Prevalence of subjects with advanced atrophic corpus gastritis (ACG), elevated
Abstract
The purpose of this chapter is to clarify the prevalence of Helicobacter pylori infection (HPI) and atrophic corpus gastritis (ACG) in patients with intellectual disability (ID) and review the literature surrounding them. We measured the levels of pepsinogen I, pepsinogen II, gastrin-17b (basal), and Helicobacter pylori antibodies from 243 patients with intellectual disability living in Rinnekoti Research Centre at Lakisto area during 2009–2011. We determined the levels of hemoglobin, mean cell volume (MCV), hematocrit, and the mean amount (MCH) and concentration (MCHC) of red cell hemoglobin, the counts of erythrocytes, leucocytes, and thrombocytes. About 43% had high level of Helicobacter pylori antibodies and 6% ACG. Our results show that Helicobacter pylori infection occurs approximately twice the rate it appears in the normal population. Also, the incidence of ACG was higher among patients with ID than normal population. ID may be a risk of getting the Helicobacter pylori infection (HPI) and ACG. In addition, it was found that the level of thrombocytes was increased in HPI group compared to normal group and decreased in ACG group compared to normal group. This study shows that there is clearly a need to investigate (test) more stomach condition in patients with ID.
Keywords
- helicobacter
- Helicobacter pylori
- pepsinogen
- gastritis
- atrophic corpus gastritis
- intellectual disability
- personalized medicine
1. Literature review
1.1. Helicobacter pylori infection
1.2. The role of epidemiology in understanding the health effects of Helicobacter pylori in intellectual disability
Intellectually disabled children are a vulnerable subgroup and may experience higher rates of infections and morbidities [4].
1.3. Helicobacter infection and gastric neoplasia
As discussed above,
Gastrointestinal problems in handicapped children with neurodevelopmental disabilities are chronic and present long-term management problems. These conditions include dysphagia (60%), chronic pulmonary aspiration (41%), gastroesophageal reflux (32%), abdominal pain and gastritis (32%), constipation (74%), and malnutrition (33%) [29]. Growth failure and malnutrition are common in children with cerebral palsy, particularly in those with spastic quadriplegia, of which 85% report feeding problems [30, 31]. In addition, 20–30% of hemiplegic and diplegic cerebral palsy children are underweight for age [26, 32]. There are multifactorial causes: insufficient food intake, feeding problems, increased nutrient losses from vomiting or diarrhea, and alterations in energy requirements in epileptic or metabolic syndromes where increased muscle tone or involuntary movements are seen. What is now clear is that undernutrition in cerebral palsy is often correctable and that providing a balanced diet and better nutrition can result in improvement in long-term spasticity, appearance, and effect of these children [33].
Good number of studies have been published in persons with intellectual disability, however, large-scale scientific studies have not been published with a population case-control study [22, 32, 34]. Harris et al. [35] (10) reported that hospital residents under 40 years of age had a 87% prevalence of HP compared with 24% for controls, whereas the overall prevalence for all ages was 87% for residents, and 43% for controls in hospital residents with severe learning disabilities. A larger study including 338 intellectually disabled and 254 controls from Holland (12) found a prevalence of 5% in children and 50% in the elderly in the general population, whereas 83% of the disabled and 27% of the healthy employees were infected. The presence of HP was significantly associated with male gender, longer duration of institutionalization, an IQ below 50, rumination, and a history of upper abdominal symptoms. Another study was conducted to determine the occurrence of HP infection in persons, who presented with severe dyspeptic symptoms and to monitor clinically the effect of treatment [36]. Over a 1-year period, a total of 43 persons (total population in care was 224) had severe dyspeptic symptoms and 42 persons (98%, 26 males, 16 females, mean age 45 years, mean institutionalization 20 years) had HP.
1.4. Treatment regimens used for H. pylori eradication
Combination drug therapy regimens commonly used to treat
1.5. Helicobacter pylori infection and oxidative stress
Oxidative stress results from the damaging action of reactive oxygen species. These molecules react with proteins, lipids, or DNA, altering their structure and causing oxidative damage to the cells. Reactive oxygen species (ROS) are produced during normal and physiological process, which inevitably leads to the generation of oxidative molecules: superoxide (O2•_), hydrogen peroxide (H2O2), or hydroxyl radical (•OH). Oxidative stress is implicated in a large number of diseases: cancer (oxidative damage to DNA causes mutations that can lead to carcinogenesis), atherosclerosis (atherosclerotic plaques are made from oxidized fat), and neurodegenerative diseases (oxidative damage is a central component of nerve cell destruction). Indicators of oxidative stress have been detected in muscles and blood of ID patients. Oxidative damage can alter the blood-brain barrier, which could explain some of the cognitive problems experienced by patients.
There is an increasing evidence that microbial pathogens induce oxidative stress in infected host cells [43, 44, 45] and this may represent an important mechanism leading to epithelial injury in
Oxidative stress could well play a role in the altered epithelial proliferation, increased apoptosis, and increased oxidative DNA damage [47, 48, 49] associated with
Evidence for this includes increased levels of reactive oxygen species (ROS) measured in the mucosae of infected patients [48, 50, 51]. While activated, ROS-releasing phagocytic leukocytes recruited to the gastric mucosa during infection represent one obvious source of oxidative stress [43, 50].
The mechanism of tissue damage and cell proliferation in H. Pylori infection remains unknown, although cytokines, chemokines, growth factors, including nitric oxide synthase and potent neutrophil. Derive reactive oxygen metabolism have all been proposed to contribute to such damage [52, 53, 54]. HP infection is associated with the increased production of free radicals in the gastric mucosa [50]. Accumulated free radicals in the tissue initiate lipid peroxidation of cell membranes and threaten cell integrity. Antioxidant may be useful in HP-related mucosal disease [47]. Evidence suggests that microbial pathogens induce oxidative stress in infected host cells [43, 44, 45], which represents an important mechanism causing damage to the epithelial in
2. Research study
2.1. Material and methods
GastroPanel test (Biohit Oyj, Helsinki) was used. The test consisted of measurement of plasma pepsinogen I, pepsinogen II (PG I, PG II and PG I/PG II ratio),
2.2. Laboratory determinations and reagents
Vacuette serum tubes were used to obtain serum samples and vacuette K2EDTA tubes were used to obtain hematological samples. Hemoglobin, mean cell volume (MCV), hematocrit, erythrocytes, thrombocytes, and leukocytes were assayed with Sysmex KX-21 N analyzer. All used reagents were reagent grade. All laboratory determinations were controlled with the control samples from Labquality Ltd., Helsinki, Finland. All enzyme immunoassays were done with BP 800 reader.
2.3. Study population
The study material consisted of blood samples from patients with intellectual disability (243 individuals). Patients with ID lived in groups containing 6–8 persons during 2009–2011. Age was from 10 to 80. The whole group consisted 157 male and 86 female patients with ID. Sanitary facilities were common for each group as normal family living. The personnel taking care of these patients was living with them for 24 hours per day with 8–10 hours shifts.
3. Results
We measured the levels of pepsinogen I, pepsinogen II, gastrin 17-beta, and
4. Discussion
This study provides an overview of the best available evidence on the prevalence of
The level of ID and environmental factors may be related to the risk of infection with
Proujansky et al. [20] stated that rumination may be a possible symptom of
Wallace et al. [63, 64] reported that 7% of institutionalized adults with ID treated for
The poor prognosis of patients with a negative
Antibiotic susceptibility should be checked in all patients, ideally, before the start of eradication treatment. The knowledge of local antibiotic resistance and consumption pattern is important in selecting a reliable regimen [71, 72, 73]. Future development for
A complete history could also do away with the need for additional testing and increased medical expenses for the patient and the healthcare system as a whole.
Acknowledgments
We would like to thank all the patients who lived at Rinnekoti Research Centre during 2009–2011. Also we want to thank the laboratory workers of Rinnekoti and we are grateful for a financial help of Rinnekoti Foundation and Finnish Brain Foundation.
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