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 distribution of 16 antigens of the HLA-A and 15 antigens of the HLA-B series of HLA system, the blood groups ABO, and Rh antigens were studied in 40 alcoholics with cirrhosis, 18 alcoholics without cirrhosis, and in normal control subjects. The group of alcoholics with cirrhosis showed a significantly high frequency of HLA-B13 (corrected P less than 0.01) when compared with normal subjects, while the frequency of HLA-B13 was similar to normal in alcoholics without cirrhosis. On the basis of these findings, its seems that the carriers of HLA-B13 are more susceptible to liver damage caused by alcohol. Both groups of alcoholics and the normal controls had a similar distribution of ABO blood groups and Rh antigens.
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PMID:Distribution of HLA histocompatibility antigens, ABO blood groups and Rh antigens in alcoholic liver disease. 10 57

A family was studied in which three middle-aged siblings had unexplained cirrhosis and steatosis. Five of nine additional family members had abnormalities of liver function. Liver biopsy in those 5 revealed steatosis in 3, steatosis and fibrosis in 1, and increase in lipofuchsin pigment in another. Detailed investigation revealed no known metabolic defect, adverse environmental exposure, or alcohol abuse. We postulate that this family represents a unique type of idiopathic familial cirrhosis. The role of steatosis in the pathogenesis of cirrhosis in this family remains unsettled. The HLA haplotype A24, B18, DRW 4 X 7 was found in several family members, but the association of the disease with the HLA system remains to be established.
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PMID:Idiopathic familial cirrhosis and steatosis in adults. 49 8

Thirteen family members of a patient with chronic active hepatitis type B were investigated. The family included both parents, 6 sons, and 5 daughters. The parents were second cousins. HBsAg, liver tests, immunological evaluation, and HLA typing were performed on all subjects. Percutaneous liver biopsies were done on the mother and 5 of the 6 sons. The mother and all 6 sons had HBs antigenemia. The mother was free from any evidence of liver disease whereas all 6 sons had abnormal liver and immunological tests. The liver biopsies of 5 sons showed chronic active hepatitis with variable degrees of progression toward cirrhosis. The 6th son could not be biopsied in view of his prolonged prothrombin time. The father and the 5 daughters were HBsAg negative and had no evidence of liver disease. Immunological abnormalities were present in all of the effected children and in the mother and 3 daughters. This is the second report in the English literature on the familial occurrence of chronic active hepatitis type B. It emphasizes the predominance of this entity in the male offspring and confirms the presence of immunological abnormalities in the relatives of such patients. There was no evidence to link the inheritance of an immunological abnormality to clear the HBsAg to the histocompatibility complex.
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PMID:Genetic and immunological aspects of familial chronic active hepatitis (type B). 66 17

Determination of histocompatibility antigens in 63 patients with alcoholic liver disease showed that HLA-B8 was more prevalent in patients with cirrhosis than in controls, but among those with fatty liver and minimal fibrosis the prevalence of this antigen was normal. Another noticeable difference was the absence of HLAA28 in the cirrhotic group. In the total series of 219 patients the prevalence of antinuclear and smooth muscle antibodies was raised; they were especially prevalent in patients with cirrhosis. Raised serum IgA and IgG concentrations were also common (found in 50% and 37% respectively) and were again significantly associated with cirrhosis. In contrast, serum IgM levels, which were raised in 46% of cases, were not significantly related to the presence of cirrhosis but correlated significantly with the degree of portacaval shunting. These results support recent evidence suggesting that immune responses may be implicated in alcohol-induced liver damage, particularly in its progression to cirrhosis.
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PMID:Histocompatibility antigens, autoantibodies, and immunoglobulins in alcoholic liver disease. 108 18

In some cases of ascitic fluid due to cirrhosis, benign mesothelial clusters may be observed, accompanied by markedly atypical cells that have been proposed to be abnormal macrophages, mesothelial cells or necrotic cells of hepatic origin. The aim of this study was to determine the origin of these cells with the use of a panel of monoclonal antibodies (MAbs) against cell surface antigens. Furthermore, the lymphocyte subpopulations were analyzed for a possible correlation with the presence of abnormal cells. Markedly atypical cells were found in 4 of 12 cases. They showed no phagocytosis of latex particles and were negative for MAbs My4 (CD14), HLE-1 (CD45), Leu M1 (CD15), CEA 3-13 and HEA-125. They reacted positively with BMA-120 and HLA-1. This staining pattern demonstrated the mesothelial origin of the markedly atypical cells. The profile of the lymphocyte subpopulations in the cases with markedly atypical cells was not different from the other cases. We propose that these cells are abortive cluster formations of mesothelial cells.
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PMID:Immunocytochemical analysis of ascitic fluid due to cirrhosis. A contribution to understanding the origin of markedly atypical cells. 154 8

One hundred and forty-six patients with chronic liver disease have been studied. Some of them (15) showed a clinical picture characterized by cryptogenetic liver cirrhosis associated with hypotriglyceridemia and hypobetalipoproteinemia. These patients had compensated cirrhosis and no history of alcohol abuse; they did not suffer major illness in the past and had no signs of portosystemic encephalopathy. The pathogenetic mechanism of this association and the possible role of genetic factors are discussed. The HLA system has been studied and the A2 antigen found with high frequency, raising the possibility that patients with this syndrome may represent a particular subgroup among these with liver cirrhosis.
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PMID:[Cryptogenetic liver cirrhosis with hypobetalipoproteinemia. Typing of the HLA histocompatibility system]. 157 90

Genetic haemochromatosis is characterised by an inappropriately high rate of iron absorption by the small intestine. The disease is transmitted as an autosomal recessive condition. The gene frequency in the Caucasian population is approximately 1 in 20 and the disease frequency is 1 in 400. Excessive iron deposition occurs in the liver, pancreas, heart, pituitary and joints and hepatic iron concentrations above approximately 400 mumol/g dry weight are always associated with fibrosis and usually with cirrhosis and progressive liver failure. Accurate diagnosis depends upon the demonstration of elevated hepatic iron stores. An hepatic iron index [hepatic iron concentration (in mumol/g dry weight) divided by patient age] of greater than 2.0 distinguishes homozygous subjects from the other conditions in which slight increases in hepatic iron concentration may occur, e.g. in a subject heterozygous for haemochromatosis or alcoholic liver disease. If cirrhosis is present, patients are at a high risk of developing hepatocellular carcinoma. Therefore, they should undergo regular abdominal ultrasound and alpha-fetoprotein estimation. In the absence of cirrhosis, phlebotomy restores life expectancy to normal. Venesection should be continued until all excess iron stores are removed as judged by failure of a rise in haemoglobin concentration on cessation of phlebotomy. Screening of first degree relatives should commence from a young age (e.g. 10 years). If serum ferritin or transferrin saturation are abnormal, liver biopsy should be undertaken. HLA typing of the family allows for the identification of those siblings who are most likely to develop the disease. Secondary iron overload is often multifactorial in origin. Iron chelation therapy with subcutaneous deferoxamine (desferrioxamine) should only commence after careful consideration of the potential benefits in each individual patient.
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PMID:Current concepts in rational therapy for haemochromatosis. 171 64

Hereditary haemochromatosis is a recessive disease in which primary hepatocellular carcinoma, complicating cirrhosis, is responsible for about one-third of deaths in affected homozygotes. We describe a unique HLA haplo-identical pedigree showing parent-to-offspring transmission of hereditary haemochromatosis in whom HLA typing studies, including class I and class II allogenotype analysis, were of no benefit in identifying affected homozygotes. However, affected siblings in the pre-cirrhotic stage of haemochromatosis, with apparent discordance between the haemochromatosis allele and class I loci on chromosome 6, were detected by undertaking a family study, using analysis of serum parameters of iron status in combination with magnetic resonance imaging (MRI). This pedigree emphasises the critical importance of genetic and non-invasive methods for the identification of asymptomatic homozygotes before cirrhosis develops.
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PMID:Detection of hereditary haemochromatosis in an HLA-identical pedigree showing discordance between HLA class I genes and the disease locus. 175 96

Epidemiological evidence suggests a direct relationship between alcohol consumption and the prevalence of cirrhosis. However, the observation that only 8-30% of alcoholics develop cirrhosis illustrates that individual susceptibility mediates the relationship between alcohol consumption and cirrhosis. This chapter examines the factors that may influence individual risk for alcoholic liver disease. These factors include individual differences in alcohol metabolism and consumption patterns, gender, HLA antigens, family alcoholism history, and immune responsiveness. Important methodological issues in each of these areas are addressed also. From the available evidence, the hypothesis is advanced that there is an underlying vulnerability to liver disease in some individuals, and that alcohol use, although a necessary condition, is not sufficient to trigger disease in all individuals.
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PMID:Vulnerability to alcoholic liver disease. 175 83

The fact that only a small percentage of excessive drinkers develop cirrhosis may be due to a genetic susceptibility to the disease. In order to identify possible genetic risk factors for cirrhosis, we studied mixed-race (Negroid-Caucasian) inhabitants of the French West Indies and compared: (1) the frequency of 51 HLA-A, -B, -C and -DR antigens in 41 subjects with alcoholic cirrhosis and in two control groups consisting of 41 excessive drinkers free of liver disease and 51 healthy non-drinkers; and (2) the frequency of Gm and Km haplotypes in the same groups. Analysis of the Gm system also determined the patients' ethnic origins. The frequency of the HLA-A2 antigen was significantly higher in the cirrhotic patients than in the control group of excessive drinkers (chi 2 = 4.47; P less than 0.05), while that of the HLA-B15 antigen was significantly lower (chi 2 = 5.14; P less than 0.05). The frequency of the Cw4 antigen was significantly higher in the cirrhotics than in the non-drinkers (chi 2 = 5.59; P less than 0.05). However, these differences did not persist when the number of comparisons was taken into account. The frequency of Gm and Km haplotypes was not significantly different in the three groups. In conclusion, complementary studies are required to determine the value of the Gm-Km system as a marker of susceptibility to alcoholic cirrhosis. Our results do not identify an association between HLA antigens and cirrhosis specific to a negroid ethnic group and support the notion that such an association is weak.
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PMID:HLA Gm systems and susceptibility to alcoholic cirrhosis: a study of mixed-race subjects. 176 53


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