5-year progression free period in the interferon group was achieved in a higher percentage (66%) than in the hydroxycarbamide group (46.7%) [19].
The most recent form of interferon approved by the
Thanks to these changes to the structure of the molecule, it was possible to achieve a significant increase in its half-life. Ropeginterferon can be administered subcutaneously to patients every 14 days. The clinical trials conducted so far have assessed the ropeginterferon dose from 50 micrograms to a maximum dose of 500 microgams administered as standard every 2 weeks. The possible dose change in case of side effects includes not only the reduction of the drug dose itself, but also the extension of the interval between doses. The extension of the dosing interval up to 4 weeks was assessed.
Ropeginterforn was approved in 2019 by the EMA for the use in patients diagnosed with polycythemia vera without splenomegaly, as monotherapy.
Ropeginterferon, like the previous forms of interferons used in treatment, is contraindicated in patients with severe mental disorders, such as severe depression. It is also a contraindication in patients with noncompensatory standard treatment of disorders of the thyroid gland as well as severe forms of autoimmune diseases. The safety profile of ropeginterferon is similar to that of other forms of alpha interferons. The most common side effects are flu-like symptoms [20].
Ropeginterferon has been shown to exhibit in vitro activity against JAK2-mutant cells. The activity of ropeginterferon against JAK2-positive cells is similar to that of other forms of interferons used actually for standard therapy. Ropeginterferon has an inhibitory effect on erythroid progenitor cells with a mutant JAK2 gene. At the same time, it has almost no effect on progenitor cells without the mutated allele (JAK2-wile-type) and normal CD34+ cells. A gradual decrease of JAK2-positive cells was observed in patients with PV during ropeginterferon treatment. The examination was performed after 6 and 12 months of treatment. In comparison, the reduction in the percentage of JAK2 positive cells in patients treated with hydroxycarbamide was significantly lower.
These results may suggest that ropeginterferon may cause elimination of the mutant clone, but further prospective clinical trials are needed to confirm this theory. The evaluation was performed on a group of patients enrolled in the PROUD-PV study who were treated in France [21].
In 2017, a multicenter study was opened in Italy. The study was of the second phase. In total, 127 patients with polycythemia vera were included in the study. All patients enrolled on the study had low-risk PV. The clinical trial consisted of two arms. Patients received phlebotomies and low-dose aspirin in one arm and ropeginterferon in the other arm. The aim of the study was to achieve a hematocrit of 45% or lower without any evidence of disease progression. Ropeginterferon was administered every 2 weeks at a constant dose of 100 μg.
The response to the treatment was assessed after 12 months. The reduction of hematocrit to the assumed level was achieved in significantly higher percentage of patients in the ropeginterferon group than of patients who received only phlebotomies and aspirin. In addition, none of the patients treated with ropeginterferon experienced disease progression during the course of the study, while among those treated with phlebotomies, 8% of patients progressed.
Grade 4 or 5 adverse events were not observed in patients treated with ropeginterferon, and the incidence of remaining adverse event (AE) was small and comparable in both arms. The most common side effects in the ropeginterferon group were flu-like symptoms and neutropenia; however, the third-grade neutropenia was the most common (8% of cases) [22].
One of the most important clinical studies on the use of ropeginterferon was the PROUD-PV study and its continuation: the CONTINUATION-PV study. These were three-phase, multicenter studies. The aim of the study was to compare the effectiveness of ropeginterferon in relation to hydroxycarbamide. The study included adult patients diagnosed with polycythemia vera treated with hydroxycarbamide for less than 3 years and no cytoreductive treatment at all. In total, 257 patients received this treatment. The patients were divided into two groups: those receiving ropeginterferon or the other being given hydroxycarbamide.
During the PROUD-study, drug doses were increased until the hematocrit was achieved below 45% without the use of phlebotomies, and the normalization of the number of leukocytes and platelets was reached.
The PROUD-PV study lasted 12 months. After this time, the patients continued the treatment under the CONTINUATION-PV study for further 36 months. After the final analysis performed in the 12th month at the end of PROUD study, it was found that the hematological response rates did not differ between the ropeginterferon and hydroxycarbamide treatment groups. These were consecutively 43% in the ropeginterferon arm and 46% in the control arm.
However, after analyzing the CONTINUATION- PV study, it turned out that after 36 months of treatment, the rates of hematological responses begin to prevail in the group of patients receiving ropeginterferon, 53% versus 38% in the control group. Thus, from the above data, it can be seen that the response rate to ropeginterferon increases with the duration of treatment [23].
Another analysis of patients participating in the PROUD and CONTINUATION studies was based on the assessment of treatment results after 24 months, dividing patients into two groups according to age (under and over 60 years).
The initial comparison of both groups of patients showed that older patients had a more aggressive course of the disease. Patients over 60 years of age had a higher percentage of cells with a mutant JAK2 allele. They experienced both general symptoms and some complications, such as thrombosis, more frequently. Both patients under 60 years of age and over 60 years of age in the ropeginterferon arm had a higher rate of molecular response, namely 77.1 and 58.7% compared with the HU remission: 33.3 and 36.1%, respectively. Significantly higher reductions in the JAK2 allele were observed in both groups of patients after ropeginterferon treatment: it was 54.8% for younger patients and 35.1% for elderly patients. For comparison, this difference in the group of patients treated with HU was 4.5 and 18.4%, respectively.
What is more, the age did not affect the frequency of ropeginterferon side effects. In addition, the incidence of adverse ropeginterferon disorders was similar to that observed in the hydroxycarbamide group [24].
Essential thrombocythemia is a clonal growth of multipotential stem cells in the bone marrow. The consequence of this is increased proliferation of megakaryocytes in the bone marrow and an increase in the number of platelets in the peripheral blood. The level of platelets above 450,000/μl is considered a diagnostic criterion.
Essential thrombocythemia may progress over time to a more aggressive form of myeloproliferation, i.e., myelofibrosis. The disease can also evolve into acute myeloid leukemia or myelodysplastic syndrome, both with very poor prognosis. Thromboembolic complications are serious, and they concern over 20% of patients. Thrombosis occurs in the artery and venous area. Moreover, in patients with a very high platelet count, above 1,000,000/μl, bleeding may occur as a result of secondary von Willebrand syndrome [1, 2].
The treatment of ET is primarily aimed to prevent thrombotic complications.
In low-risk patients, only acetylsalicylic acid is used. In cases of high-risk patients, hydroxycarbamide is the first-line drug for most patients. Anagrelide and interferon are commonly used as second-line drugs.
Due to the possible effects of hydroxycarbamide of cytogenetic changes in the bone marrow cells after long-lasting usage, some experts recommend the use of interferon in younger patients in the first line. Interferon is also used as the drug of choice in patients planning a pregnancy [25].
The efficacy of pegylated interferon alpha-2a was assessed on the basis of the group of 39 patients with essential thrombocythemia and 40 patients with polycythemia vera.
Of the overall group, 81% of patients were previously treated prior to the study entry. The patients received pegylated interferon alpha-2a in a dose of 90 μg once a week. The dose of 450 μg was associated with a high percentage of intolerance.
In patients with essential thrombocythemia, the complete remission was achieved in 76%, while the overall hematological response rate brought 81%. Moreover, the molecular remission was achieved in 38%, in 14% of cases, JAK2 transcript became not detectable.
Patients diagnosed with polycythemia vera achieved 70% complete hematological remission and 80% general hematological response to treatment. JAK2 transcript was undetectable in 6% of patients. Molecular remission was achieved in 54% of cases.
Pegylated interferon alpha-2a at the dose of 90 μg per week was very well tolerated. In total, 20% of patients experienced a grade of 3 or 4 of adverse reaction, which was neutropenia. In addition, an increase in liver function tests was observed. Grade 4 of AE was not observed among patients who started the treatment with 90 μg/week while grade 3 neutropenia was an adverse event in only 7% of cases [26].
The effect of interferon alpha-2b treatment in patients with ET and PV was investigated. The study was prospective. Some of the results concerning the group of patients with polycythemia vera are presented in the subsection on polycythemia vera. In total, 123 patients with diagnosed essential thrombocythemia participated in the study. All of them received interferon alpha-2b. The patients were divided into two groups depending on the presence of the JAK2 V617F mutation. The enrolled patients were between 18 and 65 years of age. The treatment they received was, sequentially, interferon alpha-2b in the dose of 3 million units three times a week for the first 2 years, after which time the dose was changed into a maintenance dose, which amounted to 5 million units two times a week.
The analysis showed that the patients with the JAK2 V617F mutation present in a higher percentage achieved an overall hematological response as well as a complete hematological response. The overall hematological response was achieved in 83% of patients with JAK2 mutation, and the complete hematological remission was achieved in 23 cases. In the group of ET patients without the JAK2 V617F mutation, overall hematological response was achieved in 61.4%, while the complete hematological remission was achieved in 12 patients. The 5-year progression-free survival was obtained in 75.9% in the JAKV617F group and only in 47.6% without the mutation.
A significant proportion of patients experienced mild side effects. Grade 3 and 4 of adverse events were severe, most of them being a fever. The isolated cases of elevated liver tests and nausea have also been reported [19].
Pegylated interferon alpha-2b in patients with essential thrombocythemia who were previously treated with hydroxycarbamide, anagrelide, and other forms of interferon alpha, however, due to the lack of efficacy or toxicity, the patients required a change of treatment, was assessed. Pegylated interferon alpha-2b turned out to be effective in these cases. It led to the complete hematological remission in 91% of patients after 2 months of therapy, and in 100% of patients after 4 months. However, merely 11 patients participated in the study. Also only two patients required treatment discontinuation due to the side effects such as depression and general fatigue grade 3 [27].
In case of pregnant patients, interferon is currently considered the only safe cytoreductive drug. Over the years, several analyses of the results of interferon treatment during pregnancy have been carried out.
The assessment of 34 pregnancies in 23 women diagnosed with ET was performed retrospectively. All the pregnancies included in the analysis were of high risk. This high risk was associated with a high platelet count above 1,500,000/μl, a history of thrombotic episode, severe microcirculation disorders, or a history of major hemorrhage.
It turned out that the use of interferon allowed the birth of an alive child in 73.5% of cases. There was no difference in efficacy between the basic and pegylated forms of interferon alpha. In pregnancies without interferon treatment, the percentage of live births was only 60%. Moreover, it was not found if the presence of the JAK2 V617F mutation had any influence on the course of pregnancy [28].
An analysis of the course of pregnancy in patients with ET was assessed in Italy. Data from 17 centers were taken into account. Data from 122 pregnancies were collected from 92 women. In patients diagnosed with essential thrombocythemia, the risk of the spontaneous loss of pregnancy is about 2.5 times higher than among the general population. In the contrary to the study quoted above, it was found that the presence of the JAK2 mutation increases the risk of pregnancy loss. The proportion of live births in patients exposed to interferon during pregnancy was 95%, compared with 71.6% in the group of patients not treated with interferon.
The multivariate analysis also showed that the use of acetylsalicylic acid during pregnancy had no effect on the live birth rate of patients with ET [29].
Whatever its form, interferon is the drug of first choice in pregnancy. Hydroxycarbamide and anagrelide should be withdrawn for about 6 months, and at least for 3 months, before the planned conception. Experts recommend the use of interferon in high-risk pregnancies [30]. A Japanese analysis of 10 consecutive pregnancies in ET patients showed 100% live births in patients who received interferon [31].
In myelofibrosis (MF), monoclonal megakaryocytes produce cytokines that stimulate the proliferation of normal, non-neoplastic fibroblasts and stimulate angiogenesis. The consequence of this is the gradual fibrosis of the bone marrow, impaired hematopoiesis in the bone marrow, and the formation of extramedullary location mainly in the sites of fetal hematopoiesis, i.e., in the spleen and the liver.
The production of various cytokines by neoplastic megakaryocytes leads to the proliferation of normal, noncancerous fibroblasts as well as to increased angiogenesis.
Progressive bone marrow fibrosis leads to worsening anemia and thrombocytopenia. On the other hand, the production of proinflammatory cytokines by megakaryoblasts leads to the general symptoms such as weight loss, fever, joint pain, night sweats, and consequently, progressive worsening of general condition.
The prognosis for myelofibrosis is poor. In about 20% of patients, myelofibrosis evolves into acute myeloid leukemia with poor prognosis.
Currently, the only effective method of treatment that gives a chance to prolong the life is allogeneic bone marrow transplantation. However, this method is only available to younger patients.
The goal of treatment of patients who have not been qualified for allotranspalntation is to reduce the symptoms and to improve the patient’s quality of life. In case of leukocytosis cytoreducing drugs, such as hydroxycarbamide, melphalan, or cladribine can be used. They cause a reduction in the number of leukocytes and may, to some extent, inhibit splenomegaly. Interferon alpha has been used successfully for the treatment of myelofibrosis for many years. The results of its effectiveness will be presented below [2].
Currently, the JAK2 inhibitor ruxolitinib is approved for the treatment of myelofibrosis with enlarged spleen in intermediate and high-risk patients. Ruxolitinib reduces the size of the spleen, reduces general symptoms, and improves the quality of life; however, it does not prolong the overall survival of patients [32].
In 2015, the results of a retrospective study were published to compare the histological parameters of the bone marrow before and after interferon treatment. Twelve patients diagnosed with primary myelofibrosis as well as post-PV MF and post-ET MF were enrolled in the study. Patients were treated with pegylated recombinant interferon alpha-2a or recombinant interferon alpha-2b in standard doses. The time of treatment was from 1 to 10 years. Some patients had previously been treated with hydroxycarbamide or anagrelide. In all cases, karyotype was normal. The prognostic factor of Dynamic International Prognostic Scoring System (DIPSS) was assessed at the beginning as well as during the treatment.
Bone marrow cellularity decreased in cases with increased bone marrow cellularity before the treatment. After the interferon treatment, a reduction in the degree of bone marrow fibrosis was found. The parameters, such as the density of naked nuclei and the density of megakaryocytes in the bone marrow, also improved.
It proves that if the JAK2 V617F mutation had been present, DIPSS was decreased after interferon treatment. This relationship was not observed in patients without the JAK2 V617F mutation. The improvement in peripheral blood morphological parameters and the overall clinical improvement correlated with the improvement in the assessed histological parameters of the bone marrow.
Before the initiation of interferon, seven patients had splenomegaly. During the treatment with interferon, the complete resolution of splenomegaly was achieved in 17% of patients (two cases), and its size decreased in 25% (three cases). A good clinical response was achieved in 83% during interferon therapy. There was no significant difference in response between the two types of interferon used [33].
A prospective study was also conducted in patients with low and intermediate-1 risk group myelofibrosis. Seventeen patients were enrolled. Patients received interferon alpha-2b (0.5–3 milion units/three times a week) or pegylated interferon alpha-2a (45–90 μg/week). The duration of therapy was on average 3.3 years.
Most of the patients responded to the treatment. Partial remission was found in seven patients and complete remission in two patients. Moreover, in four cases, the disease was stabilized and in one case the clinical improvement was achieved. Three patients did not respond to treatment at all and progressed to myelofibrosis. Additionally, the assessment in reducing spleen size was performed. At baseline, 15 patients have splenomegaly, nine of them achieved the compete regression of spleen size [34].
However, the efficacy of interferon in the treatment of myelofibrosis appears to be limited only to a less advanced form, when the bone marrow still has an adequate percentage of normal hemopoiesis and the marrow stroma is not significantly fibrotic. In more advanced stages, interferon was not shown to have any significant effect on the regression of the fibrosis process [35].
In 2020, the results of the COMBI study were published. That was a two-phase, multicenter, single-arm study that investigated the efficacy and safety of the combination of ruxolitinib and pegylated interferon alpha. Thirty-two patients with PV and 18 patients with primary and secondary myelofibrosis participated in the study. The patients were at age 18 and older. Remission was achieved in 44% of myelofibrosis cases, including 28% (5 patients) of complete remission. In patients with PV, the results were slightly worse: 31% of remissions, including 9% of complete remissions. Patients received pegylated interferon alpha-2a (45 μg/week) or pegylated interferon alpha-2b (35 μg/week) in low doses and ruxolitinib in doses of 5–20 mg twice a day.
For the entire group of patients (with PV and MF), the initial JAK2 allele burden was 47% at baseline, and after 2 years of treatment with interferon and ruxolitinib, it decreased to 12%.
The treatment toxicity was low. The highest incidence of side effects occurred at initiation of therapy. It was mostly anemia and thrombocytopenia.
The observations from the COMBI study show that, for the combination of interferon in lower doses with ruxolitinib, it may be effective and well tolerated even in the group of patients who had intolerance to interferon used as the only drug in higher doses. The combined treatment improved the bone marrow in terms of fibrosis and its cellularity. It also allowed to improve the value of peripheral blood counts [36].
It is currently known that some of the additional mutations are associated with a worse prognosis in patients with myelorpoliferation, including patients with myelofibrosis. Some of these mutations have been identified as high-risk molecular mutations. These are ASXL1, EZH2, IDH1/2, or SRSF2. Earlier studies have shown their association with a more aggressive course of the disease, worse prognosis, and shorter survival of patients, as well as a poorer response to treatment. Due to their importance, they have been included in the diagnostic criteria of myelofibrosis [37].
It is also known that the presence of driver mutations, i.e., JAK2, CALR, and MPL or triple negativity, may affect the course of myeloproliferation, including the incidence of thromboembolic complications.
The assessment of the influence of driver mutations and a panel of selected additional mutations on the effectiveness of interferon treatment in patients with myelofibrosis was performed on a group of 30 patients. Only the patients with low- and intermediate-1-risk were enrolled in the study. The treatment with pegylated interferon alpha-2a or interferon alpha-2b resulted in a complete remission in two patients and partial remission in nine patients. The disease progressed in three cases. One patient relapsed and four died. The remaining patients achieved a clinical improvement or disease stabilization. In the studied group, it was not found if the effectiveness of interferon treatment was influenced by the lack of driver mutations. Among the group of four patients with additional mutations, two died and one had disease progression. It was a mutation of ASXL1 and SRSF2. The treatment with interferon in patients without additional molecular mutations in the early stages of the disease may prevent further progression of the disease [38].
The side effects of interferon in the group of patients with myelofibrosis are similar to those occurring after the treatment of other chronic myeloproliferative diseases. The most frequently described are hematological toxicity- anemia and thrombocytopenia, less often is the appearance of leukopenia. Hematological toxicity usually resolves with dose reduction or extension of the dose interval. The most frequently nonhematological toxicity was fatigue, muscle pain, weakness, and depression symptoms. All symptoms are usually mild and do not exceed grade 2 [38].
However, the use of interferon in the treatment of myelofibrosis has not been recommended as a standard therapy. Interferon is still being evaluated in clinical trials, or it is used in selected patients as a nonstandard therapy in this diagnosis.
Mastocytosis is characterized by an excessive proliferation of abnormal mast cells and their accumulation in various organs.
The basis for the development of mastocytosis is ligand-independent activation of the KIT receptor, resulting from mutations in the KIT proto-oncogene. The KIT receptor is a trans membrane receptor with tyrosine kinase’s activity. Its activation stimulates the proliferation of mast cells. That excessive numbers of mast cells infiltrate tissues and organs and release mediators such as histamine, interleukine-6, tryptase, heparin, and others, which are responsible for the appearance of symptoms typical of mastocytosis. In addition, the infiltration of tissues for mast cells itself causes damage to the affected organs.
The prognosis of mastocytosis depends on the type of the disease. In the case of cutaneous mastocytosis (CM), in the majority of cases prognosis is good and the disease does not shorten the patient’s life, but in aggressive systemic mastocytosis (ASM), the average follow-up is about 40 months. Mast cell leukemia has a poor prognosis with a median follow-up of approximately 1 year.
Systemic mastocytosis usually requires the implementation of cytoreductive therapy. The first line of therapy is interferon alone or its combination with corticosteroids. In aggressive systemic mastocytosis, the first line in addition to interferon 2-CdA can be used. An effective drug turned out to be midostaurin in the case of the present KIT mutation. In patients without the KIT D816V mutation, treatment with imatinib may be effective. In the case of mast cell leukemia, multidrug chemotherapy is most often required, as in acute leukemias, followed by bone marrow transplantation [39].
Systemic mastocytosis requiring treatment is a rare disease, this is why the studies available in the literature evaluating various therapies concern mostly small groups of patients.
In 2002, the French authors presented their experiences on the use of interferon in patients with systemic mastocytosis. They included 20 patients. The patients received interferon alpha-2b in gradually increased doses.
The patients were assessed after 6 months. In cases in which bone marrow was infiltrated for mast cells at baseline, it still remained infiltrated after 6 months of treatment.
However, the responses were obtained in terms of symptoms related to mast cell degranulation. Partial remission was achieved in 35% of patients and minor remission in 30%. It concerns mainly skin lesions and vascular congestion. Moreover, the assessment of the histamine level in the plasma revealed a decrease of it in patients who previously presented symptoms related to the degranulation of mast cells, such as gastrointestinal disorders and flushing.
A high percentage of side effects were found during treatment. They concerned 35% of patients. Depression and cytopenia were most frequent ones [40].
Another analysis was a report of five patients with systemic mastocytosis treated with interferon and prednisolone. All patients received interferon alpha-2b in a dose of 3 million units three times a week and four patients additionally received prednisolone. Four patients responded to interferon treatment at varying degrees. One patient, who at baseline had bone marrow involvement by mast cells in above 10%, progressed to mast cell leukemia. In two patients, the symptoms C resolved completely and in one of them they partially disappeared. In one case, stabilizing disease was achieved [41].
In 2009, a retrospective analysis of patients treated with cytoreductive therapy due to mastocytosis was published. The authors collected data from 108 patients treated at the Mayo Clinic. This analysis allowed for the comparison of the efficacy of four drugs used in systemic mastocytosis. There were interferon alpha alone or in the combination with prednisone—among 40 patients, hydroxycarbamide—among 26 ones, imatinib—among 22 persons, and 2-chlorodeoxyadenosine (2-CdA)—among 22 patients.
After dividing the patients into three additional groups on the basis of the type of mastocytosis—indolent systemic mastocytosis, aggressive systemic mastocytosis, and systemic mastocytosis associated with another clonal hematological nonmast cell lineage disease (SM-AHNMD)—the effectiveness of each of type of therapy was assessed.
The highest response rates in indolent and aggressive mastocytosis were achieved with interferon treatment. They were 60% of the responses in both groups, and in the SM-AHNMD group of patients, the percentage was also one of the highest and amounted to 45%. The second most effective drug was 2-CdA. The response rates were 56% for indolent MS, 50% for aggressive MS, and 55% for SM-AHNMD. The patients treated with imatinib achieved response in 14, 50, and 9% by following groups, respectively. In contrast, patients with indolent and aggressive systemic mastocytosis did not respond to hydroxycarbamide treatment at all. The response rate in both groups was 0%. However, patients with MS associated with another clonal hematological nonmast cell lineage disease achieved 21% response to hydroxycarbamide. Additionally, it was found that only interferon relieved symptoms caused by the release of inflammatory mediators by mast cells.
The additional analysis showed no influence of the TET 2 mutation on the response to treatment [42].
In the literature, there are also single cases of mastocytosis presenting trials of nonstandard treatment. That is description of a patient with systemic mastocytosis with mast cell bone marrow involvement. Mutation of c-kit Asp816Val was present. Patient progressed despite treatment with dasatinib and 2-chlorodeoxyadenosine. The patient developed symptoms related to the degranulation of mast cells and increased ascites.
The patient was treated with pranlukast, which is an anti-leukotriene receptor antagonist due to an asthma episode. The rate of ascites growth decreased significantly after one administration. The patient required paracentesis every 10 days and not every 3 days, as before starting to take the drug. After 15 days of treatment with pranlukast, the patient received interferon alpha, which resulted in complete regression of ascites, resolution of pancytopenia, and complete disappearance of the c-kit mutation clone. The infiltration of mast cells in the bone marrow significantly decreased [43].
Interferon alpha was also effective in a patient with systemic mastocytosis associated with myelodysplastic syndrome with the c-kit D816V mutation, which was refractory to imatinib treatment [44].
Interferon alpha also proved to be effective in the treatment of osteoporotic lesions appearing in the course of mastocytosis.
The series of 10 cases with resolved mastocytosis and osteoporosis-related fractures was presented in 2011. The patients received interferon alpha in a dose of 1.5 million units three times a week as well as pamindronic acid. The patients were treated for an average of 60 months. For the first 2 years, pamindronate was given at a dose of 1 mg/kg every month, and then every 3 months.
During the course of the study, no patient had a new-bone fracture. The level of alkaline phosphatase decreased by 25% in relation to the value before treatment and tryptase by 34%. Bone density increased during treated with interferon and pamindronate. The increase was on average 12% in the spine bones and 1.9% in the hip bones. At the same time, there was no increase in the density of the hip bone and a minimal increase in the density of the spine in patients treated with pamindronate alone.
The results of this observation suggest that it is beneficial to add low doses of interferon alpha to pamindronate treatment in terms of bone density increase [45].
That experiences show that interferon used in systemic mastocytosis significantly improves the quality of life of patients by inhibiting the symptoms caused by degranulation of mast cells. They prevent bone fractures and, in some patients, they cause remission of bone marrow infiltration by mast cells.
Chronic neutrophilic leukemia (CNL) is a very rare disease. It is characterized by the clonal proliferation of mature neutrophils.
The diagnostic criteria proposed by the World Health Organization (WHO) comprise leukocyte counts above 25,000/μl (including more than 80% of rod and segmented
Physical examination often shows enlargement of the liver and spleen, moreover, patients complain on weight loss and weakness [1].
The prognosis varies. The average survival time for patients with CNL is less than 2 years.
Only few descriptions of chronic neutrophilic leukemia are available in the literature, and these are mostly single case reports.
Because it is an extremely rare disease, there are no established and generally accepted treatment standards. In most cases, patients are given hydroxycarbamide or interferon. Patients who are eligible for a bone marrow transplant may benefit from this treatment. Bone marrow allotransplantation remains the only method that gives a chance for a significant extension of life.
The German authors presented a series of 14 cases of chronic neutrophilic leukemia. The group of patients consisted of eight women and six men. The average age was 64.7 years. From the entire group of patients, longer survival was achieved only in three cases. One of these patients was treated with interferon alpha and achieved hematological remission, the other underwent bone marrow allotransplantation from a family donor, and the third one was treated with hydroxycarbamide and transfusions as needed. The follow-up period of the patient after allogeneic matched related donor transplantation (allo-MRD) was 73 months, and for the patient after interferon treatment it was 41 months.
The remaining patients died within 2 years of diagnosis. Six patients, the largest group, died due to intracranial bleeding, three patients died because of leukemia cell tissue infiltration, one patient because of the disease transformation into leukemia, and one patient because of pneumonia [46].
It can be seen from these experiences that treatment with interferon alpha can significantly extend the survival time of patients.
The case of a 40-year-old woman diagnosed with chronic neutrophilic leukemia is presented by Yassin and coauthors. Initially, the patient had almost 41,000 leukocytes in the peripheral blood. In a physical examination, splenomegaly and hepatomegaly were not present. Patient received pegylated interferon alpha-2a. The initially dose was 50 μg once a week for the first 2 weeks, then the dose was increased to 135 μg weekly for 6 weeks, and then the dose interval was extended to another 2 weeks. As a result of the treatment, the general condition of the patient improved and the parameters of peripheral blood counts were normalized [47].
Another case report presented in the literature describes a 41-year-old woman diagnosed with CNL accompanied by focal segmental glomerulosclerosis (FSGS). The patient had increasing leukocytosis for several months. On the admission to the hospital, leukocytosis was 94,000/μl. Moreover, the number of platelets in the morphology exceeded 1,000,000/μl. More than a year earlier, the patient had splenectomy due to splenomegaly and spleen infraction.
Additionally, JAK2 V617F mutation was found. Some authors suggest that the presence of JAK2 mutation may be associated with longer survival in CNL.
The patient received hydroxycarbamide for 3 months and reduction in the number of leukocytes was achieved. After this time, interferon alpha-2b was added to hydroxycarbamide. As a result, focal segmental glomerulosclerosis disappeared and the renal tests improved [48].
Another case of chronic neutrophilic leukemia with a JAK2 gene mutation concerns a 53-year-old man. The patient’s baseline leukocytosis was 33,500/μl, including the neutrophil count of 29,700/μl. The patient also had splenomegaly.
The treatment with interferon alpha-2b at a dose of 3 million units every other day was started. After a month of treatment, the number of leukocytes was reduced to less than 10,000/μl. Then the patient was treated chronically with interferon alpha-2b in doses of 3 million units every 2 weeks. As a result of the therapy, the number of leukocytes remains between 8 and 10,000/μl. The patient remains in general good condition [49].
A series of two CNL cases are also shown. The first patient was a 70-year-old woman with stable leukocytosis of about 35,000/μl and the remaining morphology parameters in normal range. The patient was only observed for 5 years until hepasplenomegaly progressed rapidly. Then, interferon alpha-2b was included. Due to the treatment, the rapid regression of hepatosplenomegaly was achieved.
The second case is a 68-year-old woman with baseline leukocytosis of almost 14,000/μl. In this case, the treatment with hydroxycarbamide was started immediately. However, no improvement was achieved. After 6 weeks of HU treatment, interferon alpha-2b 3 million units 3 times a week was implemented and leukocytosis decreased. Due to the interferon treatment, the disease stabilized for a long time. Because the patient experienced an adverse reaction, a severe flu-like syndrome, interferon was discontinued. After interferon withdrawal, the disease progressed gradually and the treatment attempts by busulfan and 6-mercaptopurine were unsuccessful. Therefore, interferon was readministered and the disease went into remission. Interferon treatment was continued at a reduced dose. The disease regression was achieved again.
Additionally, the patient showed an improvement in the function of granulocytes in terms of phagocytosis and an improvement in neutral killer (NK) cell function after treatment with interferon [50].
The above examples show that interferon alpha is effective in the treatment of chronic neutrophilic leukemia. The side effects are rare and can be managed with dose reductions. Moreover, in these cases, interferon is also effective in a reduced dose. Disease remission or regression can be achieved without typical of CNL complications, such as intracranial bleeding.
Interferon has been used in the past to treat chronic myeloid leukemia. The treatment with tyrosine kinase inhibitors is now a standard practice. However, in a small number of patients, they are ineffective or exhibit unmanageable toxicity. Therefore, the attempts are underway to use interferon in combination with TKI in lower doses, which is to ensure the enhancement of the antiproliferative effect while reducing the toxicity.
There are ongoing attempts to use ropeginterferon in patients diagnosed with chronic myeloid leukemia, in whom treatment with imatinib alone has not led to deep molecular response (DMR). The first phase study was conducted in a small group of patients with chronic myeloid leukemia. The patients in first chronic phase treated with imatinib who did not achieve DMR, but in complete hematologic remission and complete cytogenetic remission, were included in the study. Patients have been treated with imatinib for at least 18 months. Twelve patients were enrolled in the study, and they completed the study according to the protocol. These patients received additional ropeginterferon to imatinib and four achieved DMR. Low toxicity was observed during the treatment. Among the hematological toxicities, neutropenia was the most common. There was no nonhematological toxicity with a degree higher than 1/2 during the treatment. Moreover, it has been found that better effects and fewer side effects are obtained when ropeginterferon is administered for a longer time, but in lower doses. The comparison of the effectiveness of interferon in chronic myeloproliferative disorders based on selected articles is presented in Table 1 [51].
Source | Type of trial | Interferon | Diagnosis | No. | Prior treatment status | Response rate |
---|---|---|---|---|---|---|
Yacoubet al. [15] | Phase II, multicenter | Pegylated IFN alfa-2a | PV | 50 | Resistance to HU or HU intolerance | CR:22% PR:38% |
ET | 65 | CR:43% PR:26% | ||||
Masarova et al. [16] | Phase II, single-center | Pegylated IFN alfa-2a | PV | 43 | Untreated or previously treated with cytoreductive therapy | CR:77% PR:7% |
ET | 40 | CR:73% PR:3% | ||||
Samuelsson et al. [18] | Phase II | Pegylated IFN alfa-2b | PV | 21 | Untreated or previously treated with cytoreductive therapy | CR: 69% for the entire group |
ET | 21 | |||||
Huang BT et al. [19] | Open label, multicenter | IFN alfa-2b | PV | 136 | Untreated or previously treated with cytoreductive therapy | OHR:70% Molecular response:54.7% |
ET | 123 | OHR (JAK2+ patients):83% CHR:23 cases OHR (JAK2-patients): 61.4% CHR:12 cases | ||||
Gisslinger et al. [23] | phase III, multicenter | Ropeginterferon | PV | 257 | Previously treated | OHR:53% |
Quintás-Cardama et al. [26] | phase II | Pegylated IFN alfa-2a | PV | 40 | Untreated or previously treated with cytoreductive therapy | OHR:80% CR:70% Molecular remission:54% |
ET | 39 | OHR:81% CR:76% Molecular remission:38% | ||||
Sørensen et al. [36] | Phase III, multicenter, COMBI | Pegylated IFN alfa-2a with ruxolitinib or Pegylated IFN alfa-2b with ruxolitinib | PV | 32 | Untreated or previously treated with cytoreductive therapy | OHR:44% CR:28% |
MF | 18 | OHR:31% CR:9% | ||||
Casassus et al. [40] | Open label, multicenter | IFN alpha-2b | Mastocytosis | 20 | Untreated and previously treated | PR:35% Minor remission: 30% |
Comparison of the effectiveness of interferon in chronic myeloproliferative disorders.
PV: polycythemia vera; ET: essential thrombocythemia; MF: myelofibrosis; HU: hydroxycarbamide/hydroxyurea; CR: complete remission; PR: partial remission; and OHR: overall hematological response.
Interferon alpha appears to be an effective and safe drug in the most type of chronic myeloproliferative disorders. Nowadays, all forms of its using have similar effectiveness. Interferon alpha can be effective even in cases of resistance for first-line treatment. Trial research is currently underway to combine it with some new drugs, such as ruxolitinib, and to add it to the already well-established therapy, it is a promising option for patients with refractory disease.
From time to time, new forms of interferon, such as ropeginterferon, are introduced, which gives hope for better effectiveness, better safety profile, and greater comfort in its use for patients who have to be treated for many years. In the case of the use of interferons alpha in the treatment of chronic myeloproliferative diseases, there are still opportunities to extend its use and to study its combination with newly introduced drugs.
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Morris, Steve Croker, Amy M. Masnick and Corinne Zimmerman",authors:[{id:"154336",title:"Prof.",name:"Bradley",middleName:null,surname:"Morris",slug:"bradley-morris",fullName:"Bradley Morris"},{id:"154337",title:"Prof.",name:"Steve",middleName:null,surname:"Croker",slug:"steve-croker",fullName:"Steve Croker"},{id:"154338",title:"Prof.",name:"Amy",middleName:null,surname:"Masnick",slug:"amy-masnick",fullName:"Amy Masnick"},{id:"154339",title:"Prof.",name:"Corinne",middleName:null,surname:"Zimmerman",slug:"corinne-zimmerman",fullName:"Corinne Zimmerman"}]},{id:"60564",doi:"10.5772/intechopen.76249",title:"Ageing Process and Physiological Changes",slug:"ageing-process-and-physiological-changes",totalDownloads:7003,totalCrossrefCites:19,totalDimensionsCites:34,abstract:"Ageing is a natural process. Everyone must undergo this phase of life at his or her own time and pace. In the broader sense, ageing reflects all the changes taking place over the course of life. These changes start from birth—one grows, develops and attains maturity. To the young, ageing is exciting. Middle age is the time when people notice the age-related changes like greying of hair, wrinkled skin and a fair amount of physical decline. Even the healthiest, aesthetically fit cannot escape these changes. Slow and steady physical impairment and functional disability are noticed resulting in increased dependency in the period of old age. According to World Health Organization, ageing is a course of biological reality which starts at conception and ends with death. It has its own dynamics, much beyond human control. However, this process of ageing is also subject to the constructions by which each society makes sense of old age. In most of the developed countries, the age of 60 is considered equivalent to retirement age and it is said to be the beginning of old age. In this chapter, you understand the details of ageing processes and associated physiological changes.",book:{id:"6381",slug:"gerontology",title:"Gerontology",fullTitle:"Gerontology"},signatures:"Shilpa Amarya, Kalyani Singh and Manisha Sabharwal",authors:[{id:"226573",title:"Ph.D.",name:"Shilpa",middleName:null,surname:"Amarya",slug:"shilpa-amarya",fullName:"Shilpa Amarya"},{id:"226593",title:"Dr.",name:"Kalyani",middleName:null,surname:"Singh",slug:"kalyani-singh",fullName:"Kalyani Singh"},{id:"243264",title:"Dr.",name:"Manisha",middleName:null,surname:"Sabharwal",slug:"manisha-sabharwal",fullName:"Manisha Sabharwal"}]},{id:"56330",doi:"10.5772/intechopen.69932",title:"Russian Scientific Trends on Specific Language Impairment in Childhood",slug:"russian-scientific-trends-on-specific-language-impairment-in-childhood",totalDownloads:1955,totalCrossrefCites:0,totalDimensionsCites:23,abstract:"In Russia, there are many decades of experience in the scientific study of the problem of impaired language development in children. Today, the term “Systemic speech-and-language underdevelopment (SLU)” has firmly established in Russian science and practice, implying a complex developmental disorder of speech and language in children with a primary normal hearing and a conserved intellect, in which the main components of the language system are violated: vocabulary, grammar, phonetics, and, as a consequence, dialogic and monologic speech. Traditionally, a differentiated level-by-level analysis of the speech and language abilities of children is used. The variability of the manifestations and severity of speech-and-language disorders were initially systematized and characterized in four levels of underdevelopment: from the complete absence of phrase speech to the availability of simple and complex sentences with lexico-grammatical errors. Effective algorithms of speech therapist work with SLU are introduced. The effectiveness of the application of these models and algorithms on the material of various language groups is proved.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Tatiana Tumanova and Tatiana Filicheva",authors:[{id:"204529",title:"Dr.",name:"Tatiana Volodarovna",middleName:null,surname:"Tumanova",slug:"tatiana-volodarovna-tumanova",fullName:"Tatiana Volodarovna Tumanova"},{id:"208704",title:"Dr.",name:"Tatiana Borisovna",middleName:null,surname:"Filicheva",slug:"tatiana-borisovna-filicheva",fullName:"Tatiana Borisovna Filicheva"}]},{id:"36452",doi:"10.5772/38931",title:"Qualitative Research Methods in Psychology",slug:"qualitative-research-methods-in-psychology",totalDownloads:35899,totalCrossrefCites:13,totalDimensionsCites:17,abstract:null,book:{id:"1997",slug:"psychology-selected-papers",title:"Psychology",fullTitle:"Psychology - Selected Papers"},signatures:"Deborah Biggerstaff",authors:[{id:"123274",title:"Dr.",name:"Deborah",middleName:null,surname:"Biggerstaff",slug:"deborah-biggerstaff",fullName:"Deborah Biggerstaff"}]},{id:"56560",doi:"10.5772/intechopen.70235",title:"The Role of Speech and Language Therapist in Autism Spectrum Disorders Intervention – An Inclusive Approach",slug:"the-role-of-speech-and-language-therapist-in-autism-spectrum-disorders-intervention-an-inclusive-app",totalDownloads:2373,totalCrossrefCites:2,totalDimensionsCites:16,abstract:"The chapter describes the possibilities of involving a speech-language therapist in the assessment of the pragmatic level of communication in autism spectrum disorders (ASD), where one of the most frequently impaired areas is communication pragmatics. These difficulties lead to a disruption of social interaction, which might be one of the obstacles to speech-language intervention in these children. The text is based on an originally developed testing material aimed at selected pragmatic-oriented communication situations relating to everyday activities and real life. Based on a comparison of domestic and international resources in this area, as well as mediated and own empirical experience, our assessment approach is based on the conclusion that pragmatics can be understood in different contexts and perspectives. The text presents the results of a partial survey comparing the performance of children with ASD and children with typical development. The assessment focused on the children’s election of the correct picture of a pair of pictures that represent usual communication and social situations. The results of the research suggest fewer incorrect responses in children with ASD and in different areas compared with children with typical development. However, the results of a qualitative analysis indicate a necessity to expand the assessment of communication pragmatics by adding an individually specific qualitative analysis of children’s performance.",book:{id:"5957",slug:"advances-in-speech-language-pathology",title:"Advances in Speech-language Pathology",fullTitle:"Advances in Speech-language Pathology"},signatures:"Kateřina Vitásková and Lucie Kytnarová",authors:[{id:"203061",title:"Associate Prof.",name:"Kateřina",middleName:null,surname:"Vitásková",slug:"katerina-vitaskova",fullName:"Kateřina Vitásková"},{id:"212035",title:"MSc.",name:"Lucie",middleName:null,surname:"Kytnarová",slug:"lucie-kytnarova",fullName:"Lucie Kytnarová"}]}],mostDownloadedChaptersLast30Days:[{id:"73271",title:"Social Media and Its Effects on Beauty",slug:"social-media-and-its-effects-on-beauty",totalDownloads:3075,totalCrossrefCites:0,totalDimensionsCites:1,abstract:"Beauty is concerned with physical and mental health as both are intimately related. Short-term decisions to alter one’s body structure irrespective of genetic, environmental, occupational and nutritional needs can leave medium- and long-term effects. This chapter analyzes the role of social media and its effects on the standards of beauty. The researchers have summarized the literature on how social media plays a role in affecting beauty trends, body image and self-esteem concerns. There is support that social media affects individuals negatively, in pushing them to engage in life threatening beauty trends due to social compliance and acceptance in society. The aim was to review social networking sites’ impact on perception of standards of beauty and newer unrealistic trends gaining popularity that could alter opinions and also cause harm to individuals in the long run. This is an emerging area of research that is of high importance to the physical and mental health in the beauty, health and hospitality industry with the latter being manifested in depression, anxiety and fear of non-acceptability and being seen as a social gauche.",book:{id:"7811",slug:"beauty-cosmetic-science-cultural-issues-and-creative-developments",title:"Beauty",fullTitle:"Beauty - Cosmetic Science, Cultural Issues and Creative Developments"},signatures:"Mavis Henriques and Debasis Patnaik",authors:[{id:"320016",title:"Ph.D. Student",name:"Mavis",middleName:"Lilian",surname:"Henriques",slug:"mavis-henriques",fullName:"Mavis Henriques"},{id:"320978",title:"Dr.",name:"Debasis",middleName:null,surname:"Patnaik",slug:"debasis-patnaik",fullName:"Debasis Patnaik"}]},{id:"60564",title:"Ageing Process and Physiological Changes",slug:"ageing-process-and-physiological-changes",totalDownloads:6995,totalCrossrefCites:19,totalDimensionsCites:33,abstract:"Ageing is a natural process. Everyone must undergo this phase of life at his or her own time and pace. In the broader sense, ageing reflects all the changes taking place over the course of life. These changes start from birth—one grows, develops and attains maturity. To the young, ageing is exciting. Middle age is the time when people notice the age-related changes like greying of hair, wrinkled skin and a fair amount of physical decline. Even the healthiest, aesthetically fit cannot escape these changes. Slow and steady physical impairment and functional disability are noticed resulting in increased dependency in the period of old age. According to World Health Organization, ageing is a course of biological reality which starts at conception and ends with death. It has its own dynamics, much beyond human control. However, this process of ageing is also subject to the constructions by which each society makes sense of old age. In most of the developed countries, the age of 60 is considered equivalent to retirement age and it is said to be the beginning of old age. In this chapter, you understand the details of ageing processes and associated physiological changes.",book:{id:"6381",slug:"gerontology",title:"Gerontology",fullTitle:"Gerontology"},signatures:"Shilpa Amarya, Kalyani Singh and Manisha Sabharwal",authors:[{id:"226573",title:"Ph.D.",name:"Shilpa",middleName:null,surname:"Amarya",slug:"shilpa-amarya",fullName:"Shilpa Amarya"},{id:"226593",title:"Dr.",name:"Kalyani",middleName:null,surname:"Singh",slug:"kalyani-singh",fullName:"Kalyani Singh"},{id:"243264",title:"Dr.",name:"Manisha",middleName:null,surname:"Sabharwal",slug:"manisha-sabharwal",fullName:"Manisha Sabharwal"}]},{id:"27237",title:"Emotional Intelligence",slug:"emotional-intelligence",totalDownloads:5774,totalCrossrefCites:6,totalDimensionsCites:9,abstract:null,book:{id:"679",slug:"emotional-intelligence-new-perspectives-and-applications",title:"Emotional Intelligence",fullTitle:"Emotional Intelligence - New Perspectives and Applications"},signatures:"Adrian Furnham",authors:[{id:"85492",title:"Prof.",name:"Adrian",middleName:null,surname:"Furnham",slug:"adrian-furnham",fullName:"Adrian Furnham"}]},{id:"70731",title:"Theoretical Perspective of Traditional Counseling",slug:"theoretical-perspective-of-traditional-counseling",totalDownloads:1605,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"This chapter discusses the theoretical perspective of traditional counseling from an African context. Traditional counseling involves a broad perspective that enhances learning for transformation and integration of sociocultural values that are peculiar to each human society. A cursory review of the literature suggests that the concept of traditional counseling is rooted in traditional systems of knowledge and sociocultural customs and practices, and it promotes a collective approach to problem identification, resolution, and management. The traditional counseling process centers on four aspects: traditional counselor, client, family, and community. The key elements that inform the theoretical framework of traditional counseling from an African perspective are: cultural context, collective belief system, and initiation rituals Traditional systems of knowledge deemed essential for each generation are passed on successively to the next generation by elderly people who do not only have the necessary wisdom and experience, but are also adorned with social competences and skills.",book:{id:"9136",slug:"counseling-and-therapy",title:"Counseling and Therapy",fullTitle:"Counseling and Therapy"},signatures:"Hector Chiboola",authors:[{id:"314172",title:"Prof.",name:"Hector",middleName:null,surname:"Chiboola",slug:"hector-chiboola",fullName:"Hector Chiboola"}]},{id:"55388",title:"Beauty, Body Image, and the Media",slug:"beauty-body-image-and-the-media",totalDownloads:7764,totalCrossrefCites:5,totalDimensionsCites:12,abstract:"This chapter analyses the role of the mass media in people’s perceptions of beauty. We summarize the research literature on the mass media, both traditional media and online social media, and how they appear to interact with psychological factors to impact appearance concerns and body image disturbances. There is a strong support for the idea that traditional forms of media (e.g. magazines and music videos) affect perceptions of beauty and appearance concerns by leading women to internalize a very slender body type as ideal or beautiful. Rather than simply being passive recipients of unrealistic beauty ideals communicated to them via the media, a great number of individuals actually seek out idealized images in the media. Finally, we review what is known about the role of social media in impacting society’s perception of beauty and notions of idealized physical forms. Social media are more interactive than traditional media and the effects of self‐presentation strategies on perceptions of beauty have just begun to be studied. This is an emerging area of research that is of high relevance to researchers and clinicians interested in body image and appearance concerns.",book:{id:"5925",slug:"perception-of-beauty",title:"Perception of Beauty",fullTitle:"Perception of Beauty"},signatures:"Jennifer S. Mills, Amy Shannon and Jacqueline Hogue",authors:[{id:"202110",title:"Dr.",name:"Jennifer S.",middleName:null,surname:"Mills",slug:"jennifer-s.-mills",fullName:"Jennifer S. Mills"}]}],onlineFirstChaptersFilter:{topicId:"21",limit:6,offset:0},onlineFirstChaptersCollection:[{id:"83107",title:"Helping BIPOC LGBTQIA+ Families Through Inclusive Therapy and Advocacy",slug:"helping-bipoc-lgbtqia-families-through-inclusive-therapy-and-advocacy",totalDownloads:0,totalDimensionsCites:null,doi:"10.5772/intechopen.106695",abstract:null,book:{id:"11781",title:"Family Therapy - Recent Advances in Clinical and Crisis Settings",coverURL:"https://cdn.intechopen.com/books/images_new/11781.jpg"},signatures:"Lucy Parker-Barnes, Noel McKillip and Carolyn Powell"},{id:"83099",title:"Values-Flow in Contextual Psychotherapy: The ‘What’, ‘Why’, and ‘How’ of Sustainable Values-Based Behaviour",slug:"values-flow-in-contextual-psychotherapy-the-what-why-and-how-of-sustainable-values-based-behaviour",totalDownloads:2,totalDimensionsCites:null,doi:"10.5772/intechopen.106594",abstract:"Flow - enjoyed and fully absorbed engagement in meaningful and contextually bounded activities - is widely underutilised in psychotherapy and mental health settings. Two gold standard therapies, Acceptance and Commitment Therapy (ACT) and Dialectical Behaviour Therapy (DBT), while powerful and effective in many ways, would benefit from systematic models that move from initiating positive change to sustaining meaningful change. This chapter introduces ‘Values-Flow’ – an approach aimed at building commitment and sustainable engagement in psychotherapy and values-based behaviour in working adults struggling with sub-optimal functioning. We first introduce Values-Flow and describe how it may benefit psychotherapy skills practice in everyday life. Next, we discuss why Values-Flow is relevant and enhances the practice of ACT and DBT strategies, helping to sustain engagement and creative practice of values-based actions outside of sessions. We then describe the ‘Values-Flow’ framework, which incorporates VIVA (Virtue, Involve, Vital, Accepting) and ARIA (Attend, Reflect, Inform, Act) tools that develop commitment for values-based practice in daily life. We conclude with a case-example of how Values-Flow can build commitment and sustainable engagement in homework completion in psychotherapy.",book:{id:"11444",title:"Happiness - Biopsychosocial and Anthropological Perspectives",coverURL:"https://cdn.intechopen.com/books/images_new/11444.jpg"},signatures:"Cedomir Ignjatovic, Margaret L. Kern and Lindsay G. Oades"},{id:"83100",title:"Factors Affecting the Happiness of Korean University Students",slug:"factors-affecting-the-happiness-of-korean-university-students",totalDownloads:2,totalDimensionsCites:null,doi:"10.5772/intechopen.106296",abstract:"As of 2020, in Korea, as 72.5% of high-school graduates go on to college and college period has an impact on the social development of Korean youth, it is very important to increase the sense of happiness of college students. However, there are new terminologies to express the situation in which how young people in Korea feel the difficulties in their lives, such as “Hell Chosun, 88-Dollar-Generation, N-Give-up-Generation, and Spoon-Social-Rank.” This chapter summarizes the factors related to the happiness of college students in South Korea, such as depression, interpersonal relationships, and self-efficacy, to suggest educational programs to promote the happiness of young people in Korea.",book:{id:"11444",title:"Happiness - Biopsychosocial and Anthropological Perspectives",coverURL:"https://cdn.intechopen.com/books/images_new/11444.jpg"},signatures:"Soo-Koung Jun"},{id:"83027",title:"Coping Strategies and Meta-Worry in Adolescents’ Adjustment during COVID-19 Pandemic",slug:"coping-strategies-and-meta-worry-in-adolescents-adjustment-during-covid-19-pandemic",totalDownloads:1,totalDimensionsCites:0,doi:"10.5772/intechopen.106258",abstract:"With the beginning of the COVID-19 pandemic, several limitations and stressful changes have been introduced in adolescent’s daily life. Particularly, Italian teenagers were the first among western populations to experience fears of infection, home confinement, and social restrictions due to a long lockdown period (10 weeks). This study explores the role of coping strategies (task-oriented, emotion-oriented, and avoidance coping) and meta-beliefs about worry as vulnerability factors associated with adolescents’ anxiety. A community sample of adolescents (N = 284, aged 16–18 y.o.) answered questionnaires assessing anxiety symptoms (RCMAS-2), meta-cognitive beliefs and processes about worry (MCQ-C), and coping strategies (CISS). Results show that 37% of participants report clinically elevated anxiety. Emotion-centered coping predicted higher anxiety, whereas task-centered coping resulted associated with decreased anxiety. Cognitive monitoring about their own worry contributes, but to a lesser extent, to higher levels of anxiety. The implications for the intervention are discussed, especially the need to enhance the coping skills of adolescents and mitigate the stress of the COVID-19 pandemic, which could last for a long time.",book:{id:"10671",title:"Adolescences",coverURL:"https://cdn.intechopen.com/books/images_new/10671.jpg"},signatures:"Loredana Benedetto, Ilenia Schipilliti and Massimo Ingrassia"},{id:"83023",title:"Gestational Tryptophan Fluctuation Underlying Ontogenetic Origin of Neuropsychiatric Disorders",slug:"gestational-tryptophan-fluctuation-underlying-ontogenetic-origin-of-neuropsychiatric-disorders",totalDownloads:5,totalDimensionsCites:0,doi:"10.5772/intechopen.106421",abstract:"Neuropsychiatry underlies personality development and social functioning. Borderline personality disorder exhibits high trait aggression and is associated with tryptophan hydroxylase polymorphisms. The acute tryptophan depletion reduces plasma and cerebrospinal fluid tryptophan availability and brain serotonin concentrations, leading to alterations in personality and trait-related behaviors. Tryptophan is essential for fatal neurodevelopment and immunomodulation in pregnancy. Gestational tryptophan fluctuation induced by maternal metabolic disorders or drug administrations may account for the maternal-fetal transmission determining neurogenesis and microbial development, consequentially shaping the long-standing patterns of thinking and behavior. However, it is not possible to assess the gestational tryptophan exposure effects on fetal brain and gastrointestinal system in humans for ethical reasons. The maternal–fetal microbe transmission in rodents during gestation, vaginal delivery, and breastfeeding is inevitable. Chicken embryo may be an alternative and evidence from the chicken embryo model reveals that gestational tryptophan fluctuation, i.e., exposed to excessive tryptophan or its metabolite, serotonin, attenuates aggressiveness and affects peer sociometric status. This chapter discusses the gestational tryptophan fluctuation as a risk factor of personality disorders in offspring and the prevention of personality disorders by dietary tryptophan control and medication therapy management during pregnancy.",book:{id:"11782",title:"Personality Traits - The Role in Psychopathology",coverURL:"https://cdn.intechopen.com/books/images_new/11782.jpg"},signatures:"Xiaohong Huang, Xiaohua Li and Heng-Wei Cheng"},{id:"82982",title:"The Well-Being in the Children and Adolescents with ADHD: Possible Influencing Factors and How to Improve It",slug:"the-well-being-in-the-children-and-adolescents-with-adhd-possible-influencing-factors-and-how-to-imp",totalDownloads:2,totalDimensionsCites:0,doi:"10.5772/intechopen.106596",abstract:"In recent years, academics have increasingly emphasized the importance of research into the well-being of children and adolescents. This is because well-being plays an important role in the development of children and adolescents. The literature reports that high levels of well-being facilitate positive functioning in children and adolescents. They contribute to the overall development of the individual and are a key factor in helping children and adolescents to integrate into society. ADHD, the most prevalent neurodevelopmental disorder, affects more than 5% of children and adolescents, and the distress caused by its symptom can seriously undermine the well-being of children and adolescents. Therefore, this chapter discusses this noticeable issue focusing on the following key parts: An understanding of the well-being in children and adolescents, the factors that affect the well-being of children and adolescents with ADHD, and how to improve the well-being of children and adolescents with ADHD.",book:{id:"11444",title:"Happiness - Biopsychosocial and Anthropological Perspectives",coverURL:"https://cdn.intechopen.com/books/images_new/11444.jpg"},signatures:"Jenson Yin and Jie Luo"}],onlineFirstChaptersTotal:67},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:90,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:108,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:33,numberOfPublishedChapters:330,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:14,numberOfPublishedChapters:145,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:9,numberOfPublishedChapters:141,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:124,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:112,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:22,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:11,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:"2753-6580",doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. The whole process of submitting an article and editing of the submitted article goes extremely smooth and fast, the number of reads and downloads of chapters is high, and the contributions are also frequently cited.",author:{id:"55578",name:"Antonio",surname:"Jurado-Navas",institutionString:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRisIQAS/Profile_Picture_1626166543950",slug:"antonio-jurado-navas",institution:{id:"720",name:"University of Malaga",country:{id:null,name:"Spain"}}}},{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}}]},series:{item:{id:"11",title:"Biochemistry",doi:"10.5772/intechopen.72877",issn:"2632-0983",scope:"Biochemistry, the study of chemical transformations occurring within living organisms, impacts all areas of life sciences, from molecular crystallography and genetics to ecology, medicine, and population biology. Biochemistry examines macromolecules - proteins, nucleic acids, carbohydrates, and lipids – and their building blocks, structures, functions, and interactions. Much of biochemistry is devoted to enzymes, proteins that catalyze chemical reactions, enzyme structures, mechanisms of action and their roles within cells. Biochemistry also studies small signaling molecules, coenzymes, inhibitors, vitamins, and hormones, which play roles in life processes. Biochemical experimentation, besides coopting classical chemistry methods, e.g., chromatography, adopted new techniques, e.g., X-ray diffraction, electron microscopy, NMR, radioisotopes, and developed sophisticated microbial genetic tools, e.g., auxotroph mutants and their revertants, fermentation, etc. More recently, biochemistry embraced the ‘big data’ omics systems. Initial biochemical studies have been exclusively analytic: dissecting, purifying, and examining individual components of a biological system; in the apt words of Efraim Racker (1913 –1991), “Don’t waste clean thinking on dirty enzymes.” Today, however, biochemistry is becoming more agglomerative and comprehensive, setting out to integrate and describe entirely particular biological systems. The ‘big data’ metabolomics can define the complement of small molecules, e.g., in a soil or biofilm sample; proteomics can distinguish all the comprising proteins, e.g., serum; metagenomics can identify all the genes in a complex environment, e.g., the bovine rumen. This Biochemistry Series will address the current research on biomolecules and the emerging trends with great promise.",coverUrl:"https://cdn.intechopen.com/series/covers/11.jpg",latestPublicationDate:"August 2nd, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:33,editor:{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:4,paginationItems:[{id:"14",title:"Cell and Molecular Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/14.jpg",isOpenForSubmission:!0,editor:{id:"165627",title:"Dr.",name:"Rosa María",middleName:null,surname:"Martínez-Espinosa",slug:"rosa-maria-martinez-espinosa",fullName:"Rosa María Martínez-Espinosa",profilePictureURL:"https://mts.intechopen.com/storage/users/165627/images/system/165627.jpeg",biography:"Dr. Rosa María Martínez-Espinosa has been a Spanish Full Professor since 2020 (Biochemistry and Molecular Biology) and is currently Vice-President of International Relations and Cooperation development and leader of the research group 'Applied Biochemistry” (University of Alicante, Spain). Other positions she has held at the university include Vice-Dean of Master Programs, Vice-Dean of the Degree in Biology and Vice-Dean for Mobility and Enterprise and Engagement at the Faculty of Science (University of Alicante). She received her Bachelor in Biology in 1998 (University of Alicante) and her PhD in 2003 (Biochemistry, University of Alicante). She undertook post-doctoral research at the University of East Anglia (Norwich, U.K. 2004-2005; 2007-2008).\nHer multidisciplinary research focuses on investigating archaea and their potential applications in biotechnology. She has an H-index of 21. She has authored one patent and has published more than 70 indexed papers and around 60 book chapters.\nShe has contributed to more than 150 national and international meetings during the last 15 years. Her research interests include archaea metabolism, enzymes purification and characterization, gene regulation, carotenoids and bioplastics production, antioxidant\ncompounds, waste water treatments, and brines bioremediation.\nRosa María’s other roles include editorial board member for several journals related\nto biochemistry, reviewer for more than 60 journals (biochemistry, molecular biology, biotechnology, chemistry and microbiology) and president of several organizing committees in international meetings related to the N-cycle or respiratory processes.",institutionString:null,institution:{name:"University of Alicante",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"15",title:"Chemical Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/15.jpg",isOpenForSubmission:!0,editor:{id:"441442",title:"Dr.",name:"Şükrü",middleName:null,surname:"Beydemir",slug:"sukru-beydemir",fullName:"Şükrü Beydemir",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003GsUoIQAV/Profile_Picture_1634557147521",biography:"Dr. Şükrü Beydemir obtained a BSc in Chemistry in 1995 from Yüzüncü Yıl University, MSc in Biochemistry in 1998, and PhD in Biochemistry in 2002 from Atatürk University, Turkey. He performed post-doctoral studies at Max-Planck Institute, Germany, and University of Florence, Italy in addition to making several scientific visits abroad. He currently works as a Full Professor of Biochemistry in the Faculty of Pharmacy, Anadolu University, Turkey. Dr. Beydemir has published over a hundred scientific papers spanning protein biochemistry, enzymology and medicinal chemistry, reviews, book chapters and presented several conferences to scientists worldwide. He has received numerous publication awards from various international scientific councils. He serves in the Editorial Board of several international journals. Dr. Beydemir is also Rector of Bilecik Şeyh Edebali University, Turkey.",institutionString:null,institution:{name:"Anadolu University",institutionURL:null,country:{name:"Turkey"}}},editorTwo:{id:"13652",title:"Prof.",name:"Deniz",middleName:null,surname:"Ekinci",slug:"deniz-ekinci",fullName:"Deniz Ekinci",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002aYLT1QAO/Profile_Picture_1634557223079",biography:"Dr. Deniz Ekinci obtained a BSc in Chemistry in 2004, MSc in Biochemistry in 2006, and PhD in Biochemistry in 2009 from Atatürk University, Turkey. He studied at Stetson University, USA, in 2007-2008 and at the Max Planck Institute of Molecular Cell Biology and Genetics, Germany, in 2009-2010. Dr. Ekinci currently works as a Full Professor of Biochemistry in the Faculty of Agriculture and is the Head of the Enzyme and Microbial Biotechnology Division, Ondokuz Mayıs University, Turkey. He is a member of the Turkish Biochemical Society, American Chemical Society, and German Genetics society. Dr. Ekinci published around ninety scientific papers, reviews and book chapters, and presented several conferences to scientists. He has received numerous publication awards from several scientific councils. Dr. Ekinci serves as the Editor in Chief of four international books and is involved in the Editorial Board of several international journals.",institutionString:null,institution:{name:"Ondokuz Mayıs University",institutionURL:null,country:{name:"Turkey"}}},editorThree:null},{id:"17",title:"Metabolism",coverUrl:"https://cdn.intechopen.com/series_topics/covers/17.jpg",isOpenForSubmission:!0,editor:{id:"138626",title:"Dr.",name:"Yannis",middleName:null,surname:"Karamanos",slug:"yannis-karamanos",fullName:"Yannis Karamanos",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002g6Jv2QAE/Profile_Picture_1629356660984",biography:"Yannis Karamanos, born in Greece in 1953, completed his pre-graduate studies at the Université Pierre et Marie Curie, Paris, then his Masters and Doctoral degree at the Université de Lille (1983). He was associate professor at the University of Limoges (1987) before becoming full professor of biochemistry at the Université d’Artois (1996). He worked on the structure-function relationships of glycoconjugates and his main project was the investigations on the biological roles of the de-N-glycosylation enzymes (Endo-N-acetyl-β-D-glucosaminidase and peptide-N4-(N-acetyl-β-glucosaminyl) asparagine amidase). From 2002 he contributes to the understanding of the Blood-brain barrier functioning using proteomics approaches. He has published more than 70 papers. His teaching areas are energy metabolism and regulation, integration and organ specialization and metabolic adaptation.",institutionString:null,institution:{name:"Artois University",institutionURL:null,country:{name:"France"}}},editorTwo:null,editorThree:null},{id:"18",title:"Proteomics",coverUrl:"https://cdn.intechopen.com/series_topics/covers/18.jpg",isOpenForSubmission:!0,editor:{id:"200689",title:"Prof.",name:"Paolo",middleName:null,surname:"Iadarola",slug:"paolo-iadarola",fullName:"Paolo Iadarola",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSCl8QAG/Profile_Picture_1623568118342",biography:"Paolo Iadarola graduated with a degree in Chemistry from the University of Pavia (Italy) in July 1972. He then worked as an Assistant Professor at the Faculty of Science of the same University until 1984. In 1985, Prof. Iadarola became Associate Professor at the Department of Biology and Biotechnologies of the University of Pavia and retired in October 2017. Since then, he has been working as an Adjunct Professor in the same Department at the University of Pavia. His research activity during the first years was primarily focused on the purification and structural characterization of enzymes from animal and plant sources. During this period, Prof. Iadarola familiarized himself with the conventional techniques used in column chromatography, spectrophotometry, manual Edman degradation, and electrophoresis). Since 1995, he has been working on: i) the determination in biological fluids (serum, urine, bronchoalveolar lavage, sputum) of proteolytic activities involved in the degradation processes of connective tissue matrix, and ii) on the identification of biological markers of lung diseases. In this context, he has developed and validated new methodologies (e.g., Capillary Electrophoresis coupled to Laser-Induced Fluorescence, CE-LIF) whose application enabled him to determine both the amounts of biochemical markers (Desmosines) in urine/serum of patients affected by Chronic Obstructive Pulmonary Disease (COPD) and the activity of proteolytic enzymes (Human Neutrophil Elastase, Cathepsin G, Pseudomonas aeruginosa elastase) in sputa of these patients. More recently, Prof. Iadarola was involved in developing techniques such as two-dimensional electrophoresis coupled to liquid chromatography/mass spectrometry (2DE-LC/MS) for the proteomic analysis of biological fluids aimed at the identification of potential biomarkers of different lung diseases. He is the author of about 150 publications (According to Scopus: H-Index: 23; Total citations: 1568- According to WOS: H-Index: 20; Total Citations: 1296) of peer-reviewed international journals. He is a Consultant Reviewer for several journals, including the Journal of Chromatography A, Journal of Chromatography B, Plos ONE, Proteomes, International Journal of Molecular Science, Biotech, Electrophoresis, and others. He is also Associate Editor of Biotech.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorTwo:{id:"201414",title:"Dr.",name:"Simona",middleName:null,surname:"Viglio",slug:"simona-viglio",fullName:"Simona Viglio",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRKDHQA4/Profile_Picture_1630402531487",biography:"Simona Viglio is an Associate Professor of Biochemistry at the Department of Molecular Medicine at the University of Pavia. She has been working since 1995 on the determination of proteolytic enzymes involved in the degradation process of connective tissue matrix and on the identification of biological markers of lung diseases. She gained considerable experience in developing and validating new methodologies whose applications allowed her to determine both the amount of biomarkers (Desmosine and Isodesmosine) in the urine of patients affected by COPD, and the activity of proteolytic enzymes (HNE, Cathepsin G, Pseudomonas aeruginosa elastase) in the sputa of these patients. Simona Viglio was also involved in research dealing with the supplementation of amino acids in patients with brain injury and chronic heart failure. She is presently engaged in the development of 2-DE and LC-MS techniques for the study of proteomics in biological fluids. The aim of this research is the identification of potential biomarkers of lung diseases. She is an author of about 90 publications (According to Scopus: H-Index: 23; According to WOS: H-Index: 20) on peer-reviewed journals, a member of the “Società Italiana di Biochimica e Biologia Molecolare,“ and a Consultant Reviewer for International Journal of Molecular Science, Journal of Chromatography A, COPD, Plos ONE and Nutritional Neuroscience.",institutionString:null,institution:{name:"University of Pavia",institutionURL:null,country:{name:"Italy"}}},editorThree:null}]},overviewPageOFChapters:{paginationCount:42,paginationItems:[{id:"82914",title:"Glance on the Critical Role of IL-23 Receptor Gene Variations in Inflammation-Induced Carcinogenesis",doi:"10.5772/intechopen.105049",signatures:"Mohammed El-Gedamy",slug:"glance-on-the-critical-role-of-il-23-receptor-gene-variations-in-inflammation-induced-carcinogenesis",totalDownloads:15,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Chemokines Updates",coverURL:"https://cdn.intechopen.com/books/images_new/11672.jpg",subseries:{id:"18",title:"Proteomics"}}},{id:"82875",title:"Lipidomics as a Tool in the Diagnosis and Clinical Therapy",doi:"10.5772/intechopen.105857",signatures:"María Elizbeth Alvarez Sánchez, Erick Nolasco Ontiveros, Rodrigo Arreola, Adriana Montserrat Espinosa González, Ana María García Bores, Roberto Eduardo López Urrutia, Ignacio Peñalosa Castro, María del Socorro Sánchez Correa and Edgar Antonio Estrella Parra",slug:"lipidomics-as-a-tool-in-the-diagnosis-and-clinical-therapy",totalDownloads:9,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Fatty Acids - Recent Advances",coverURL:"https://cdn.intechopen.com/books/images_new/11669.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82440",title:"Lipid Metabolism and Associated Molecular Signaling Events in Autoimmune Disease",doi:"10.5772/intechopen.105746",signatures:"Mohan Vanditha, Sonu Das and Mathew John",slug:"lipid-metabolism-and-associated-molecular-signaling-events-in-autoimmune-disease",totalDownloads:17,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Fatty Acids - Recent Advances",coverURL:"https://cdn.intechopen.com/books/images_new/11669.jpg",subseries:{id:"17",title:"Metabolism"}}},{id:"82483",title:"Oxidative Stress in Cardiovascular Diseases",doi:"10.5772/intechopen.105891",signatures:"Laura Mourino-Alvarez, Tamara Sastre-Oliva, Nerea Corbacho-Alonso and Maria G. Barderas",slug:"oxidative-stress-in-cardiovascular-diseases",totalDownloads:10,totalCrossrefCites:0,totalDimensionsCites:0,authors:null,book:{title:"Importance of Oxidative Stress and Antioxidant System in Health and Disease",coverURL:"https://cdn.intechopen.com/books/images_new/11671.jpg",subseries:{id:"15",title:"Chemical Biology"}}}]},overviewPagePublishedBooks:{paginationCount:33,paginationItems:[{type:"book",id:"7006",title:"Biochemistry and Health Benefits of Fatty Acids",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/7006.jpg",slug:"biochemistry-and-health-benefits-of-fatty-acids",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Viduranga Waisundara",hash:"c93a00abd68b5eba67e5e719f67fd20b",volumeInSeries:1,fullTitle:"Biochemistry and Health Benefits of Fatty Acids",editors:[{id:"194281",title:"Dr.",name:"Viduranga Y.",middleName:null,surname:"Waisundara",slug:"viduranga-y.-waisundara",fullName:"Viduranga Y. Waisundara",profilePictureURL:"https://mts.intechopen.com/storage/users/194281/images/system/194281.jpg",biography:"Dr. Viduranga Waisundara obtained her Ph.D. in Food Science\nand Technology from the Department of Chemistry, National\nUniversity of Singapore, in 2010. She was a lecturer at Temasek Polytechnic, Singapore from July 2009 to March 2013.\nShe relocated to her motherland of Sri Lanka and spearheaded the Functional Food Product Development Project at the\nNational Institute of Fundamental Studies from April 2013 to\nOctober 2016. She was a senior lecturer on a temporary basis at the Department of\nFood Technology, Faculty of Technology, Rajarata University of Sri Lanka. She is\ncurrently Deputy Principal of the Australian College of Business and Technology –\nKandy Campus, Sri Lanka. She is also the Global Harmonization Initiative (GHI)",institutionString:"Australian College of Business & Technology",institution:{name:"Kobe College",institutionURL:null,country:{name:"Japan"}}}]},{type:"book",id:"6820",title:"Keratin",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/6820.jpg",slug:"keratin",publishedDate:"December 19th 2018",editedByType:"Edited by",bookSignature:"Miroslav Blumenberg",hash:"6def75cd4b6b5324a02b6dc0359896d0",volumeInSeries:2,fullTitle:"Keratin",editors:[{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}}]},{type:"book",id:"7978",title:"Vitamin A",subtitle:null,coverURL:"https://cdn.intechopen.com/books/images_new/7978.jpg",slug:"vitamin-a",publishedDate:"May 15th 2019",editedByType:"Edited by",bookSignature:"Leila Queiroz Zepka, Veridiana Vera de Rosso and Eduardo Jacob-Lopes",hash:"dad04a658ab9e3d851d23705980a688b",volumeInSeries:3,fullTitle:"Vitamin A",editors:[{id:"261969",title:"Dr.",name:"Leila",middleName:null,surname:"Queiroz Zepka",slug:"leila-queiroz-zepka",fullName:"Leila Queiroz Zepka",profilePictureURL:"https://mts.intechopen.com/storage/users/261969/images/system/261969.png",biography:"Prof. Dr. Leila Queiroz Zepka is currently an associate professor in the Department of Food Technology and Science, Federal University of Santa Maria, Brazil. She has more than fifteen years of teaching and research experience. She has published more than 550 scientific publications/communications, including 15 books, 50 book chapters, 100 original research papers, 380 research communications in national and international conferences, and 12 patents. She is a member of the editorial board of five journals and acts as a reviewer for several national and international journals. 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