Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric abnormalities are more common in diabetics than in the normal population. They seem to be related to gastric parietal cell autoantibodies (GPCA). We have studied 168 patients affected with non-insulin-dependent diabetes mellitus (NIDDM), and assessed the GPCA in the serum and haematologic disorders. We have also assessed the endoscopic and histological findings of atrophic gastritis in patients with GPCA. GPCA were found in 15.74% of diabetic patients and in 2% of a control group of blood donors. 80% of GPCA positive patients showed signs of atrophic gastritis. Such presence of GPCA seems to be a good marker to identify patients affected by atrophic gastritis and its complications.
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PMID:[Gastric and hematologic changes in patients with gastric parietal cell autoantibodies and non-insulin-dependent diabetes mellitus]. 146 30

Surface electrogastrograms were recorded in 95 patients. There were 6 groups of patients: chronic superficial gastritis (20), chronic atrophic gastritis (20), duodenal ulcer (20), gastric ulcer (17), gastric cancer (8), and diabetes mellitus (10). Electrogastrographic examination was continuously carried out for 60 minutes both in fasting and postprandial state. (1) During the fasting state, in 72% of the cases, there was a 50% to 100% change in the mean of the amplitude among six 10-minute periods of recording. (2) In 23 cases (25%), there was no amplitude increase in the postprandial electrogastrogram. Feeding caused an increase in amplitude by 30-240 microV over the prefeeding state in 70 cases (75%). (3) The distribution of amplitude in various groups of disease overlapped each other. The difference in amplitude or frequency would not be used as a diagnostic parameter of gastric diseases. (4) Tachygastria of 5-7.3 cycles per minute was observed in 15 of the 95 patients. The longest episode was a wave with 7.3 cycles per minute lasting for 20 minutes. It is difficult to evaluate the clinical significance of the observed tachygastria.
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PMID:[Electrogastrography: the clinical significance of changes during fasting and postprandial state]. 191 65

We evaluated the basal and postprandial circulating levels of gastrin in 20 diabetic patients and in 20 normal subject. The basal gastrin concentrations were not statistically different in comparison to controls. The blood tests provoked increased circulating levels of gastrin. In our study diabetes significantly enhanced that response, particularly in diabetics with severe disease, peripheral neuropathy and in untreated patients. Histologic evidence of antral hyperplasia was obtained in 7 patients; atrophic gastritis and intestinal metaplasia were found in 3 diabetics. We postulate that postprandial gastrin levels raised secondary to achlorhydria, common in diabetics.
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PMID:[Serum gastrin in patients with diabetes]. 210 51

We report a case of dorsal pancreatic hypoplasia complicated with atresia of the vagina, type-A chronic atrophic gastritis, duodenal papillary dysfunction, and insulin-requiring diabetes mellitus, in a 32-yr-old woman. The laboratory data showed elevated hepatobiliary enzymes. Endoscopic retrograde cholangiopancreatography (ERCP) revealed a slightly dilated common bile duct and a short major pancreatic duct connected with a minor pancreatic duct. Ultrasonography and computerized tomography could not identify any pancreatic tissue in the region of the body or tail of the pancreas. The pancreatic tissue weight calculated by the serial thin slice of computerized tomography was 43.1 g, approximately 45% of the standard Japanese adult pancreas. Reevaluated pancreatic exocrine function based on this weight showed a hypersecretory state. The pancreatic ductal pressure was slightly increased, and the motility of the sphincter of Oddi (SO) was abnormal when measured with a 4Fr. microtransducer inserted through a duodenoscope. These findings suggest that dysfunction of the sphincter of Oddi may play some role in the pathophysiology in the hypoplasia of the dorsal pancreas and pancreaticobiliary diseases associated with it.
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PMID:Congenital hypoplasia of the dorsal pancreas: with special reference to duodenal papillary dysfunction. 219 55

We describe a child with Down's syndrome who developed an insulin-dependent diabetes mellitus at the age of 8 years and hypothyroidism at the age of 17 years. Because of the well known tendency to autoimmune diseases of patients with Down's syndrome, an autoantibody screening was undertaken. Only a low titre for gastric parietal cell antibodies was repeatedly found, but a gastric biopsy did not reveal chronic atrophic gastritis. Thyroid function should be checked periodically in patients with Down's syndrome since they might suffer from hypothyroidism which may not be recognized for a long time because of its latent onset.
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PMID:Down's syndrome, hypothyroidism and insulin-dependent diabetes mellitus. 294 78

Tolbutamide significantly decreased fasting plasma gastrin after 5 min of intravenous infusion in patients with atrophic gastritis, duodenal ulcer, or insulin-dependent diabetes mellitus (IDDM) as well as in healthy volunteers. Increased plasma insulin and decreased blood glucose were observed in patients with atrophic gastritis, duodenal ulcer and healthy volunteers, but not in patients with IDDM. Suppression of plasma gastrin in healthy volunteers was also observed following oral administration of tolbutamide. Despite the observed decrease in plasma gastrin, neither basal nor tetragastrin-stimulated acid output was changed for 30 min following tolbutamide infusion in healthy volunteers. Thus, our data suggest that tolbutamide inhibits gastrin release in man via mechanisms independent of changes in plasma insulin, blood glucose or acid secretion.
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PMID:Tolbutamide inhibits gastrin release in man. 306 96

Spontaneous insulin-dependent diabetes mellitus (IDDM) and other autoimmune manifestations, such as lymphocytic thyroiditis and atrophic gastritis, develop in diabetes-prone (high-risk) lines of Wistar-derived BioBreeding (BB) rats. To examine whether Cyclosporin A (CsA) would abrogate multiple autoimmune manifestations in BB rats, we treated them prophylactically with CsA from 5-6 weeks to 23-25 weeks of age. IDDM developed in 0/58 CsA-treated rats; 47% (29 out of 62) of sex- and age-matched controls treated with vehicle developed IDDM (p less than 0.001). CsA-treated rats had no or minimal lymphocytic infiltration and parenchymal changes in the pancreas, stomach and thyroid at the time of cessation of treatment. IDDM, glycosuria and hyperglycemia developed in 0/22 rats followed up to 370 days of age (up to 210 days following the cessation of CsA therapy); histologic examination of their islets was normal. We conclude that CsA completely abrogates the development of clinical IDDM in the BB rat, and that it inhibits or abolishes lymphocyte infiltration in several organs against which there is autoimmunity. The data also suggest that the protective effect of CsA persists well past the duration of therapy, and that cell-mediated autoimmunity (with or without humoral immunity) may be an important pathogenetic mechanism in the destruction of beta cells in the BB rat.
Diabetes Res 1986 Jan
PMID:Cyclosporin prophylaxis induces long-term prevention of diabetes, and inhibits lymphocytic infiltration in multiple target tissues in the high-risk BB rat. 351 66

Although no absolute certainty exists about the role of nutrition in the etiology of cancer, many facts in favor of the relationship became available during the last decades. Correlation studies, experimental work and to a lesser extent case-control studies made it possible to clarify the role of certain nutrients and foods in carcinogenesis. The most important cancer sites where nutrition could play a role are esophagus, stomach, colon, rectum, prostate and breast. Esophageal cancer is of a very complex etiology, in which alcohol intake plays an important role, at least in western countries. The cancer-promoting properties of alcohol intake are enhanced by smoking. Three factors from nutrition are probably related to stomach cancer, namely salt, nitrate/nitrite and vitamin C. Salt is caustic to the stomach mucosa, resulting in atrophic gastritis. Salt is also co-carcinogenic and stomach cancer-promoting in experimental animals. Nitrate is probably important at the stage of atrophic gastritis, where bacterial overgrowth, due to the high pH, converts nitrates in nitrites, making the loco synthesis possible of potent nitrosocarcinogens. Vitamin C inhibits the latter step. The epidemiological evidence for the role of those factors is provided. The most important among them is the strong and consistent association of stomach cancer mortality with stroke. Rectum, colon, prostate and breast cancer are related in some way to fat intake. They all seem positively related to saturated fat intake, whereas breast cancer is probably also promoted by polyunsaturated fat intake. However, polyunsaturated fat seems to be without effect on rectum cancer. Colon and prostate cancer are probably also influenced by polyunsaturated fat but to a lesser degree than breast cancer. An important argument for this are the positive ecological correlations between changes in rectum, colon and breast cancer mortality from 1968 on, and changes occurring in coronary heart diseases, stroke and diabetes mortality. Those six types of mortality are decreasing, or only slightly increasing in the USA, Belgium, France, the Netherlands, etc. They are strongly increasing in East European countries. The intake of saturated fat has generally decreased in the first group of countries, and has markedly increased in the second group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and cancer. 353 16

Abnormalities in the function of the stomach in patients with long-standing diabetes mellitus, usually insulin-dependent, may provide difficult management problems. There is a reduced frequency of peptic ulcer disease in diabetics. Gastric atrophy, often with parietal cell antibodies, is common and the frequency of pernicious anemia with its expected intrinsic factor antibodies is increased. Gastric analysis results have been conflicting but generally suggest that long-standing diabetics have lower acid levels than normals, possibly secondary to vagal neuropathy. Gastric atony occurring in a small but significant number of patients with longstanding insulin-dependent diabetes, usually with a clinically apparent peripheral neuropathy, has been associated with upper abdominal discomfort, vomiting, and a clinical picture of gastric outlet obstruction. Various degrees of subclinical delays in gastric emptying are probably present in many asymptomatic patients and, indeed, are underemphasized contributors to poor control of blood sugar levels. Studies utilizing radioactive-labeled physiological meals have demonstrated abnormalities in the gastric emptying of solids, in particular, and sometimes liquids in the latter stages of the disease. Metoclopramide, a dopamine antagonist, which stimulates upper gastrointestinal smooth musculature, results in accelerated gastric emptying; clinical trials have shown that it is capable of alleviating symptoms related to diabetic gastroparesis and with its recent approval and release in this country, it promises improved management of this entity. Another agent, domperidone, a selective peripheral dopamine antagonist with no appreciable side effects, is in this country an investigational drug which has shown clinical efficacy in Europe in improving gastric stasis syndromes.
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PMID:Diabetes and the stomach. 665 60

The frequency and significance of gastric parietal cell autoimmunity was assessed in 771 patients with insulin-dependent diabetes (IDD) of onset before 30 yr of age. Gastric parietal autoantibodies (PCA) were found 4 times more frequently in the patients with IDD (9%) than among 600 matched nondiabetic controls (2%). Caucasian female patients with IDD had PCA twice as frequently as male patients. Thyroid microsomal autoantibodies were more frequent in patients with IDD and PCA, than in those with IDD alone (Caucasian 46% versus 18%, black 25% versus 2.5%). A history of pernicious anemia and/or PCA was found in 25 or 40 families of IDD probands with PCA. Achlorhydria was demonstrated in 6 of 11 patients (54%) with PCA but in none of seven IDD patients without PCA. The six patients with achlorhydria had significantly lower uptakes of oral radiolabeled cobalamin, lower serum cobalamin levels, lower intrinsic factor-R protein ratios in their gastric aspirates, and lower plasma ferritin levels than patients with IDD but without PCA. None of the study group had IF antibodies in their serum or gastric juice. Overt pernicious anemia and neuropathy were found in one patient with PCA. Young patients with IDD at risk for atrophic gastritis and cobalamin deficiency can initially be identified by screening for PCA. Many of these young patients with PCA already have achlorhydria and evidence of decreased absorption of cobalamin. These patients can then be followed with cobalamin levels and/or with complete blood counts to identify those requiring therapy.
Diabetes 1982 Dec
PMID:Predictive value of gastric parietal cell autoantibodies as a marker for gastric and hematologic abnormalities associated with insulin-dependent diabetes. 717 96


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