Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The basal acid output (BAO), post-pentagastrin acid output (MAO), fasting and post-prandial gastrin levels in 40 patients with proven cirrhosis of the liver were compared with those in 20 normal controls. The mean BAO and MAO were significantly lower than normal, the mean fasting gastrin level was significantly higher than normal, and the postprandial gastrin response was significantly increased and prolonged. These differences were still significant even when the patients were divided into cryptogenic and alcoholic subgroups. A significant inverse relationship between MAO and the integrated gastrin response to meal was observed both in the normal controls and in the cirrhotic patients. The MAO and integrated gastrin response of the cirrhotic patients did not correlate with the degree of liver function impairment. In five cirrhotic patients fasting and postprandial gastrin levels were unchanged after splenorenal shunt operation. A more consistent abnormality of the gastric mucosa as assessed by endoscopy and biopsies appeared to be mucosal congestion with occasional atrophic gastritis. the severity of mucosal abnormality, however, was unrelated to the degree of hypoacidity. these results indicate, firstly, that the hypergastrinaemia in cirrhotic patients is a reflection of gastric hypoacidity and bears no direct relationship to hepatic dysfunction. Secondly, the gastric hypoacidity does not accrue solely from mucosal abnormality. It is suggested that this hypoacidity may result from the presence of excessive amounts of circulating acid-inhibiting intestinal peptides, which the diseased liver fails to metabolise.
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PMID:Hypergastrinaemia in cirrhosis of liver. 97 11

To investigate whether hypergastrinemia and low serum levels of pepsinogen I are associated with gastric hypoacidity in cirrhosis with capillary ectasia of gastric mucosa and whether this alteration is secondary to the presence of atrophic gastritis, two groups of patients were studied: 1) 12 cirrhotic patients with diffuse gastric red spots at the endoscopic examination, and 2) 12 cirrhotic patients with endoscopically normal mucosa. Vascular ectasia of the gastric mucosa was histologically confirmed in all patients with gastric red spots. The study of base-line and stimulated acid gastric secretion showed that 9 of 12 (75%) cirrhotics with gastric vascular ectasia had achlorhydria and that 8 of these 9 patients had high base-line gastrin serum levels (greater than 130 pg/ml) and low base-line pepsinogen I serum levels (less than 20 ng/ml). Base-line gastrin and pepsinogen I serum levels were significantly greater and lower, respectively, in patients with gastric vascular ectasias than in cirrhotics without these lesions. None of the patients of either group had complete atrophy in the corpus of the stomach, and only 4 of the 9 cirrhotics with gastric vascular ectasia and achlorhydria had moderate atrophy. These results show that achlorhydria is frequently associated with hypergastrinemia and low pepsinogen I serum levels in patients with cirrhosis and gastric vascular ectasias and suggest that this disturbance is not secondary to a morphologic abnormality of the gastric mucosa.
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PMID:Gastric vascular ectasias in cirrhosis: association with hypoacidity not related to gastric atrophy. 259 68

The part played by the human hepatocytic antigens in the self-perpetuation of the inflammatory processes was investigated in two groups of patients with chronic active liver disease (CALD). In the 26 patients of the first group (14 with chronic active hepatitis and 12 with active cirrhosis), their serum was put in contact with a suspension of hepatocytes in a culture of liver from a 5.5 month-old human embryo, in presence of rabbit complement. The hepatocytic lysis was evaluated by the test of microcytotoxicity (MCT), considered positive at values above 60%. Ten healthy subjects and 8 patients with atrophic gastritis were used as controls. In 12 other patients with CALD (2nd group), the authors performed the test of inhibition of the macrophage migration (IMM) and that of lymphoblastic transformation (LT) in presence of an autologous liver antigen, obtained by liver biotic puncture. In the first group, the MCT test was positive in 57.6% of the patients, in correlation with a particular biomorphologic aggressivity and marked immune disturbances, while in controls it was negative in 17 of the 18 cases. In the second group, the extract of autologous hepatocytes induced a marked inhibition of the macrophage migration and a significantly increased lymphoblastic transformation. It is concluded to the existence, in the patients with CALD, of cytotoxic hepatocytic antibodies, as well as to a stimulation of the macrophagic-lymphocytic function in presence of the autologous liver antigen. The participation af an autoimmune mechanism in the perpetuation of the hepatocytic lesions in such patients is also suggested.
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PMID:The interference of an autoimmune mechanism in the pathogeny of chronic active liver diseases. 274 58

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

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.
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PMID:Autoimmune hepatitis, autoimmune gastritis, and gastric carcinoid in a type 1 diabetic patient: a case report. 1095 74

This report describes a 60-yr-old white male presenting with decompensated liver cirrhosis. He had a history of Addison's disease for 36 yr, primary hypothyroidism for 5 yr, and moderate alcohol consumption. His laboratory studies and a liver biopsy supported the diagnosis of autoimmune hepatitis. Furthermore, he was found to be heterozygous for the piZ allele of the alpha1-antitrypsin gene with normal serum alpha1-antitrypsin levels and absence of pulmonary affection. Mucosal biopsies revealed moderately severe atrophic gastritis; however, signs of pernicious anemia were missing. An association of autoimmune hepatitis with endocrine disorders and atrophic gastritis has been described. Long term hydrocortisone therapy for his adrenal insufficiency may have prevented a faster course of the liver disease, whereas the heterozygous alpha1-antitrypsin deficiency and moderate alcohol consumption constituted additional risk factors ultimately leading to the development of cirrhosis.
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PMID:A patient with autoimmune hepatitis type I, Addison's disease, atrophic thyroiditis, atrophic gastritis, exocrine pancreatic insufficiency, and heterozygous alpha1-antitrypsin deficiency. 1200 88

A 67 year-old female with a 10-year history of cirrhosis due to hepatitis C virus who developed a gastric carcinoid tumor of the corpus is described. Carcinoid tumor was identified during her last routine gastroscopic evaluation for portal hypertension. In the case, serum parietal cell antibodies, hypergastrinemia and atrophic gastritis were also found. Chronic hepatitis C virus infection is known to induce clinical and laboratory signs of autoimmunity. But the question of whether hepatitis C virus plays a pathogenic role in the development of gastric carcinoid tumor is unknown. As far as we know, this is the first report describing gastric carcinoid tumor in hepatitis C virus induced chronic liver disease. We suggest that the possibility of the development of autoimmune atrophic gastritis and carcinoid tumors should be considered in patients with chronic hepatitis C that coexists with autoimmune diseases and has positive parietal cell antibodies.
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PMID:Type 1 gastric carcinoid tumor: another extrahepatic manifestation of hepatitis C virus infection? 1465 65

This article describes changes in the basic digestive functions (motility, secretion, intraluminal digestion, absorption) that occur during aging. Elderly individuals frequently have oropharyngeal muscle dysmotility and altered swallowing of food. Reductions in esophageal peristalsis and lower esophageal sphincter (LES) pressures are also more common in the aged and may cause gastroesophageal reflux. Gastric motility and emptying and small bowel motility are generally normal in elderly subjects, although delayed motility and gastric emptying have been reported in some cases. The propulsive motility of the colon is also decreased, and this alteration is associated with neurological and endocrine-paracrine changes in the colonic wall. Decreased gastric secretions (acid, pepsin) and impairment of the mucous-bicarbonate barrier are frequently described in the elderly and may lead to gastric ulcer. Exocrine pancreatic secretion is often decreased, as is the bile salt content of bile. These changes represent the underlying mechanisms of symptomatic gastrointestinal dysfunctions in the elderly, such as dysphagia, gastroesophageal reflux disease, primary dyspepsia, irritable bowel syndrome, primary constipation, maldigestion, and reduced absorption of nutrients. Therapeutic management of these conditions is also described. The authors also review the gastrointestinal diseases that are more common in the elderly, such as atrophic gastritis, gastric ulcer, colon diverticulosis, malignant tumors, gallstones, chronic hepatitis, liver cirrhosis, Hepato Cellular Carcinoma (HCC), and chronic pancreatitis.
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PMID:Changes, functional disorders, and diseases in the gastrointestinal tract of elderly. 2247 8

Gastric antral vascular ectasia (GAVE) syndrome is an uncommon but well-described cause of recurrent upper gastrointestinal bleeding or iron deficiency anaemia. Atiology is unknown but several associated diseases have been reported like connective tissue or autoimmune disorders or cirrhosis. Cases have been reported in systemic sclerosis, achlorhydia, atrophic gastritis and chronic renal failure. The most common cause is portal hypertension and portal hypertensive gastropathy. This is especially so after eradication of oesophageal varices by sclerotherapy or banding. Diabetic complications are characterised by microvascular diseases especially in the retina, glomerulus and vasa nervorum. It involves apoptosis and remodelling of endothelial cells. Hyperglycaemia is an essential cause of reactive oxygen species (ROS)-mediated oxidative stress in this complication. Angiopathy of gastric mucosa in diabetes mellitus has not been reported so far in the literature. We are presenting an interesting case of diabetes mellitus with gastric vascular ectasia without evidence of any other systemic illness.
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PMID:Gastric antral vascular ectasia (GAVE) in a non-cirrhotic patients with diabetes: case report and possible pathophysiological mechanism. 2273 55