Low molecular weight URS.
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"654",leadTitle:null,fullTitle:"Current Topics in Children's Learning and Cognition",title:"Current Topics in Children's Learning and Cognition",subtitle:null,reviewType:"peer-reviewed",abstract:"As a whole, the essays in this book address theoretical and empirical issues related to children's learning and cognition. 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\r\n\r\n\tLikewise, we are interested in focusing on the results of the mechanisms of interaction with living organisms and the effects on animal models. Very importantly, we are interested in capturing clinical trials that reveal the potential and beneficial effects on human patients.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"500a7cef20d52569986689d1f93b0263",bookSignature:"Dr. Elena Franco-Robles",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/9736.jpg",keywords:"Sources, Degree of Polymerization, Fructans in Plants, Stress Environment, Food Products, Properties, Probiotic Effect, Antimicrobial Effect, Animal Models, Models of Health and Disease, Metabolism, Gastrointestinal Disorders",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 9th 2019",dateEndSecondStepPublish:"March 27th 2020",dateEndThirdStepPublish:"May 26th 2020",dateEndFourthStepPublish:"August 14th 2020",dateEndFifthStepPublish:"October 13th 2020",remainingDaysToSecondStep:"a year",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"219102",title:"Dr.",name:"Elena",middleName:null,surname:"Franco-Robles",slug:"elena-franco-robles",fullName:"Elena Franco-Robles",profilePictureURL:"https://mts.intechopen.com/storage/users/219102/images/system/219102.jpeg",biography:"Dr. Elena Franco Robles is Professor in the Department of Veterinary and Zootechnics, Division of Life Sciences, Irapuato-Salamanca Campus, University of Guanajuato, Mexico, and is member of the National System of Investigators (SNI I). She graduated from Faculty of Chemistry, Universidad de Guanajuato, México, in 2006. She obtained her M.S. degree in Medical Science from the same University in 2010. She obtained her Ph.D from the same University. She obtained a Posdoctoral Position in Biotechnology in Center for Research and Advanced Studies of the National Polytechnic Institute in 2014-2016. \nDr. Elena Franco Robles has done research mainly in immunology of the intestine and oxidative stress in murine models with various pathologies. Her research focused on the role of nutraceutical and functional ingredients as immunomodulators for the prevention and / or treatment of diseases in animals. In addition, the study of toll-like receptors and gut microbiota as new therapeutic targets in zoonotic infections.",institutionString:"Universidad de Guanajuato",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"1",institution:{name:"Universidad de Guanajuato",institutionURL:null,country:{name:"Mexico"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"6",title:"Biochemistry, Genetics and Molecular Biology",slug:"biochemistry-genetics-and-molecular-biology"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"278926",firstName:"Ivana",lastName:"Barac",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/278926/images/8058_n.jpg",email:"ivana.b@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"56795",title:"Uremic Retention Solutes",doi:"10.5772/intechopen.70461",slug:"uremic-retention-solutes",body:'\nChronic kidney disease (CKD) is defined by estimated glomerular filtration rate (eGFR). Uremic syndrome occurs as this eGFR declines over time. Uremia is due to the accumulation of uremic retention solutes (URS) that affect multiple organ systems most notably the cardiovascular, neurologic, endocrine, and skeletal systems. These URS become elevated during the course of CKD and reach their peak during end-stage renal disease (ESRD). Organ dysfunction due to URS is seen, at times, long before patients reach the stage of dialysis dependency. Patients with early stages of CKD are much more likely to die from cardiovascular disease than to progress to ESRD [1]. While accelerated cardiovascular disease in patients undergoing chronic hemodialysis has been attributed to traditional cardiovascular risk factors, e.g., hypertension, diabetes, and lipid abnormalities, Lindner identified an accelerated risk of atherosclerosis in CKD patients without these risk factors [2]. During the past 10 years, there has been growing interest in characterizing the relationship between URS and cardiovascular disease. Since accelerated cardiovascular disease is seen in well-dialyzed patients, attention has been focused on solutes that are poorly dialyzed. Protein-bound URS, specifically indoxyl sulfate and p-cresyl sulfate, have been the focus of many studies over the past several decades. The interest is a result of their strong association with cardiovascular disease, their poor dialyzability, and their propensity to act on receptors (organic anion transporters) on the endothelium. Many different strategies for enhancing their removal and novel methods for reducing their generation have evolved over this period of time. The focus of this chapter will be to describe the classification of URS, describe their physiology, review their negative effects in the setting of uremia, and outline the different strategies currently being investigated to reduce levels of these solutes.
\nThe established classification system for URS is dependent on carrier protein binding and molecular weight [3]. The first class, termed low molecular weight (LMW) solutes, is categorized as less than 500 Da and is efficiently removed via hemodialysis. The next class is known as middle molecular weight (MMW) solutes. These molecules have molecular weights greater than 500 Da and require high-flux dialysis membranes, which have greater transport capacity and larger pore size for removal [4]. Protein-bound solutes comprise the last group, which are typically less than 500 Da though there is no official size demarcation. Their defining feature is their limited dialytic removal due to protein binding that impedes their movement across a dialysis membrane. A brief survey of LMW and MMW solutes will be given before focusing more in depth on the protein-bound solutes.
\nSome of the most prominent examples of the LMW category are urea, creatinine, asymmetric dimethylarginine (ADMA), trimethylamine-N-oxide (TMAO), and uric acid.
\nUrea has long been known to be elevated in patients with acute and chronic kidney diseases (Table 1). Today, urea levels are used as a surrogate for kidney function and for assessing the adequacy of hemodialysis sessions [5]. However, the data that has been gathered over the past several decades has been conflicting over whether urea is harmful or inert [6]. While research has shown that increasing the plasma levels of urea to ten times the upper limit can produce moderate uremic symptoms (lethargy and headache), there is no evidence of a survival benefit with aggressive reductions in urea during dialysis [7, 8]. In vitro and in vivo studies have linked urea to gut epithelial damage, endothelial dysfunction, and vascular smooth muscle apoptosis [6, 9]. Despite this data, it is difficult to determine the true effect of urea reduction on uremic syndrome and patient survival due to numerous confounding factors [6].
\n\n | MW (Da) | \nSource | \nMetabolism | \nToxicity | \n
---|---|---|---|---|
Urea [6] | \n60.05 | \nDietary proteins | \nHepatic | \nVascular disease, insulin resistance (in vivo data) | \n
ADMA [24] | \n202.25 | \nProtein metabolism | \nEndogenous enzymes | \nVascular disease | \n
TMAO [15] | \n75.11 | \nDiet | \nHepatic | \nVascular disease, renal fibrosis | \n
Uric acid [18, 19, 20] | \n168.11 | \nPurine metabolism | \nEndogenous enzymes | \nAccelerated CKD, vascular disease, hypertension | \n
Low molecular weight URS.
URS, uremic retention solutes; MW, molecular weight; ADMA, asymmetric dimethylarginine; TMAO, trimethylamine-N-oxide
Creatinine is formed from creatine, as part of the metabolic breakdown of the muscle. Clinically, serum creatinine levels are used to estimate glomerular filtration rate (eGFR) [10]. In CKD, creatinine accumulates as a result of decreased renal clearance, but no compelling evidence has linked it to pathology in kidney disease.
\nTwo other LMW solutes (Table 1) with possible links to the pathophysiology of cardiovascular disease in CKD patients are asymmetric dimethylarginine (ADMA) and trimethylamine-N-oxide (TMAO). ADMA has been shown to inhibit nitric oxide synthase causing endothelial dysfunction and has been correlated with vascular damage as evidenced by increased vessel wall thickness [3, 11, 12]. For ADMA, removal strategies (other than dialysis) have focused on the enzyme dimethylaminohydrolase. Inhibition of this enzyme has been linked to ADMA accumulation, whereas enzyme upregulation has shown decreased coronary damage in mice [13, 14]. TMAO is a small amine oxide with a well-documented association with cardiovascular disease [15]. However, the mechanism by which it leads to atherosclerosis remains speculative with research focusing on endothelial adhesion molecule dysfunction [15, 16]. Considering that the removal of TMAO via dialysis is already highly efficient, therapeutic strategies have targeted the generation of TMAO by the gut microbiome [17].
\nUric acid is a LMW molecule (Table 1) that is generated as a result of purine metabolism. Most animals, with the exception of humans and other primates, break down uric acid utilizing the enzyme uricase. Humans lack this enzyme and therefore excrete uric acid via the gut and kidney. Elevated uric acid levels are implicated in the pathophysiology of gout, but it has been proposed that it also plays a role in cardiovascular disease among the CKD population. Numerous studies have looked at the relationship of uric acid on cardiovascular events and mortality in the setting of early CKD [18, 19, 20]. The results have not been consistent, and this topic remains controversial. Hyperuricemia is believed to cause chronic stimulation of the renin angiotensin system leading to hypertension and progressive kidney disease [21]. Numerous randomized controlled trials have been conducted to determine whether the administration of urate-lowering therapy has an effect on CKD progression [22, 23]. There is a trend toward benefit, but it remains controversial due to significant heterogeneity among study groups and a lack of blinded studies.
\nThese solutes range from a MW of 500 to many tens of thousands of Daltons (Da). It is difficult at times to differentiate between solutes that are elevated due to reduced renal excretion (such as β2-microglobulin and leptin) versus those that are elevated due to other reasons (such as parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23), and advanced glycation end products (AGEP), among others). This section will focus on the former group.
\nThe most prominently studied MMW solute is β2-microglobulin (Table 2), an important component of the major histocompatibility complex [4]. β2-Microglobulin is recognized to be related to the deposition of amyloid in bones and joints. Speculation exists that it is not only a URS marker but additionally plays an active role in cardiovascular damage [25]. The removal of MMW solutes has centered on high-flux membranes containing wider pores to accommodate these larger molecules. However, the survival benefit of high flux versus low flux has not been definitively demonstrated in the dialysis population [26].
\n\n | MW (Da) | \nSource | \nToxicity | \n
---|---|---|---|
β2-Microglobulin [25] | \n11,729 | \nMajor histocompatibility complex | \nAmyloid bone and joint disease, vascular wall infiltration | \n
Leptin [28] | \n16,000 | \nEndogenous | \nMalnutrition | \n
Middle molecular weight URS.
URS, uremic retention solutes; MW, molecular weight
The discovery of the obesity gene in 1994 and its subsequent protein product, leptin, was an important step in understanding obesity [27]. Leptin accumulates in CKD/ESRD (Table 2). It is produced by white adipose tissue in response to an increase in body fat. It is found in a free form as well as bound to leptin-soluble receptor, which has a molecular weight of >150,000 Da. Exogenous administration of leptin, in an in vitro study, led to a reduction in food intake, increased energy expenditure, and a subsequent decrease in body weight [28]. Leptin is predominantly cleared by the kidneys, and it has been demonstrated that chronic hemodialysis patients have supraphysiological levels of this protein [29]. Using a mouse model, in which uremia was induced via subtotal nephrectomy, it has been demonstrated that the level of malnutrition was lower in leptin-receptor-deficient mice compared to wild-type mice [30].
\nProtein-bound URS are generally <500 Da. As mentioned earlier, protein-bound URS are poorly dialyzable due to their high affinity for carrier proteins such as albumin. Albumin binding is complex and determined by numerous factors that are not fully understood. This section will focus on two binding sites found on albumin, Sudlow’s sites I and II, which were first described in 1975 [31]. Sudlow’s site I is also known as the warfarin site, and Sudlow’s site II is the diazepam site. But there are numerous drugs and URS that bind to these sites. Sudlow’s site I is the binding site of 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF), indomethacin, salicylates, and many others. 3-Carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) is considered to be one of the most potent inhibitors of drug binding to albumin compared to other URS [32, 33]. Sudlow’s site II is the binding site of IS, PCS, hippuric acid, and ibuprofen. Observational studies have demonstrated a link between indoxyl sulfate (IS) and p-cresyl sulfate (PCS) concentrations and increased cardiovascular morbidity and mortality in CKD/ESRD. Both of these compounds have a shared quality of possessing high affinity to Sudlow’s site II [34]. As such, they both exist primarily in the bound form (Table 3).
\n\n | MW (Da) | \nSource | \nMetabolism | \nToxicity | \nPercent unbound | \n
---|---|---|---|---|---|
Indoxyl sulfate [37, 38, 45, 46, 47, 48] | \n251.30 | \nTryptophan | \nGut microbiome, hepatic | \nCardiovascular | \n~10% | \n
p-Cresyl sulfate [37, 38, 45, 46] | \n188.19 | \nTyrosine | \nGut microbiome, hepatic | \nCardiovascular | \n5–10% | \n
Kynurenine [41, 42, 43] | \n208.21 | \nTryptophan | \nPrimarily hepatic, also immune cells | \nCNS | \nN/A | \n
Kynurenic acid [41, 42, 43, 52] | \n189.17 | \nTryptophan | \nCNS | \nCNS | \n14% | \n
Quinolinic acid [41, 44] | \n167.12 | \nTryptophan | \nBrain microglia | \nBone marrow, CNS | \nN/A | \n
CMPF [38] | \n240.25 | \nFuranoid fatty acids | \nEndogenous enzymes | \nBone marrow, thyroid, albumin drug binding | \n<1% | \n
Protein-bound URS.
URS, uremic retention solutes; MW, molecular weight; CMPF, 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid
There are known differences in the rate of production of protein-bound URS, and this likely explains why their plasma levels do not correlate well with creatinine, urea levels, or estimated GFR [3]. Organic anion transporters (OAT1 and OAT3) on the basolateral membrane of the proximal tubule are responsible for URS entry into the cell, and subsequent secretion into the tubular lumen appears to be mediated by OAT4 [35, 36, 37]. This important physiological process is hindered by nephron loss in advanced CKD and almost nonexistent in ESRD leading to significant elevation of protein-bound URS.
\nCMPF is a highly protein-bound URS (see Table 3). It is very poorly dialyzable, and there is in vitro data that it leads to radical oxygen species (ROS) production in endothelial cells. Unlike other protein-bound URS, CMPF does not demonstrate any significant removal during dialysis, but dialysate effluent levels were not measured to determine whether there is filtration [38]. The probable explanation, offered by the authors, for the paradoxical rise of CMPF levels after dialysis is hemoconcentration. CMPF has significant effects on drug binding to albumin. CMPF has also been implicated in numerous pathological pathways including anemia, hypothyroidism, and others [39, 40].
\nTryptophan metabolism via the kynurenine pathway produces several solutes (including kynurenine and quinolinic acid) relevant to renal failure. In ESRD patients, elevated levels of kynurenine and quinolinic acid have been associated with endothelial dysfunction, inflammation, and carotid artery thickening [41]. Metabolic products of kynurenine, specifically kynurenic acid, are also known to have neural activity at several neurotransmitter receptors, and alterations in kynurenine removal are thought to be sufficient to produce CNS effects [42, 43]. Researchers have demonstrated that quinolinic acid inhibits erythropoietin release in vitro, possibly contributing to the anemia seen in ESRD patients [44].
\nOver the last few decades, microbial metabolism in the human gut has been recognized as offering beneficial effects to the host. These effects include fermentation of carbohydrates resistant to our own enzymatic processes, formation of several vitamins, and unique contributions to the mammalian metabolome [49, 50]. Important to the current discussion of uremic retention solutes is that a significant amount of protein-bound solutes (IS and PCS included) are formed by dietary protein metabolism in the large intestine [51]. In fact, a 2011 study with dialysis patients comparing the URS levels of individuals with a total colectomy versus those with an intact colon showed IS and PCS to be nearly absent in those patients without colons [52]. Similarly, IS and PCS levels are very low in germ-free rodents.
\nProtein metabolism in the large intestine generates IS and PCS along parallel pathways (Figure 1). For IS the process starts with dietary tryptophan being acted upon by bacterial tryptophanase enzymes that convert tryptophan to indole. Indole is then absorbed in the large intestine and travels to the liver where it is oxidized and sulfated to form indoxyl sulfate [53]. Similarly, bacterial metabolism of tyrosine generates p-cresyl, which is absorbed and converted to p-cresyl sulfate by the liver. Both IS and PCS become bound to albumin and circulate in the plasma until they are secreted by the kidneys via OATs found on the basolateral and luminal membranes of proximal renal tubular cells. The relationship between gut bacterial metabolites, normal human metabolism, and renal excretion has been termed the gut-kidney axis [51, 54, 55, 56]. In fact, an additional classification of URS has been proposed, organizing solutes based on their origin (human metabolism, microbial metabolism, or diet) as opposed to their behavior during dialysis [49].
\nThe gut-kidney axis of indoxyl sulfate (IS) and p-cresyl sulfate (PCS). Adapted from [55] with permission.
In addition to the colon microbiota species, the main determinants of gut microbial metabolism are diet and transit time [56]. With diet, the ratio of carbohydrate catabolism to protein catabolism by the microbiota determines the extent to which protein metabolism (and therefore URS generation) takes place. In the case of carbohydrate excess such as with a high-fiber diet, there is a large amount of energy available for bacterial growth and cell division. The nitrogen sources in the gut are consequently utilized for the bacteria’s own growth and replication as opposed to being fermented for energy [49]. However, in carbohydrate deficiency, the nitrogen sources are predominantly metabolized to phenols, indoles, and amines, thereby contributing to URS generation [51].
\nAnother modifiable determinant of microbial metabolism is the colonic transit time. In vivo human data has demonstrated that the majority of the variance seen in the urinary phenol excretion rate was due to colonic transit time and dietary protein intake. In fact, a doubling of the colonic transit time corresponded to a 60% increase in urinary excretion of phenols [57]. It is thought that longer transit times induce the development of large populations of many proteolytic bacteria. This, in addition to the relative carbohydrate deficit in the colon, contributes to greater protein metabolism and URS generation [51, 56]. The role of the gut-kidney axis when considering possible therapeutics to lower URS will be discussed in a later section.
\nPatients with CKD or ESRD have high morbidity and mortality from cardiovascular disease. Unfortunately, a patient with CKD is much more likely to die of cardiovascular disease than to reach the stage of dialysis dependency [1]. Due to their possible contribution to cardiovascular disease, indoxyl sulfate and p-cresyl sulfate have attracted a lot of research attention.
\nA number of human studies have shown a clinical association between high indoxyl sulfate levels and various adverse outcomes. Especially in the early stages of CKD, there have been associations of higher IS levels with left ventricular dysfunction, coronary atherosclerosis, coronary stent restenosis, and cardiac death [58, 59, 60, 61]. However, with more advanced CKD (such as with hemodialysis patients), the associations of higher IS levels with cardiovascular events and cardiac death are mixed [62, 63, 64, 65]. Several studies specifically show no association between higher IS levels and cardiovascular morbidity and mortality [64, 65]. This might be related to the fact that with advanced CKD, there is already end organ damage, and so the levels of URS are not as significant.
\nStudies with isolated cells or tissues have demonstrated a number of mechanisms by which IS could possibly lead to cardiovascular disease. One of these mechanisms is via increased tissue factor expression. Multiple studies examining this feature have found evidence that IS acts as an agonist for the aryl hydrocarbon receptor (AHR) in vascular smooth muscle cells. The AHR-IS complex is translocated to the nucleus where it dysregulates a host of genes leading to inhibition of the degradation of tissue factor [66]. This concept was further demonstrated by showing that AHR antagonists reduce tissue factor expression [67]. Additionally, AHR activation has been linked to increased progression of atherosclerosis in a mouse model [68]. Another mechanism might be via leukocyte endothelial adhesion. Studies have demonstrated increased leukocyte recruitment with IS exposure, as well as increased leukocyte adhesion to endothelial cells which is accompanied by increased expression of NF-kB, TNFα, and E-selectin. IS pretreatment of endothelial cells significantly increased IL-1β–induced E-selectin expression, monocyte adhesion, and phosphorylation of various MAP kinases and transcription factors such as NF-kB [69]. These findings support the hypothesis that altered E-selectin shedding may play a central role in the cardiovascular disease that complicates the course of many CKD patients [70].
\nAdditionally, increased vascular calcifications seem to accompany increased IS levels. In vivo rodent studies demonstrated that uremic-level IS administration resulted in vascular calcifications [71]. The mechanism by which IS leads to vascular calcification is unknown, but it may be related to altered osteoblast signaling [72]. Additional evidence regarding the effects of IS includes disrupted adherens junctions on endothelial cells, impaired proliferation and self-repair of endothelial cells, endothelial microparticle release, free radical production, and increased advanced glycation end products [73, 74, 75, 76, 77].
\nClinical studies have identified an association between elevated PCS levels (total and unbound) and cardiovascular complications in CKD patients. These cardiovascular complications include an increased rate of coronary artery disease, vascular calcifications, and cardiovascular and all-cause mortality [78, 79, 80, 81, 82].
\nCell culture and isolated tissue studies have demonstrated a variety of effects of increased levels of PCS. Several studies have focused on the oxidative stress that results from PCS exposure. Elevated PCS levels have been demonstrated to induce leukocyte-free radical production, oxidative stress in both human umbilical vein endothelial cells and vascular smooth muscle cells, as well as increase NADPH oxidase activity and ROS production in cardiomyocytes leading to cardiac cell apoptosis [83, 84, 85, 86]. Other effects include the release of endothelial microparticles, vascular remodeling, and the observation that an increase in PCS appears to stimulate leukocyte rolling along the vascular endothelium, suggesting there is cross talk between leukocytes and endothelial cells [85, 87, 88]. The mechanisms behind these findings are not yet clear.
\nIn response to the mounting evidence that supraphysiological levels of URS likely contribute to the morbidity and mortality of CKD/ESRD, there has been significant interest in developing methods to lower URS levels. Two major approaches have substantial research behind them—increasing removal via dialysis and decreasing production by gastrointestinal flora. Broadly speaking, both have shown the ability to lower URS levels, but no method has definitively shown a mortality benefit as of yet.
\nThere have been several investigational strategies that have proven successful in removing protein-bound URS during hemodialysis. The method with the fewest obstacles to being incorporated into clinical practice is the addition of a pressure gradient across the dialysis membrane (otherwise known as convection). Despite data indicating that it can effectively remove more protein-bound solutes than traditional dialysis, the clinical benefits have yet to be proven [4, 89, 90]. Another area of research concerns altering the dialysis milieu in order to affect the binding of URS to plasma proteins. Examples of this effort which have data supporting their use include using hypertonic solution, the use of albumin-binding site competitors such as tryptophan and docosahexaenoic acid, increasing temperature, plasma dilutions, and pH manipulation of the dialysate [47, 90, 91, 92, 93, 94].
\nOther techniques have been proposed and studied, but they involve technologies which would profoundly alter the way dialysis is delivered, therefore making their incorporation into clinical practice more difficult. Given the importance of renal tubular secretion in protein-bound URS removal, there has been interest in incorporating bioengineered renal tubules in the dialysis membrane. In vitro data has demonstrated that secretion of protein-bound URS (indoxyl sulfate and kynurenic acid) can be achieved in immortalized proximal tubule epithelial cells by integrating transport proteins such as organic anion transporters (OAT) [95]. The use of sorbent containing extracorporeal devices (SCED) uses an additional circuit within the hemodialysis setup to cleanse albumin of URS before returning them to circulation. The use of SCEDs has even demonstrated effective removal of these solutes from post-dialysis patient plasma. However, this strategy has been limited due to biocompatibility problems with the sorbent, although the development of newer sorbents may circumnavigate this obstacle [96, 97].
\nThere is growing interest in affecting URS levels by intervening at the level of the gut-kidney axis. This approach has significant potential because URS accumulate in all stages of CKD, not just in dialysis-dependent ESRD. By intervening upstream in the gut-kidney axis, clinicians could empirically inhibit the production and absorption of URS and their potential cardiovascular effects. The major strategies being investigated in this area include those that affect URS generation and those that act as gastrointestinal adsorbents. Altering URS generation involves using either probiotics or prebiotics to theoretically shift microbial metabolism toward carbohydrate metabolism and away from the generation of proteolytic fermentation end products such as URS.
\nThe administration of live microorganisms in order to alter an individual’s microbiome (otherwise known as probiotics) has been utilized as a treatment for various illnesses. While some initial studies utilizing probiotics showed a promise in decreasing URS, these studies were performed in patients with healthy kidneys. Only a few studies were performed which looked at URS in CKD patients, and the results for Lactobacillus and Bifidobacterium genera have been promising [98, 99, 100, 101, 102]. As opposed to introducing a living organism, prebiotics are selectively fermented molecules that result in changes to the composition or activity of the gut microbiota, conferring a benefit to the host. The limited studies that exist in utilizing prebiotics have used ingredients belonging to either the inulin-type fructans or the galacto-oligosaccharides [99, 103].
\nDue to the advancement of DNA sequencing technology, research on the gut microbiome has accelerated and includes many different conditions. The effect of the gut microbiome on URS production has been studied. Nazzal et al. demonstrated the effect of oral vancomycin on the gut microbiome [104]. They demonstrated that plasma levels of protein-bound indoxyl sulfate and p-cresyl sulfate were reduced in an ESRD population after a single dose of oral vancomycin, but the effect was transient and reversed itself by the end of the follow-up period. The diversity of the gut microbiome was significantly reduced, and the effect did not resolve by the end of the study period.
\nLimiting the uptake of colonic solutes by using an oral adsorbent, such as the spherical carbon adsorbent AST-120, has been an additional approach to lowering URS levels. AST-120 binds to a number of URS precursor molecules, and some of the initial studies were very promising, showing a decrease in the levels of several URS, including IS and PCS [105, 106, 107]. A randomized controlled trial was performed in CKD patients, which sought to evaluate the effect of AST-120 on intima-media thickness and carotid artery stiffness. The results were encouraging, finding that the AST-120 group had reduced intima-media thickness along with less arterial stiffness compared to the non-AST-120 group [108]. However, EPICC (a large randomized, placebo-controlled, double-blind study) failed to show a benefit of AST-120 for clinical outcomes such as CKD progression and mortality, thereby failing to support the widespread use of AST-120 in advanced CKD [109].
\nTo this day, our understanding of URS is limited. One major limitation of uremia research is that URS accumulate in synchrony. This makes it difficult to establish a causal relationship. Ideally, URS research should be performed in the early CKD population and should include long follow-up. Another limitation is the lack of targeted methods to decrease the level of a specific URS. Once specific URS can be targeted, prospective randomized control trials will able to elucidate each URS’ true effects.
\nIn addition, it is becoming clear that interventions outside of the realm of hemodialysis could have great potential. As described above, URS accumulate in all stages of CKD, not just in dialysis-dependent ESRD. Considering the prevalence of early CKD and its significant mortality, this would be the ideal population for further research on therapeutic options. By focusing on the gut-kidney axis, we could learn how to halt the production of URS. There is a need for randomized control trials to evaluate the effectiveness of prebiotics, probiotics, dietary alterations, adsorbents, and antibiotics in leading to better outcomes for this patient population.
\nThe word “migraine” comes from the
Migraine is self-limiting, usually presenting as recurrent severe
The best solutions to medical conditions come only from understanding the pathophysiology of the disease state. As per Wolff’s vascular theory, vascular constriction leading to hypoperfusion of the cortex later followed by vascular dilation was put forward as the main pathophysiological mechanism. Currently neurovascular hypothesis involving the trigeminovascular system is considered. Another hypothesis includes mutations of neuronal calcium channels, leading to hypersensitivity, resulting in migraine attacks. It is also postulated that increased dopaminergic activity in the thalamus/hypothalamus causing modulation in central pain pathways also plays a role in migraine attacks. Other mechanisms put forward include cortical spreading depression; release of vasoactive peptides like substance P, calcitonin gene-related peptide (CGRP) from trigeminal neural endings, nitric oxide, and serotonin; excess activation of N-methyl-
It can be divided into treatment of acute attacks and treatment of chronic migraine. As per the US consortium (2000), recommended guidelines [13] for treatment of acute migraine include pharmacological and non-pharmacological modalities as shown in Table 1.
|
Treatment of acute migraine attacks.
Triptans are selective agonists of 5-HT1B and 5-HT1D receptors. The mechanism of action includes intracranial vessel vasoconstriction (5-HT1B), peripheral neuronal inhibition (5-HT1D), and presynaptic dorsal horn stimulation (5-HT1D), producing second-order brain stem neuronal inhibition. Triptans influence the function of 5-hydroxytryptamine 1F (5-HT1F) receptors and enhance descending inhibitory pain pathways. Triptans reduce—to a considerable extent—pain severity in 2 h as per randomized controlled trials. Oral formulations are usually preferred over other formulations, but 6 mg subcutaneous injection of sumatriptan appears to be the most efficacious. As per current evidence, all oral formulations have equal efficacy except for frovatriptan which is less efficacious but has longer duration action. Parenteral preparations are more useful than oral ones, but the choice of medications depends on the clinician as well as the patient. Triptans are the first-line drugs used in acute treatment of moderate-to-severe migraine with the best pain relief occurring if it is taken within 30 min of attack, and a second dose is usually recommended after 2–4 h of initial dose. It is best used in combination with antiemetics and NSAIDs. Adverse effects include serotonin syndrome when used in combination with selective serotonin reuptake inhibitors (SSRIs), and it should be used with caution in patients having ischemic heart disease [14, 15, 16, 17, 18, 19, 20, 21, 22]. Characteristics of triptans are summarized in Table 2.
Drugs | Half life | Maximum daily dose |
---|---|---|
Group 1: fast-acting triptans | ||
Sumatriptan | 3 h | 200 mg oral 40 mg intranasal 12 mg subcutaneous |
Rizatriptan | 2–3 h | 30 mg (15 mg if on propranolol) |
Almotriptan | 3–4 h | 25 mg |
Zolmitriptan | 3 h | Two tablets or 10 mg maximum oral daily dose. Two sprays or 10 mg intranasal |
Eletriptan | 4 h | 80 mg |
Group 2: slow-acting triptans | ||
Frovatriptan | 26 h | 7.5 mg |
Naratriptan | 6 h | 5 mg |
Triptan characteristics.
Ergots act on multiple receptors including the 5-HT ones, and these account for a robust side effect profile. It is used in acute management of migraine. Side effect includes nausea as well as severe vasoconstriction. It is contraindicated in patients with vascular disease, hepatic problems, renal dysfunction, and hypertension. It is avoided in pregnancy. Dihydroergotamine (DHE) is the only preparation available and is used both parentally and intranasally. Repeated administration of DHE is very effective in refractory cases as well as status migrainosus. It is relatively safe and effective but it requires hospital administration [23, 24, 25].
Good quality evidence supports the use of NSAIDs alone or in combination with specific agents. These drugs in combination with antiemetics are comparable to lower doses of oral triptans. Recently, powdered preparation of diclofenac sodium is approved for treatment of acute attack. Ketorolac, administrated IV, can be used for emergency management of migraine. NSAIDs need to be used with caution in patients with renal toxicity [26, 27, 28, 29]. Characteristics of different drugs in this group are summarized in Table 3.
Drugs | Formulation | Dose used (the dose wording should be mg’) |
---|---|---|
Aspirin | Tablet/oral solution | 650–1000 mg |
Ketorolac | Tablet | 10 mg |
Ketoprofen | Capsule | 50–75 mg |
Ketoprofen-extended release | Capsule | 200 mg |
Diclofenac potassium | Tablet/powder | 50 mg |
Meclofenamate | Capsule | 50 mg, 100 mg |
Ibuprofen | Capsule, tablet, oral suspension | 400–1, 0 g |
Etodolac | Tablet/capsule | 200–500 mg |
Naproxen | Tablet | 120–550 mg |
Naproxen-controlled release | Tablet | 750–850 mg maximum |
NSAID characteristics.
Dopamine D2 receptor antagonists can be used alone or in combination to treat headache as well as nausea. It is mostly used in emergency settings and is available in oral, parenteral, and suppository forms, but concerns over extrapyramidal side effects, tardive dyskinesia, and lack of familiarity in their effect on migraine attacks restrict their use to a great extent [30, 31, 32, 33]. Characteristics of antiemetics are summarized in Table 4.
Drug | Formulation | Dose of migraine |
---|---|---|
Prochlorperazine | Tablet, suppository | 5–10 mg 25 mg |
Metoclopramide | Tablet | 10 mg |
Chlorpromazine | Tablet | 10–25 mg |
Promethazine | Tablet | 25–50 mg |
Ondansetron | Tablet, oral disintegrating tablet | 4 mg 8 mg |
Antiemetic characteristics.
Steroids are suggested for acute treatment as well as for status migrainosus [34]. They act by reducing the neurogenic inflammation and vasogenic edema and also play an important role in central serotonergic pathways [35]. One study showed that addition of dexamethasone 4 mg per oral to triptans plus NSAID reduces recurrence and is well tolerated in patients with frequent attacks [36, 37].
Opioids are the most prescribed drug for acute and rescue therapy in migraine in America. Recent studies have discouraged the use of opioids mainly because it decreases gray matter, increases CGRP release, releases pro-inflammatory peptides, and also causes glutamate receptor activation. It also results in degranulation of mast cells and causes vasodilation. There are many side effects, such as overuse headache and disease progression [38, 39].
Based on migraine pathology theories, trigeminal ganglion activation causes the activation of nociceptive neurons which leads to subsequent release of CGRP. Increased CGRP levels cause plasma protein extrusion, vasodilation, and mast cell degranulation, ultimately leading to neurogenic inflammation. Drugs which antagonize CGRP include olcegepant, telcagepant, and latest approved monoclonal antibodies, namely, erenumab, fremanezumab, and galcanezumab [40]. They prevent binding of endogenous CGRP on its receptors and suppress the stimulation of CGRP on trigeminal ganglion neurons. They inhibit cortical spreading depression [40]. They lack vasoconstrictive effect. Olcegepant is as effective as oral triptans with less cardiovascular side effects such as blood pressure increase and tachycardia. But one major limitation is intravenous dosing. Telcagepant was initially claimed to be as potent as rizatriptan, causing pain relief in 2 h and also sustained pain relief at 24 h and relief of migraine-associated symptoms with overall good tolerability profile, but later the phase II trial was terminated, claiming the drug showed increase in liver transaminases [40]. Eptinezumab is a new drug in this class under trial and is not yet approved by the Food and Drug Administration (FDA).
It is a 5-HT1F receptor agonist. In experimental model, it blocks neurogenic inflammation, decreases c-fos expression, and lacks vasoconstriction. The main postulated mechanisms include inhibition of protein leakage, blockage of secondary trigeminal neuronal activation, and inhibition of neuropeptide release like glutamate. In a double-blind placebo-controlled parallel group study in 512 patients, the oral form and dose of 50, 100, 200, and 400 mg in moderate-to-severe migraine attacks proved that it is as effective as sumatriptan without causing vasoconstriction, but the significant drawback is its major side effects in the central nervous system. Studies also show a great improvement in headache response in 2 h but also show high 24-h headache recurrence rate [41].
Tezampanel acts as a competitive antagonist of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate receptor (subtype GluR5) of the ionotropic glutamate receptor family. A randomized triple-blind parallel group double-dummy, multicenter trial showed 1.2 mg tezampanel had 69% headache response rate when compared to 6 mg s.c. sumatriptan which had a response rate of 86%. It is effective and well tolerated in migraine. It can be used only via intravenous route. Dasolampanel is an orally bioavailable analog of tezampanel. Both drugs were never marketed [42]. Other newer agents are summarized in Table 5.
Newer targets and drugs | Current status |
---|---|
1. Adenosine receptor agonists [43] |
|
2. NXN-188 [44] |
|
3. LY2951742 [45] |
|
4. Orexin receptor antagonism [46] (filorexant) | Orexin: trigeminal nociceptive and CSD RCT: failed efficacy |
5. TRPV1 antagonism (SB-705498) [47] |
|
6. Melatonin [48] |
|
7. P2Y purinergic receptors [49] |
|
Newer targets and drugs.
It is indicated when a patient meets the following criteria [50]:
Four or more migraine days per month.
Recurring migraines significantly interfere with daily activity.
Contraindication/failure/overuse—acute therapies.
Overwhelming costs of acute therapies.
Uncommon migraine conditions—hemiplegic and basilar migraine.
Various beta blockers used are summarized in Table 6. The mechanisms by which they act include inhibition of central beta receptors and antagonism of 5-HT1A and 5-HT1B receptors, thereby reducing neuronal excitability. It inhibits nitric oxide (NO) production by blocking inducible nitric oxide synthase and inhibits excitatory activity of glutamate, thereby reducing neuronal activity. They also inhibit kainate-induced currents (synergistic with NMDA blockers) and reduce neuronal activity and also have additional membrane-stabilizing action [51, 52].
Drugs | Daily doses |
---|---|
Propranolol | 40–400 mg |
Nadolol | 20–160 mg |
Metoprolol | 100–200 mg |
Atenolol | 50–200 mg |
Timolol | 20–60 mg |
Beta blockers and dosage.
In an open-label trial of 76 patients, a dose of 3.125–6.25 mg twice a week was used, and it was found that 60% of patients had 50% reduction in monthly migraine attack frequency and severity, but in 26% of patients, there was lack of efficacy with the drug [53].
It inhibits calcium entry and prevents intoxication of cells exposed to cerebral hypoxia due to cortical spreading depression [54]. Various drugs used are summarized in Table 7. Other possible mechanisms include inhibition of 5-HT release, inhibition of neurovascular inflammation, and cortical spreading depression.
Drugs | Comment |
---|---|
1. Flunarizine |
|
2. Verapamil |
|
Calcium channel blockers and dosage.
It is a combination of valproic acid and sodium valproate. It is used at a dose of 500–1500 mg/day. Mechanisms include prolongation of sodium channel inactivation, suppression of calcium-mediated T current, and inhibition of gamma-aminobutyric acid (GABA) transaminase. Adverse effect includes nausea, vomiting, gastrointestinal distress, alopecia, and craniofacial abnormalities in fetus [56].
Topiramate is a recently approved drug for migraine prophylaxis. Starting dose of 15–25 mg at bedtime and increase 15–25 mg/week [57]. Mechanisms include blocking of the voltage-gated sodium channel and inhibition of activation of AMPA-kainate receptor of glutamate, and it also enhances postsynaptic GABAA receptor current. Adverse effects include somnolence, fatigue, weight loss, nervousness, and precipitation of renal calculi.
It inhibits GABA transporter (GAT-1) and thereby reduces GABA uptake into the neurons and glia. It is still not approved by the FDA. In an open-label trial of 41 patients who failed with treatment of valproates with 4 mg QID, 33/41 patients showed 50% reduction in migraine attacks, and 5 patients showed complete remission in migraine [58].
It modifies synaptic release of glutamate/GABA by binding to specific synaptic protein (SV2A). Anecdotal evidence says prevention of migraine. A 10-week open-label study, evaluating efficacy and safety of LCT for pediatric migraine in a population of 30 children or adolescents aged 6–19 years, showed a reduction in headache frequency and severity [59].
It blocks voltage-dependent sodium and T-type calcium channels and decreases glutamate-mediated excitatory neurotransmission. Also, it inhibits excessive NO production and helps in scavenging NO and hydroxyl radicals. In an open-label trial, 33 patients with migraine headache, refractory to other preventive therapies, were given a dose of 100–600 mg every third day. Results showed that 65% of patients had a reduction in frequency of migraine attacks [60].
Possible mechanisms include reuptake inhibition of serotonin and noradrenaline, α-adrenergic and NMDA-receptor antagonism, sodium and calcium channel blocking action, and potassium channel activation. Increase in GABAB receptor action and opioid receptor binding/opioid-mediated effect is another minor action. It reduces inflammation by decreasing prostaglandin (PGE2) and tumor necrosis factor (TNF-α). Various drugs are summarized in Table 8. Venlafaxine is used at a dose of 75–225 mg: a double-blind placebo controlled trial showed that the drug was better than placebo, starting with 37.5 mg extended release tablet/week followed by 75 mg for another week and then 150 mg extended release in the morning [61].
Drugs | Daily doses |
---|---|
Amitriptyline | 10–400 mg |
Doxepin | 10–300 mg |
Nortriptyline | 10–150 mg |
Protriptyline | 5–60 mg |
Antidepressant dosage.
The renin-angiotensin system plays a role in neurogenic inflammation and causes increased susceptibility to oxidative stress. It also causes endothelial dysfunction and neuromodulator in nociception. Lisinopril alters sympathetic activity and inhibits free radical activation. It also increases prostacyclin synthesis and blocks the degradation of bradykinin, substance P, and encephalin. In a double-blind placebo-controlled crossover study, patients aged 19–59 years with migraine were treated with 20 mg Lisinopril for 11 weeks—21% of patients showed 50% reduction in migraine attacks [62]. In a comparative study of candesartan vs propranolol for migraine prophylaxis in 72 patients, 43% of patients showed greater than 50% reduction in migraine, and it was equally efficacious to propranolol [63].
It is the FDA-approved drug for prophylaxis of chronic migraine at doses ranged from 155 to 195 IU, and it is injected in seven craniofacial and neck muscles, usually the temporalis. It inhibits neurogenic inflammation by inhibiting the release of nociceptive mediators like glutamate, substance P, and CGRP from the peripheral terminals of the efferent nerves. The analgesic action of onabotulinum toxin is central but yet to be proved. It will effect 3 h after injection and last for at least 7 days. Novel delivery routes such as topical/subcutaneous applications are under research [64].
It is used to limit the excessive inflammatory response through H3 receptor activation. Drugs include Nα-methylhistamine and investigational drug SCH 50971. Phase III double-blind placebo-controlled trial for 12 weeks in 60 patients with a dose of 1–3 mg twice a week caused a reduction in headache frequency, intensity, and duration in 80% of patients. It helps in reducing the dose of analgesics used [65].
Preclinical studies showed inhibition of cortical spreading depression by the drug. It inhibits neurogenic inflammation and also the gap junctional intercellular communication (GJIC) between the neurons and satellite glial cells. Various randomized double-blind parallel group placebo-controlled multicenter studies for acute migraine were tried. There are conflicting reports of headache relief at 2/4 h and reasons are not found. In one study with 40 mg on 39 patients, it was found to be effective for migraine with aura when compared to that without it, reinforcing its inhibitory effect on CSD [66].
Multiple studies show migraine is associated with low levels of magnesium. It causes an influx of calcium into the neurons, causing glutamate release into the neurons, which results in neuronal activation. The onset and propagation of cortical spreading depression is delayed and decreases. It also causes change in neurotransmitter secretion and intensifies the secretion of substance P. It is used in patients with aura and premenstrual migraine and is used at a dose of 1, 0 g IV and 300–600 mg orally in chelated magnesium (taurate, glycinate, oxide) [67]. Magnesium plus
It promotes electron transfer from complex I and II to cytochrome C and helps in ATP production. It protects the mitochondria from free radical damage. A study of 1478 migraine patients of age range 3–22 years showed low levels of CoQ in 33% of patients. A randomized controlled trial of 42 patients receiving 100 mg TID for 3 months found it superior to placebo, and 48% of subjects have greater than 50% reduction in migraine attacks [68].
It is a cofactor in the Krebs cycle. Abnormal phosphorylation of ADP to ATP is prevented with riboflavin. A randomized controlled trial with 400 mg riboflavin taken daily for 3 months was superior to placebo for reduction of migraine frequency [69]. A randomized controlled trial with 400 mg of riboflavin plus feverfew and low-dose magnesium was comparable to a 25 mg active riboflavin. Greater than 40% of patients showed 50% reduction in migraine attacks [70].
It helps in the conversion of homocysteine to methionine. Studies show vitamin B12 deficiency causes increase levels of urine methylmalonic acid levels in patients and worsens migraine. A possible mechanism of vitamin B12 action in migraine includes its excitatory role in the CNS by acting on NMDA receptors. It also plays a significant role in initiation, duration, and progression of migraine and activation of trigeminovascular system [71].
It is sold as capsules of dried leaves of the weed plant Tanacetum parthenium. Animal models show feverfew acts by inhibition of nitroglycerine-induced fos expression and inhibition of nuclear factor-kappa β. An open-label trial with T. parthenium (300 mg) plus Salix alba (white willow) for 12 weeks showed a decrease in pain intensity and duration of migraine. A randomized double-blind placebo-controlled trial (riboflavin 400 mg + magnesium 300 mg + feverfew 100 mg) for 3 months showed positive results. Recently two randomized clinical trials (RCT) of a purified stable extract of feverfew, MIG99, were ineffective in migraine, and clinical effects were very low with various complications [72].
Petasites hybridus is a potential poisonous plant but the detoxified root extract is safe. Mechanisms include inhibition of the synthesis of leukotrienes. It also decreases the intracellular concentration of calcium. It is used in the prophylaxis of migraine in children. A small study of 100 mg/day and a larger one of 150 mg/day vs placebo have shown efficacy [73].
With many newer agents now under clinical trials as well as in use, physicians should be aware of these drugs and their side effects, so they can use these agents for treating recurrent and chronic cases of migraine. Also, further well-designed clinical trials are needed to prove the efficacy of these agents in treatment of migraine. So, further research is needed to find out the safest and most effective treatment for chronic migraine, further designing proper animal models for studying migraine, to identify newer drug targets and how to prevent the migraine at the patient level from acute attack going in for chronic attack.
Nil.
NSAIDS | nonsteroidal anti-inflammatory drugs |
GJIC | gap junctional intercellular communication |
CGRP | calcitonin gene-related peptide |
NO | nitric oxide |
NMDA | N-methyl-d-aspartate receptor |
DHE | dihydroergotamine |
ATP | adenosine triphosphate |
ADP | adenosine diphosphate |
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\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
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