Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study aimed to describe the clinical manifestations of celiac sprue related to malnutrition and to analyze the associations between celiac sprue and other diagnoses. A case-control study compared the occurrence of comorbid diagnoses in case and control subjects with and without celiac sprue, respectively. All patients with a primary or secondary diagnosis of celiac sprue (ICD-579.0) who were discharged from hospitals of the Department of Veterans Affairs between 1986 and 1995 were selected as case subjects. In a multivariate logistic regression analysis, the occurrence of celiac disease served as outcome variable, while age, gender, ethnicity, and the comorbid occurrences of other diagnoses served as predictor variables. A total of 458 individual patients with celiac sprue were identified. The data confirmed the known associations of celiac sprue with dermatitis herpetiformis, lactase deficiency, enlargement of lymph nodes, and lymphoma. Celiac sprue was also found to be statistically significantly associated with pancreatic insufficiency, Crohn's disease, functional bowel symptoms, chronic nonalcoholic hepatitis, and pulmonary eosinophilia. The nutritional manifestations associated with celiac disease included nutritional marasmus, cachexia, weight loss, hypocalcemia, osteoporosis, vitamin B-complex deficiency, and various types of iron- and vitamin-deficiency anemias. The large variety of complex associations clearly indicates that celiac sprue is a systemic disease that involves multiple organs and exceeds an isolated nutritional intolerance to gluten.
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PMID:Celiac sprue among US military veterans: associated disorders and clinical manifestations. 1023 5

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

CoQ transfers electrons from complexes I and II of the mitochondrial respiratory chain to complex III. There are very few reports on human CoQ deficiency. The clinical presentation is usually characterized by: epilepsy, muscle weakness, ataxia, cerebellar atrophy, migraine, myogloblinuria and developmental delay. We describe a patient who presented with neonatal liver and pancreatic insufficiency, tyrosinemia and hyperammonemia and later developed sensorineural hearing loss and Leigh syndrome. Liver biopsy revealed markedly reduced complex I+III and II+III. Addition of CoQ to the liver homogenate restored the activities, suggesting CoQ depletion. Histological staining showed prominent bridging; septal fibrosis and widening of portal spaces with prominent mixed inflammatory infiltrate, associated with interface hepatitis, bile duct proliferation with numerous bile plugs. Electron microscopy revealed a large number of mitochondria, which were altered in shape and size, widened and disordered intercristal spaces. This may be the first case of Leigh syndrome with liver and pancreas insufficiency, possibly caused by CoQ responsive oxphos deficiency.
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PMID:Neonatal liver failure and Leigh syndrome possibly due to CoQ-responsive OXPHOS deficiency. 1294 44

1. With Conn.-5 strain of Coxsackie virus, pancreatic disease can be regularly produced in adult mice. 2. The lesions consist of widespread necrosis, followed by repair; there occurs more or less complete loss of glandular acini, with fatty or fibrous replacement. The islands of Langerhans and pancreatic ducts persist. 3. Injection of virus suspensions by the intraperitoneal, subcutaneous, intramuscular, or intracerebral route is followed by selective necrosis of the pancreas. 4. The liver, in the earlier stages of the disease, is the seat of fat infiltration. There may be necrosis of individual hepatic cells, but the diffuse hepatitis described in suckling mice does not occur. In the later stages of the disease, the liver is not significantly altered. 5. Localized areas of fat necrosis, scattered through intra-abdominal adipose tissue, are usually present in the acute phase of the disease. These undergo fibrosis without calcification. 6. No lesions have been found in the skeletal muscle, even at the site of intramuscular injection. Central nervous system, heart, lungs, and peripheral fat lobules show no lesions comparable to those described in suckling mice. 7. Multiplication of virus takes place in the pancreas. Serial passage in adult mice, by injection of pancreas suspensions prepared from organs removed on the 4th day after infection, is readily accomplished. Five consecutive passages in adult mice have thus far been carried out. Pancreas suspension from 4th passage material produced typical disease in suckling mice when diluted 10(-6). No virus could be demonstrated in pancreas obtained 25 days after inoculation. 8. Complete protection against the pancreatic disease is obtained when the virus is neutralized, before injection, with Conn.-5 antiserum. Normal mouse serum and antiserum against the Ohio-R strain of Coxsackie virus have no protective effect. 9. Mice surviving the initial necrotizing effect of the virus, develop chronic pancreatic insufficiency. This is manifested by extreme weight loss-in some cases, 40 per cent or more of the body weight-and by hypoproteinemia, sometimes leading to anasarca. 10. The substitution of fox-chow which has been predigested with hog pancreas brings about a restoration of weight. 11. The possibility is considered that similar lesions of the pancreas in human beings may be due to virus infection.
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PMID:Passage of Coxsackie virus (Connecticut-5 strain) in adult mice with production of pancreatic disease. 1485 Jun 35

We report a 9-year-old girl with cereulide-producing Bacillus cereus food poisoning, who developed fulminant hepatitis, renal and pancreatic insufficiency, shock, and prolonged seizures. She was transferred to our institution for hepatic transplantation before her diagnosis was established. As a result of rapid identification of the microorganism and supportive care, liver transplantation was avoided, and she recovered fully.
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PMID:Food poisoning as a cause of acute liver failure. 1866 29

Sjogren syndrome (SS) is an autoimmune disease that affects exocrine glands and therefore may affect the gastrointestinal system, from the mouth, esophagus, and bowel to the liver and pancreas. Oral involvement in SS is mainly characterized by dryness, with a wide spectrum of symptoms, from mild-to-severe xerostomia with dysgeusia and tooth decay. The dysphagia, although common, does not correlate with the reduced salivary flow rate or the dysmotility that may be present. Dyspepsia, found in up to 23% of patients, may be associated with gastritis, reduced acid production, and antiparietal cell antibodies, but rarely pernicious anemia. Pancreatic involvement, although rare, includes pancreatitis and pancreatic insufficiency. The most common causes of liver disease are primary biliary cirrhosis, autoimmune hepatitis, nonalcoholic fatty liver disease, and hepatitis C virus (HCV). Although abnormal liver tests are found in up to 49% of patients, they are usually mild. Although sicca syndrome, abnormal histology of the salivary glands, and abnormal sialograms are common in primary biliary cirrhosis, the antibodies to Ro/SSA or La/SSB antigens are infrequent. Xerostomia, sialadenitis, abnormal salivary flow rates, and abnormal Schirmer test in HCV vary widely among the studies, although the antibodies to Ro/SSA or La/SSB are only 1%. Several studies show that HCV is in saliva, although how this may impact sicca syndrome or SS in HCV is unclear. SS as a disease of exocrine glands affects many parts of the gastrointestinal system.
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PMID:Gastrointestinal and hepatic manifestations of Sjogren syndrome. 2215 20

A 50-year-old man was investigated for painless jaundice. The histologic pattern on the liver biopsy study met the criteria of autoimmune hepatitis. Further clinical and laboratory investigation revealed multi-organ involvement, including Mikulicz's disease of the salivary glands and pancreatic insufficiency. The diagnosis of IgG4-related disease was suggested by a finding of elevated blood levels of IgG4. IgG4-related disease is an inflammatory fibrosing condition characterized by T-cell infiltration of affected organs, presence of IgG4-positive plasma cells, and elevated levels of IgG4 in serum. In the present case, the liver histopathology was compatible with one of several well-defined types of liver involvement in IgG4-related disease. IgG4-related disease may mimic malignant tumors of the biliary tract, pancreas, or liver. Undiagnosed patients may progress to end-stage fibrosis or undergo unnecessary surgery. It is highly important that IgG4-related disease be recognized because it is a treatable condition that responds well to steroids.
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PMID:[IGg4 related autoimmune hepatitis]. 2333 Feb 63

Changes in the liver and bile ducts observed in patients diagnosed with cystic fibrosis result from inflammatory processes as well as fibrosis, remodeling, apoptosis, and cholestasis. As a consequence, portal hypertension, cirrhosis, and hepatic failure may develop. So far, the complexity of these processes has not been elucidated. Study Objectives. The aim of the study was to evaluate the selected parameters of hepatitis and fibrosis (Fibrotest, Actitest, and APRI) in patients diagnosed with cystic fibrosis. Material and Methods. The study included 79 patients with cystic fibrosis, aged 1 to 20 years (mean age 9.8 years), 49 girls (62%) and 30 boys (38%). The analysis involved the following: age, sex, clinical manifestations, laboratory tests evaluating pancreas function, parameters of liver damage, and cholestasis. Fibrotest, Actitest, and APRI were performed in all subjects. Results. Elevated parameters of hepatic cell damage (hypertransaminasemia) were found in 31/79 (39.2%) patients, while abnormal cholestasis parameters in 21/79 (26.6%). The abnormal results of Fibrotest were reported in 15% of patients (12/79), while of Actitest in 10% (8/79). In contrast, elevated APRI values were found in only 7.6% (6/79) of subjects. There was a statistically significant correlation between APRI and age (higher values were observed in younger children) and between Fibrotest and Actitest and pancreatic insufficiency (higher values were found in subjects without this abnormality). Moreover, Fibrotest values were significantly higher in girls. There was no correlation between Fibrotest, Actitest, and APRI values and the type of mutation. Conclusion. It appears that Fibrotest may be used as an early marker of liver fibrosis in patients with cystic fibrosis. Increased APRI values were only found in subjects with advanced hepatic lesions, most often in the form of portal hypertension.
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PMID:Assessment of Selected Parameters of Liver Fibrosis and Inflammation in Patients with Diagnosed Cystic Fibrosis. 3230 56