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)

Vitamin D metabolism was investigated in 10 patients with cirrhosis. Mean plasma 25 hydroxycholecalciferol (25 OHD) centration in alcoholic cirrhosis was lower than in controls but the difference was not significant. In three patients restudied after the summer, plasma 25 OHD had risen. In contrast to the finding in normal subjects, the half-life of intravenously administered 3H cholecalciferol was short in cirrhotics and showed no correlation with plasma 25 OHD. Furthermore, the appearance of 3H 25 OHD from 3H cholecalciferol was reduced compared to the control group four hours after injection. Increased rate of metabolism of cholecalciferol and deficient production of 25 ohd contribute to vitamin D deficiency in liver disease.
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PMID:Abnormal vitamin D metabolism in cirrhosis. 20 89

Consecutive liver biopsies in a large general hospital for Blacks over the period 1959 - 1960 were compared with those in the 2-year period 1975 - 1976. Changes were noted in the histological appearances of micronodular cirrhosis. With the liberalization of the liquor laws and the granting of access to hard liquor to Blacks, fatty change, alcoholic hepatitis, alcoholic hyalin and alcoholic cirrhosis are making their appearance in the micronodular cirrhosis of the South African Blacks, features which were never observed when alcohol consumption was confined to homebrewed beverages containing large quantities of iron derived from the metallic containers in which liquor is brewed. No change in the histological picture or incidence of macronodular cirrhosis and hepatocellular carcinoma was observed.
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PMID:The changing pattern of liver disease in South African Blacks. 20 77

Twelve male patients with advanced alcoholic cirrhosis of the liver were found to have markedly low serum lipid and lipoprotein concentrations. Serum triglyceride and cholesterol concentrations were about 50% of matched control values. The very low density lipoprotein-triglyceride concentration was only one-third of control values and the cholesterol concentrations in very low density and low density lipoproteins were far below control values. The mean high density lipoprotein cholesterol concentration was not significantly decreased, but in three of 12 patients extremely low values were found. These findings may reflect a failure of lipoprotein synthesis secondary to a bad nutritional state and metabolic disturbances in this advanced stage of liver cirrhosis. By means of the intravenous fat tolerance test with Intralipid it could be shown that substantial amounts of triglycerides could be cleared from the plasma in these patients. However, studies on the long-term Intralipid clearance capacity have to be performed before any general recommendations about the inclusion of fat emulsions in parenteral nutrition of these patients can be made.
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PMID:Intralipid clearance and lipoprotein pattern in men with advanced alcoholic liver cirrhosis. 22 49

The frequencies of histocompatibility antigens (HL-A) have been determined in patients with chronic active hepatitis, cryptogenic cirrhosis, and alcoholic cirrhosis, and were compared with those in a control group of 900 healthy subjects. No significant differences were found and the previously reported increased frequency of HL-A8 in chronic active hepatitis has not been confirmed. The discrepancy from some previous reports could not be explained by different histological, immunological, or biochemical features. However, in view of the variation in incidence of a number of features of the disease from series to series, it seems possible that our findings may reflect differences in the selection of patients or real differences in the disease entity seen by different workers.
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PMID:Histocompatibility antigens in chronic liver disease. 29 25

Results in 44 patients with esophageal bleeding who underwent a mesocaval shunt utilizing a prosthetic graft are presented. Portal hypertension was secondary to alcoholic cirrhosis in 30 patients, to chronic active hepatitis in eight, to primary biliary cirrhosis in four, to cirrhosis secondary to inflammatory bowel disease in one, and to portal vein thrombosis following splenectomy in one. Thirty-six shunts were performed during the emergent or semiemergent time period, and only eight were performed electively. Sixteen of the patients were Child's class A, 16 were class B, and 12 were class C. There were no hospital deaths in the emergency shunt group (of eight patients); there was a 12% mortality rate for patients undergoing semiemergency shunts (two of 17 patients) and a 42% mortality rate for patients who had emergency shunts (eight of 19 patients). Death was related more closely to hepatic reserve, however, than to timing of the shunt. Among the 32 class A and B patients, there were only three deaths in hospital (9%), as compared with seven deaths among the 12 class C patients (58%). Portal-systemic encephalopathy was high in the period immediately after operation (13 of 34 patients, 38%), but it was a chronic problem following discharge from the hospital in only three of 34 patients (9%). The mesocaval shunt is a safe, effective procedure for the control of variceal bleeding in class A and class B patients in any time period, but it carries a high operative mortality risk in the class C patient when it is performed as an emergency operation.
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PMID:Mesocaval shunts for the control of bleeding esophageal varices. 31 25

In patients who have impaired hepatic reserve, the Warren shunt has been proposed as an effective operation because it decompresses the esophageal varices without disturbing portal perfusion of the liver. However, early reports of high operative mortality and technical difficulties have impeded acceptance of the procedure. The operation was done in a series of 17 patients. All patients in whom elective variceal decompression with a patent splenic vein was required and without clinical ascites were candidates for this operation. Follow-up ranged from 2 to 48 months. Six patients had alcoholic cirrhosis, two had primary biliary cirrhosis and seven had postnecrotic cirrhosis; in two the cause of the liver disease was unknown. Five patients were categorized as Child's class A, nine as class B and three as class C. No intraoperative or early postoperative deaths owing to hemorrhage occurred. However, there was one death two weeks postoperatively from pulmonary sepsis and one death five weeks postoperatively due to antigen-positive hepatitis. Two patients died from hepatic failure six weeks and five months after operation, respectively; in the first of these, chronic active hepatitis was diagnosed at the time of operation. In one patient hemorrhage recurred and transfusion was required. Although ascites, which eventually resolved, developed in eight patients after operation, the results in 76 percent of patients have been good without new episodes of hemorrhage or encephalopathy. We conclude that the Warren shunt is a safe and effective elective operation for the treatment of patients in whom hemorrhage from esophageal varices has occurred.
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PMID:The Warren shunt in treating bleeding esophageal varices. 31 64

Elevated circulating CEA levels occur in patients with benign gastrointestinal and hepatic disorders. These are usually less than 10 ng/ml. Of clinical importance is the influence of liver disease on the interpretation of CEA. At least 50% of patients with severe benign hepatic disease have elevated CEA levels, most often active alcoholic cirrhosis, and also chronic active and viral hepatitis, and cryptogenic and biliary cirrhosis. Patients with benign extrahepatic biliary obstruction may have increased plasma CEA, the highest in patients with co-existent cholangitis and especially liver abscess. The liver appears to be essential for the metabolism and/or excretion of CEA. Hence, liver work-up is needed to assess any patient with an elevated CEA. A damaged liver may further augment elevated CEA levels due to cancer. The increased circulating CEA observed in some patients with active ulcerative colitis tends to correlate with severity and extent of disease and usually returns to normal with remission. CEA levels also may be mildly elevated in patients with pancreatitis and in adults with colonic polyps. Smoking may contribute to the increased CEA levels seen in patients with alcoholic liver disease and pancreatitis. Therefore, in interpreting mildy elevated circulating CEA levels in patients with GI tract diseases, one must consider benign as well as malignant etiologies.
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PMID:Carcinoembryonic antigen (CEA) levels in benign gastrointestinal disease states. 36 Dec

IgA bound in vivo was shown by immunofluorescence on the plasma membrane of isolated hepatocytes from subjects with normal liver and patients with liver cirrhosis, chronic active hepatitis or fatty liver. IgA in sera with elevated IgA concentrations, especially from cases with alcoholic cirrhosis, was bound in vitro to isolated hepatocytes from rabbit and mouse. This was not due to the high IgA concentration per se. Moreover, polyclonal polymeric serum-type and secretory IgA, and three of ten polymeric monoclonal IgA preparations, showed similar binding properties. Conversely, purified polyclonal and monoclonal monemeric IgA did not show affinity for the hepatocytes. The binding of polymeric IgA did not seem to depend on the proportion of dimers and larger polymers, kappa- or lambda-type light chains, heavy-chain subclasses, content of J chain or affinity for secetory component. The in vivo binding of IgA by hepatocytes is probably a physiological phenomenon which in part may explain the normal clearance of polymeric IgA from serum.
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PMID:In vivo and in vitro binding of IgA to the plasma membrane of hepatocytes. 36 35

The authors describe a case of cirrhogenic hepatitis due to Pexid which was given for 8 months at 400 mg/day for a severe angina pectoris. We find here the anatomo-clinical profile of perhexiline maleate hepatiits already described in approximately 20 cases. There was a cirrhogenic evolution in our case as in 5 others : but here cirrhosis was revealing and seems stabilized since the treatment was stopped. The cirrhogenic evolution could be due to a cumulative effect of the drug and/or to an immuno-allergic mechanism as in alcoholic cirrhosis which is very similar, especially from an anatomical point of view. However cirrhogenic hepatitis differs by a characteristic lysosomal overload : brown pigment under microscopic observation and lipolysosomes with in some cases a lamellar structure under electron microscopic observation. The prescription of such a drug should be limited to cases of refractory angina pectoris and needed a regular clinical and biological survey.
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PMID:[Cirrhogenic hepatitis due to perhexiline maleate: general review based upon one new case with ultrastructural study (author's transl)]. 36 26

The relative importance of malnutrition and alcohol toxicity in the pathogenesis of cirrhosis has been controversial. In epidemiological studies the incidence of cirrhosis can be correlated with the duration and amount of alcohol imbibed. The importance of nutrition has been discounted. In these studies few analyses of dietary intake were included. Diets of patients with alcoholic cirrhosis characteristically are poor. Furthermore, alcohol toxicity impairs nutrition by interfering with absorption, transport, and utilization of essential nutrients. Patients with cirrhosis respond favorably to nutritious diets despite the concurrent intake of alcohol, although in lesser amount than their usual intakes. In long-term studies highly nutritious diets have protected rats against cirrhosis from alcohol. However, in acute experiments with "loading" doses there was evidence of direct hepatotoxicity in animals and man. Recently, cirrhosis has been produced in baboons with alcohol and a diet considered adequate. The findings are important, but there is some question whether dietary factors (imbalance) may have played a role. Also of recent interest has been the occurrence of lesions simulating alcoholic hepatitis and cirrhosis after jejunoileal bypass surgery. The evidence suggests that malnutrition may have been a major factor in this disease. The roles of alcohol toxicity and of malnutrition in the pathogenesis of cirrhosis are not fully understood. Further studies are needed to clarify these relationships.
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PMID:Alcohol, malnutrition, and alcoholic cirrhosis. 37 14


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