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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating parietal cell antibodies (PCA) were fund in 8 (5.4%) out of 147 diabetic children screened. Both sexes were equally represented, but the titres were higher in the girls. No clear relationship between the presence of these antibodies and age or the duration of diabetes was observed. Gastric studies were performed on 8 children with PCA (group A) and 41 without PCA (group B). Both basal (BAO) and maximal acid output (MAO) were significantly (p < 0.05) lower and fasting serum gastrin elevated (p < 0.01) in group A as compared with the control group. Two patients were achlorhydric. In group B, 17 patients out of the 41 studied had hyposecretion and one achlorhydria. The result became most obvious in the group with a duration and diabetes over 10 years, where MAO was significantly diminished (p < 0.05). Gastric morphology revealed atrophic gastritis in 3 patients from seven biopsies in group A and one out five biopsies for severe hyposecretion in group B. Two other children in group A had superficial gastritis. Serum ferritin levels decreased along with the duration of diabetes. Those with gastric mucosa had the lowest values.
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PMID:Parietal cell antibodies and gastric secretion in children with diabetes mellitus. 744 98

Autoimmune gastritis, induced by day-3 thymectomy of BALB/c mice, is a destructive CD4+ T cell-mediated disease characterized by leukocyte infiltrates in the gastric mucosa, loss of parietal and chief cells and anti-gastric H/K ATPase autoantibodies. Our previous studies have indicated that a T cell response to the H/K ATPase beta subunit is required for the onset of autoimmune gastritis (Alderuccio, F., Toh, B. H., Tan, S. S., Gleeson, P. A. and van Driel, I. R., J. Exp. Med. 1993. 178: 419). To determine whether a response to the beta subunit autoantigen is alone sufficient to induce autoimmunity, or whether other tissue-specific factors are required, we have generated transgenic mice expressing the gastric H/K ATPase beta subunit in beta islet cells of the pancreas (RIP-H/K beta). RIP-H/K beta mice developed autoimmune gastritis and insulitis after day-3 thymectomy. Significantly, insulitis, observed as a peri-islet infiltrate, was only detected in thymectomized mice with autoimmune gastritis. There was no apparent immune destruction of the pancreas as insulitis did not progress to invasion of the islets or diabetes. Double transgenic mice, expressing the gastric H/K ATPase beta subunit in the thymus and in the pancreas, were protected from both gastritis and insulitis after day-3 thymectomy. Therefore, insulitis in the RIP-H/K beta mice appears to be dependent on a T cell response to the H/K ATPase beta subunit. This is the first example where an organ-specific initiating autoantigen has been expressed in another peripheral tissue. Autoimmune destruction in the stomach, but not the pancreas, indicates that tissue-specific factors play a fundamental role in the development of organ-specific autoimmunity.
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PMID:Expression of a gastric autoantigen in pancreatic islets results in non-destructive insulitis after neonatal thymectomy. 758 46

The etiology, prognosis, and optimal management of primary gastric carcinoids remain controversial. Records of 36 consecutive patients with gastric carcinoid (15 men) were reviewed retrospectively between 1975 and 1990. Follow-up was complete in 97% of cases. Mean age at diagnosis was 58.4 years (range 24-82 years). The clinical presentations included anemia (72%), pain (69%), and carcinoid syndrome (11%). Associated autoimmune and endocrine abnormalities were common and included atrophic gastritis (67%), pernicious anemia (58%), hypothyroidism (39%), diabetes (19%), Addison's disease (6%), and hyperparathyroidism (6%). Lesions were nonantral in 78%, involving only the corpus in 42%, the fundus in 28%, and only the antrum in 8%; 42% were multiple. Urinary 5-hydroxyindoleacetic acid (5-HIAA) and serum gastrin levels were elevated in 17% and 50% of those tested, respectively. Histologic examination revealed that 28% of lesions were > or = 2 cm, and 33% had liver metastases on presentation or developed them during follow-up. Eight patients (22%) died of tumor with a median survival of 39 months. The presence of metastases, atypical histology, serosal involvement, and size > 2 cm were adverse prognostic factors. In patients without hypergastrinemia (n = 6), 66% developed metastases, 60% had elevated 5-HIAA, and 50% died of carcinoid tumor. In sharp contrast, those patients with hypergastrinemia and "typical" gastric carcinoids (n = 15), metastases and death did not occur (p < 0.003 and p < 0.005, respectively, compared with eugastrinemic patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diverse clinical and pathologic features of gastric carcinoid and the relevance of hypergastrinemia. 772 31

The author discusses in the submitted paper the important subject of manifestations of diabetes in the digestive tract--oesophagus, stomach, small and large intestine. Autonomous neuropathy, in particular a reduced tonus of the vagus, leads to a number of functional disorders which can produce diabetic dysphagia, gastroparesis, diarrhoea and constipation. The reduced tonus of the vagus, along with other factors, may lead to atrophy of the gastric mucosa and reduced gastric secretion. This explains the higher incidence of atrophic gastritis and other complications in diabetic patients. The author discusses also basic clinical aspects of these disorders and outlines therapeutic procedures.
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PMID:[Diabetes mellitus and the digestive tract]. 835 70

With respect to the inverse association of serum ferritin level (SFL) with the risk of gastric cancer (GC) observed in some recent epidemiologic studies, possible mediation by achlorhydria as well as atrophic gastritis (AG), both of which are strongly associated with GC risk at not only the individual but also the population level, was examined in a cross-sectional study of 634 men aged 40 to 49 years randomly selected from 5 populations in Okinawa, Iwate, Nagano, Akita and Tokyo. AG and achlorhydria were serologically diagnosed based on the criteria of pepsinogen (Pep) I level < 70 ng/ml and Pep I/Pep II ratio < 3.0, as described previously, and a serum gastrin level of over 140 pg/ml, respectively. In the results, while the mean SFL for all the subjects differed significantly by area, similar areal differences in SFL were also found even when only the non-AG cases were considered. However, both of the above differences were eliminated with the exception of those between Okinawa and each of the other 4 areas, when adjustments were made for medical histories of diabetes mellitus, ulcers and liver disease, body mass index and gamma-glutamyltranspeptidase level. Therefore, no correlation among the 5 areas was observed between the adjusted areal mean SFLs and GC mortality in either case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does high gastric cancer risk associated with low serum ferritin level reflect achlorhydria? An examination via cross-sectional study. 840 48

Helicobacter pylori (H. pylori) is the most common cause of peptic ulcers, and is considered as carcinogenic with respect to gastric cancer and MALT lymphoma. The role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional dyspepsia has been investigated in hundreds of works, but little is done about what role H. pylori may play in non gastric diseases. Gastro-esophageal reflux disease does not seem to be related to H. pylori but Barrett's esophagus might be. Inflammatory bowel diseases tend to be reverse correlated with H. pylori. In coronary heart disease some studies have shown a connection, others not. Diabetes is not likely to be H. pylori-associated and nor do liver diseases with exception for cirrhosis, where a correlation is possible. Respiratory diseases are little examined but bronchiectasis might have a correlation with H. pylori. A small series of children, who had died in sudden infant death, showed a high rate of H. pylori infection.
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PMID:Non-gastric effects of H. pylori infection: a literature review with respect to non gastric diseases which might be associated with H. pylori infection. 1002 62

Helicobacter pylori (HP) is the most common cause of nonerosive nonspecific gastritis. Gastric and duadenal ulcer both are found to be associated with HP infection. Another consequence of HP infection is that it may progress to chronic atrophic gastritis which is a well recognized risk factor for adenocarcinoma of the stomach. So by extension, HP infection can be accepted as a risk factor for gastric cancer. From this aspect, identification of risk groups is increasingly important. It is well-known that patients with diabetes mellitus are more prone to infection. Besides this, presence of gastroparesis diabeticorum may lead to bacterial overgrowth in the upper gastrointestinal (GI) tract. The present crossectional study was planned to study the presence of HP infection in diabetic patients with alterations in upper GI motility and to compare the results with healthy control group. Group I consisted of 51 patients with type II diabetes mellitus (as defined by National Data Group criteria) without any dyspeptic symptoms. Twenty-five age-matched healthy people served as a control in group II. Radionuclide-labelled solid meals were used to calculate gastric emptying time (GET). According to the results, patients in group I were divided into two groups. Patients with prolonged GET were grouped as group IA, while group IB consisted of patients with normal or shortened GET. Presence of HP gastritis is determined by histopathologic examination of endoscopic biopsy specimen. The results showed that the prevalence of HP gastritis in group I and II were 80.4% and 56% respectively and the difference was significant statistically (p: 0.03). In group IA, the prevalence of HP infection was estimated to be 88.2%, while in group IB it was 76.5% but the difference was not significant (p: 0.31). We have not found any correlation between HbA1c levels and the presence of HP infection in both group IA and IB (p values 0.26 and 0.15 respectively). We conclude that the prevalence of HP gastritis is higher in asymptomatic diabetic patients compared with healthy people. But there is no association between the alterations in GET and the presence of HP gastritis as indicated by our results. So prolonged GET may not be regarded as a specific pathogenic mechanism or a cause of HP infection in NIDDM patients.
Exp Clin Endocrinol Diabetes 1999
PMID:Helicobacter pylori associated gastric pathology in patients with type II diabetes mellitus and its relationship with gastric emptying: the Ankara study. 1037 41

Previous studies have shown a high prevalence of gastric parietal cell antibodies (PCA) in type 1 diabetes, which can be accompanied by (sub)clinical autoimmune gastric disease. This study aimed to determine the grade of associated autoimmunity and to assess the pattern of prevalence of PCA by gender, age, duration of disease, age at onset of diabetes, and human leukocyte antigen (HLA) type in an adult type 1 diabetic population. Furthermore, to examine the clinical significance of being PCA positive, manifestations of gastric autoimmune disease were studied in PCA-positive and PCA-negative patients. The population studied consisted of 497 type 1 diabetics (men/women, 252/245; mean age, 40.8 +/- 12.1 yr; mean duration of disease, 16.4 +/- 10.4 yr; mean age at onset, 26.9 +/- 13.5 yr; mean hemoglobin A1c, 8.1 +/- 1.6%). Associated autoantibodies were present in 39% and PCA were present in 20.9% of the subjects, particularly in older patients. Gender, duration, and age at onset of diabetes did not influence the appearance of PCA. Antithyroid peroxidase antibodies (aTPO) were more frequent in PCA-positive patients than in those without PCA (33.6% vs. 22.4%; P = 0.025), suggesting an association between gastric and thyroid autoimmunity. We could demonstrate an association between PCA and the HLA DR5 haplotype (P = 0.001) as well, but not with HLA DR3 and/or DR4. In the PCA-positive group, iron deficiency anemia was detected in 15.4%, and pernicious anemia was found in 10.5% of subjects. These autoimmune gastric manifestations were significantly more prevalent in PCA-positive diabetics than in PCA-negative subjects, in whom the percentages were 6.9% and 0.5%, respectively (P = 0.01 and P < 0.0001). PCA were prevalent in 84.6% of patients with pernicious anemia. A gastroscopic and anatomopathological examination performed in a subgroup of 30 patients with gastric symptoms revealed atrophic gastritis in 13 of 14 PCA-positive patients and in 9 of 16 PCA-negative subjects (P = 0.04). PCA were present in 59.1% of patients with atrophic gastritis. In conclusion, a high prevalence of parietal cell antibodies and associated autoimmune gastric disease is present in PCA-positive type 1 diabetics, recommending its screening. Early detection of PCA and iron deficiency anemia, pernicious anemia, and atrophic gastritis and the subsequent care could reduce the morbidity of type 1 diabetes.
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PMID:High prevalence of manifestations of gastric autoimmunity in parietal cell antibody-positive type 1 (insulin-dependent) diabetic patients. The Belgian Diabetes Registry. 1056 50

The history of a 45-year-old male type 1 diabetic patient is presented. At the age of 29 years, he was diagnosed to have an autoimmune hepatitis with incipient liver cirrhosis. Five years later, a successful liver/pancreas transplantation was performed. Eighteen months later, however, pancreatic insufficiency occurred due to thrombosis of the pancreatic graft. Besides these conditions, iron deficiency, pernicious anemia, and autoimmune gastritis were also diagnosed. Serum parietal cell antibodies (PCA) and intrinsic factor antibodies (AIF) were positive. At 45, this patient was found to have a gastric carcinoid tumor. The clinical importance of PCA is discussed with regard to chronic atrophic gastritis and pernicious anemia, which both predispose toward gastric carcinoid tumors. Autoimmune type 1 diabetic patients who have a high prevalence of PCA should be screened for gastric autoimmune manifestations and tumors, as the history of this patient illustrates.
J Diabetes Complications
PMID:Autoimmune hepatitis, autoimmune gastritis, and gastric carcinoid in a type 1 diabetic patient: a case report. 1095 74

The mechanisms driving the immune-mediated destruction of hepatic tissues in autoimmune hepatitis (AIH) are unknown. Recently the autoimmune regulator (AIRE), a gene associated with the development of the autoimmune polyglandular syndrome type 1 (APS-1), was cloned. About 15% to 20% of APS-1 patients develop hepatitis. However, the role of AIRE mutations in AIH, primary sclerosing cholangitis (PSC), and primary biliary cirrhosis (PBC) is not known. To address this issue patients with AIH (n = 94), PSC (n = 60), and PBC (n = 30) were analyzed for the presence of mutations in exons 6, 8, and 10 of AIRE by single stranded conformation polymorphism and sequence analysis. Autoantibody patterns of patients with defects in AIRE were analyzed by indirect immunofluorescence, enzyme-linked immunosorbent assay and Western blot. Heterozygous mutations of AIRE were identified in 3 patients: a patient with PBC and a patient with AIH type 1 carried a R257X mutation, and a patient with AIH type 2, diabetes mellitus type 1 (IDDM), thyroid disease, and atrophic gastritis carried a G305S mutation in the first PHD ring finger domain of the AIRE protein. None of the 3 patients with a defective AIRE allele showed autoantibodies, which are known to associate with APS-1. These findings show a differential genetic association of autoimmune liver diseases and hepatitis in APS-1. The subgroup of patients with heterozygous mutations in AIRE does not represent patients with an incomplete APS-1 syndrome. However, the Aire gene defect showed that genes involved in the induction of immunologic tolerance provide candidates for etiologic factors in autoimmune liver diseases.
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PMID:Autoimmune regulator AIRE: evidence for genetic differences between autoimmune hepatitis and hepatitis as part of the autoimmune polyglandular syndrome type 1. 1134 30


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