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 case is reported of an 18-year-old woman hospitalized with severe dyspnea and high temperature. Chest X-ray showed pneumonia with interstitial and air-space consolidation patterns. Serologic tests revealed a cytomegalovirus infection (CMV). The blood findings showed anemia of infectious origin. Liver biopsy was consistent with CMV-hepatitis. CMV-pneumonia in an otherwise healthy patient is extremely rare; a review of the literature revealed only four other cases.
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PMID:[Cytomegalovirus pneumonia in primarily healthy adults]. 626 84

A syndrome of acquired immunodeficiency has been identified in a group of rhesus monkeys (Macaca mulatta) which died at the California Primate Research Center. Clinical evaluation of these animals revealed that 50% or more had lymphadenopathy, weight loss, and diarrhea. At least 30% had splenomegaly, fever, cutaneous abscesses and/or arthritis/myositis. Two animals had fibrosarcomas. Anemia was seen in 19 animals, lymphopenia in 14, granulocytopenia in four and thrombocytopenia in three. Hepatitis was diagnosed histopathologically in 13. Electrophoresis revealed hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. Numerous bacterial, protozoal, and viral agents were identified including cytomegalovirus and leukocyte-associated herpesvirus. Pathologic lesions included severe post-reactive depletion of lymphocytes in germinal centers and paracortical regions of lymph nodes. Clinical and pathologic changes indicate an acquired immunodeficiency syndrome which has some similarities to AIDS in humans. This disease in monkeys may provide a model for studying that disease.
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PMID:Clinical features of simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys. 632 13

There are reports in the literature that infection with hepatitis A virus in hepatitis B carriers can result in resolution of the carrier state. In an attempt to induce clearance of the carrier state of hepatitis B virus in two persistently infected chimpanzees, the chimpanzees were infused with documented non-A, non-B infectious material. Biochemical and histopathological evidence of hepatitis was accompanied by the unique abnormalities of endoplasmic reticulum associated with non-A, non-B hepatitis in the chimpanzees. Elevation of alanine aminotransferase was accompanied by fourfold reduction in one chimpanzee and sixfold reduction in the other in the plasma levels of HBV-associated DNA polymerase activity and simultaneously by twofold reduction in the concentration of hepatitis B surface antigen in both chimpanzees. A mediator may account for these changes in markers of hepatitis B virus infection, and this mechanism may also explain the occurrence of spontaneous regression in some persistently infected carriers. The significance of transient red cell anaemia in non-A, non-B hepatitis, which was observed in one of the chimpanzees, is yet to be established.
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PMID:Non-A, non-B hepatitis in persistent carriers of hepatitis B virus. 640 22

A 38-year-old male chronic alcoholic developed spur-cell anemia during an episode of non-A, non-B hepatitis. Lipid evaluation showed a marked decrease in cholesterol (1.98 mmol/l), in triglycerides (0.41 mmol/l) and in phospholipids (1.38 mmol/l) in total serum as well as in VLDL and LDL. Serum apolipoprotein B was also low. Cholesterol (C) and phospholipid (PH) content of the erythrocytic membrane was increased, as was the intraerythrocytic C/PH ratio. Hemolysis ceased with correction of the hypobetalipoproteinemia. The relationship between acquired acanthocytosis and lipid disorders is discussed.
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PMID:[Reversible acquired acanthocytosis and hemolytic anemia associated with hypobetalipoproteinemia in a chronic alcoholic]. 641 78

Severe congestive cardiac failure developed in a few weeks in a 44 year old man who had undergone porto-caval anastamosis for post-hepatitis cirrhosis one year previously and then treated for anaemia by repeated blood transfusion and chronic daily oral iron therapy. Infiltrative, congestive and restrictive cardiomyopathy was diagnosed in the presence of global cardiomegaly, electrocardiographic changes (microvoltage, diffuse ST-T wave changes), echocardiographic appearances (dilatation of the left ventricle, with hypertrophic and hypokinetic walls), and hemodynamic signs of adiastole with equalisation of filling pressures at 15 mmHg and a cardiac index of 1,88 l/min/m2. Cardiac haemochromatosis was confirmed by the laboratory (serum iron: 35 mumol/l; siderophilin saturation: 100 p. 100; serum ferritin: 1854 ng/ml; induced siderouria: 51 mg/24 hours) and histological findings (endomyocardial biopsy showing pigment overload). The absence of a family history, of homozygote A3 antigen, of diabetes, of iron overload on hepatic biopsy one year previously, excluded the diagnosis of familial idiopathic haemochromatosis. A secondary form of the disease was diagnosed on a possible genetic predisposition (heterozygote A3 antigen) and on environmental factors (blood transfusions, iron therapy, cirrhosis, alcoholism and perhaps the porto-caval anastamosis. Cardiac haemochromatosis was cured in this case by iron chelating therapy comprising daily subcutaneous infusions of 2 g of desferrioxamine for 2 months. The cure was confirmed by regression of the signs of clinical cardiac failure and of cardiomegaly, the increase in QRS voltages and the near normalisation of the hemodynamic and laboratory findings.
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PMID:[Adiastole caused by a secondary cardiac hemochromatosis. Successful treatment with an iron chelating agent]. 641 3

The incidence of haematological abnormalities has been evaluated in 1170 patients affected by acute viral hepatitis. Of these patients, 665 were HBsAg+, 427 HBsAg-, 31 with IgM anti-HAV, 26 non A and non B hepatitis. 21 patients were not classified due to lack of data relating to markers for HAV or HBV. Anemia, leucopenia, thrombocytopenia and pancytopenia were found with some frequency at the haemochromocytometric examination. It is emphasized that these haematological abnormalities are often of minor relevance whereas the rarer and more serious complications such as persistent bone marrow hypoplasia or pure aplastic anemia can present difficult clinical problems regarding prognosis and therapy: in 4 cases of bone marrow hypoplasia a recovery was obtained in 1 case only, whereas the remaining cases had a fatal outcome after a period varying from 20 days to 15 months from the appearance of pancytopenia. We suggest the advisability of a closer study of the haematological and immunological aspects in patients with viral hepatitis in order to discover those elements which are useful towards a better understanding of the etiopathogenesis of the haematological abnormalities studied above. Such a detailed study would also enable further improvement in existing therapeutic measures.
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PMID:[Hematological complications of viral hepatitis. Case-list contribution]. 644 May 80

An unusual case of obstructive jaundice due to metastatic pancreatic plasmacytoma is described. Initially post-transfusion hepatitis was suspected in the patient who suffered from multiple myeloma (IgA) and had received numerous transfusions for severe anemia. Clinical and laboratory findings indicated obstructive jaundice and the ecographic examination showed a dishomogeneous mass at the level of the pancreas. The investigators suggest that after this type of ecographic finding a percutaneous biopsy should be performed eliminating exploratory laparotomy, a high risk procedure in this type of patient, and eventually radiotherapy should be initiated since this type of tumor is radiosensitive.
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PMID:[Clinical and diagnostic considerations on a case of pancreatic plasmacytoma]. 652 54

Idiopathic perforation of the bile duct is rare in children. Sixty-seven cases were reported in the English literature to 1980. It is, nevertheless, the second commonest surgical cause of jaundice in the neonate. The etiology is unknown though distal obstruction and weakness in the bile duct wall have been postulated. Limited surgical treatment with external drainage is the preferred therapy. In isolated cases internal drainage procedures or repeated aspiration have been successful. The diagnosis should be suspected in the presence of jaundice and ascites with or without abdominal pain and signs of peritoneal irritation. We describe a 3-month-old girl presenting with anemia, vomiting, jaundice, and ascites. This was initially diagnosed as hepatitis but bilious fluid was found on paracentesis. Computerized tomography with cholangiography and 99 MTC Diisopropyl IDA cholescintigraphy confirmed the diagnosis. The latter seems to be more accurate than I-131 Rose Bengal. The perforation was at the junction of the hepatic and cystic ducts. It was treated successfully by external drainage and a cholecystostomy. Direct attempts to close the perforation, or more complicated surgical procedures, are unnecessary while nonoperative treatment carries a high mortality. At follow-up after 1 year the IV cholangiogram and liver-function tests are normal. Cholecystostomy provided good drainage of the biliary ducts as well as easy access for follow-up cholangiography.
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PMID:Idiopathic perforation of the biliary tract in infancy. 664 92

A 25-year-old woman underwent plateletpheresis 101 times over a 33-month period. The equivalent of 5.8 to 7.5 units of platelet concentrate was removed during each pheresis. Two machine-related complications occurred, resulting in the loss of one unit of blood and 150 milliliters of plasma. Other complications included a mild anemia consistent with iron deficiency. The donor's platelet count decreased but remained in the normal range. There were no significant changes in the serum proteins or immunoglobulins. Serum hepatic enzymes became elevated and were consistent with a mild, subclinical hepatitis. These returned toward normal during continued pheresis.
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PMID:Long-term plateletpheresis of a donor. 677 93

Clinical sarcocystosis was studied in 37 goats after inoculation with graded doses of sporocysts of Sarcocystis capracanis. Eight uninoculated goats served as controls. Clinical response varied with the dose. Goats inoculated with 10-40 million sporocysts died between 11 and 13 days after inoculation (DAI), from interstitial pneumonia, vasculitis, and necrosis of mesenteric lymph nodes. All goats inoculated with 100,000 or 1 million sporocysts died between 19 and 23 DAI; clinical signs were anorexia, fever (40-41 C), anemia, and weight loss. Four of 4 goats inoculated with 50,000 sporocysts and 1 of 4 inoculated with 10,000 sporocysts died 24, 28, 39, 68, and 61 DAI, respectively. Goats inoculated with 1,000 sporocysts and uninoculated goats remained clinically normal. After day 18 and before day 68, packed cell volume and hemoglobin content decreased to as low as 11% and 3.6 g/dl, respectively. Alanine aminotransferase and lactic dehydrogenase activities were inconsistently increased. Blood urea nitrogen and bilirubin values were increased, reaching as high as 63 mg/dl and 10 mg/dl, respectively. Histologically, thymic atrophy, vasculitis, hepatitis, cholangitis, myocarditis, generalized myositis, and encephalomyelitis were the main microscopic findings. The cause of the anemia in goats that died after day 19 was not determined.
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PMID:Sarcocystosis in goats: clinical signs and pathologic and hematologic findings. 678 65


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