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)

371 males admitted to a special hospital for withdrawal treatment of alcoholics were investigated on admission and repeatedly controlled during a follow-up of 3-6 months. In only 15% of all patients without delirium tremens there were no signs of liver disease on admission. 62% showed evidence of moderate or severe liver disease. 2-6 months after admission the percentage with moderate or severe liver disease had decreased (26%) while normal findings were obtained in 49%. On admission no correlation between frequency or degree of liver damage and the duration of alcohol abuse or daily intake of alcohol was demonstrated. Following abstinence of 2 months or more incidence of severe liver changes was nearly unchanged (16%) in patients drinking for more than 20 years, while it dropped distinctly in the groups with shorter duration of abuse (abuse less than 10 years: 5%). Histological alterations were distinctly more frequent in patients with abuse of more than 15 years (pronounced fibrosis 26%, cirrhosis 20%), as compared to alcoholics who drank less than 15 years (5 and 9%, respectively). In the patients with delirium tremens signs of severe liver disease were more frequent than in those without delirium. The trend towards normalisation of liver function tests was less in the former than in the latter (marked pathological findings following 2 months of alcohol abstinence in alcoholics with delirium tremens: duration of alcoholism less than 10 years: 16%; 11-20 years: 33%).
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PMID:[Liver damage in chronic alcoholics with and without delirium tremens (author's transl)]. 127 49

Two hundred twelve Italian patients with genetic hemochromatosis (181 men, mean age 50 +/- 11 yr; and 31 women, mean age 49 +/- 10 yr) were followed for a median period of 44 mo (range = 3 to 218 mo). Alcohol abuse was present in 31 subjects (15%), and chronic HBV and HCV infection were seen in 19 (9%) and 35 (24%) of 145 cases tested, respectively. Twenty-four patients (11%) had concomitant beta-thalassemia trait. Liver biopsy revealed cirrhosis in 146 and a noncirrhotic pattern in the other 66. Perls' stain was degree III in 37 patients and IV in 171 patients. One hundred eighty-five patients underwent weekly venesection, and iron depletion was achieved in 122 cases after total iron removal of 3 to 41 gm. Death occurred in 44 patients after 3 to 198 mo and was due to hepatocellular carcinoma in 20 cases, liver failure in 10, extrahepatic cancer in six, heart failure in three and hemochromatosis unrelated causes in five. Cancer has developed in seven other patients still alive (hepatocellular in five and extrahepatic in two). No deaths were observed among noncirrhotic patients; cumulative survival rates in cirrhotic patients were 85%, 75%, 60% and 47% at 3, 5, 8 and 10 yr, respectively. Univariate analysis in the 146 cirrhotic patients showed that age greater than 60 yr, alcohol abuse, cardiomyopathy, skin pigmentation, portal hypertension, hypoalbuminemia, hypergammaglobulinemia and Child class B or C had significant negative prognostic value. At multivariate analysis, only alcohol abuse, gamma-globulins greater than 2.0 gm/dl and Child class B or C maintained their negative prognostic values (p less than 0.01, hazard ratio 2.7; p less than 0.001, hazard ratio 2.8; and p less than 0.001, hazard ratio 4.3, respectively).
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PMID:Survival and prognostic factors in 212 Italian patients with genetic hemochromatosis. 131 85

The present paper is devoted to overview the basic concepts of ethanol-induced hepatic injury and therapeutic modalities by which alcoholic liver disease can be alleviated. The role of alcohol dehydrogenase of both hepatic and gastric origin as well as the importance of the number one metabolite acetaldehyde are discussed, furthermore the effects of microsomal ethanol oxidizing system are also described. The features of the major clinicopathological consequences of alcohol abuse fatty liver, alcoholic hepatitis are briefly outlined, and the basic pathogenetic mechanisms that lead to cirrhosis--cell necrosis, regeneration and fibroplasia--are shown. The understanding of the pathophysiology of alcohol-induced liver injury may improve the therapy with drugs and nutritional factors, and allow successful prevention through the early recognition of heavy drinkers before their social or medical disintegration. In the management of alcoholic liver diseases, among the true hepatoprotective agents a naturally occurring flavonoid silymarin and an active methyl-donor metabolite S-adenosyl-L-methionine seem to be promising. An antifibrotic treatment with colchicine might also be of importance. Further prospective, well-designed, controlled clinical trials are still warranted to evaluate real efficacy of these drugs. The hepatic consequences of alcohol abuse may be treatable, however, prevention would be the true resolution of the major global health problem of alcoholism.
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PMID:Pathogenesis and management of alcoholic liver injury. 134

Porphyria cutanea tarda in human beings is believed to be due to reduced hepatic uroporphyrinogen decarboxylase activity. However, extrinsic factors such as alcohol abuse and drug intake are required for clinical manifestation of the disease. In addition to typical cutaneous lesions, patients with porphyria cutanea tarda usually have chronic liver disease and moderate iron overload. Of 74 Italian patients with porphyria cutanea tarda, hepatitis C virus antibodies were detected in 76% by enzyme-linked immunoassay and in 82% by recombinant immunoblot assay. Viral genome, studied with nested polymerase chain reaction, was found in the sera of 49 subjects--47 positive and 2 indeterminate on recombinant immunoblot assay. Five percent of the patients were HBsAg-positive, and about 40% had had past hepatitis B contacts. Alcohol abuse was present in 38%. Liver biopsies performed in 42 patients showed chronic persistent hepatitis in 7 patients, chronic active hepatitis in 22 patients, fibrosis in three patients and cirrhosis in 10 patients. Hepatitis C virus antibody was detected in 100% of patients with chronic active hepatitis and in about 80% of all other groups. Alcohol abuse was more frequent in patients with cirrhosis (80%) than in the other groups. In Italian patients with porphyria cutanea tarda, the prevalence of hepatitis C virus infection was very high, comparable to that in non-A, non-B hepatitis and high-risk patient groups. Hepatitis C virus is probably the main pathogenetic factor of the liver disease of patients with porphyria cutanea tarda.
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PMID:Hepatitis C virus and porphyria cutanea tarda: evidence of a strong association. 753 99

Studies have been made of the presence of bile acid metabolites in ten patients with liver cirrhosis as a consequence of alcohol abuse. Eight of the patients were categorized as Child group A, indicating only mild impairment of liver function, whereas the remaining two patients comprised Child group C. A complex mixture of bile acids was isolated from serum, urine, and faeces, and 26 bile acids were identified by gas-liquid chromatography coupled to mass spectrometry. Identification was made of the primary bile acids, cholic (C) and chenodeoxycholic (CDC) acid, and metabolites of these bile acids converted through 7-dehydroxylation, keto-formation, 6-hydroxylation, 1 beta-hydroxylation, allo-formation or nor-formation. All of the bile acids have previously been described either in healthy humans or patients with hepatobiliary disease. With the exception of C, CDC, and deoxycholic acid, all of the bile acids were present only infrequently, and none of the bile acids was pathognomonic for liver cirrhosis. The proportion of metabolites of the primary bile acids C and CDC was similar to that previously reported in healthy humans, the lowest proportion being recorded in the Child group C patients. Repeated determinations of the metabolite pattern in two patients showed large variations, indicating that the bile acid metabolism varies from time to time. We conclude that in mild cirrhosis, no significant alterations in microbial or hepatic transformation of bile acids seem to occur.
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PMID:Presence of bile acid metabolites in serum, urine, and faeces in cirrhosis. 141 Dec 66

A poor nutritional status has repeatedly been described in advanced liver cirrhosis, but the exact prevalence of the defect and its relation to the aetiology and severity of liver disease in the Italian population are only partly known. Anthropometric measurements were carried out in 200 patients with cirrhosis (135 M, 65 F). Liver disease was related to alcohol abuse in 77 cases, but most patients had stopped alcohol for at least 6 months before study. In comparison to a normal elderly Italian and to an age-matched North-American population, 5 to 45% of male patients with cirrhosis and 10 to 30% of females had signs of malnutrition, the proportion being variable according to the test used. Male patients showed a remarkable reduction in muscle mass (30-45% of patients, mainly in the presence of moderate-to-severe or severe liver failure), whereas female patients showed a more remarkable reduction of fat stores (15-30% of cases), with advancing liver failure, and a less severe reduction in muscle mass. No direct effect of alcohol was demonstrated in this selected population.
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PMID:Anthropometric assessment of the nutritional status of patients with liver cirrhosis in an Italian population. 142 44

One hundred and one patients with cirrhosis resulting from alcohol abuse, admitted to Broussais University Hospital, Paris, between January, 1986 and December, 1989 were assessed for infection of the ascitic fluid using clinical and cytobacteriological criteria. All of 46 patients (45.5%) with clinical signs and symptoms of peritonitis had an ascitic fluid polymorphonuclear (PMN) count > 250 cells/mm3. Bacteria could be isolated from the ascitic fluid of 23 patients (50%). Twenty-six bacterial strains were isolated (there was more than one strain in two samples). Escherichia coli was found in 14 cases. It is noteworthy that no anaerobes were grown. Mortality, biochemical parameters and clinical features correlated significantly with an ascitic fluid PMN count > 250 cells/mm3. High mortality correlated with a PMN count > 1000 cells/mm3 (70% vs. 33%).
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PMID:Spontaneous peritonitis in cirrhotic hospital in-patients: retrospective analysis of 101 cases. 143 75

The purpose of the study was evaluation of the usefulness of selected indices of humoral immune responsiveness in the differential diagnosis of post-alcoholic hepatocellular damage. The study was carried out in 105 patients: 10 patients with a history of alcohol abuse without clinical and biochemical evidence of hepatocellular damage, 2) patients with alcoholic cirrhosis, 3) patients with post-inflammatory cirrhosis. The prognostic usefulness of the determinations of serum IgM, C3 and C4 complement components and circulating immune complexes in early diagnostic of alcoholic liver disease was demonstrated. It was noted also that increased serum IgA level may be a useful index differentiating of cirrhosis after hepatitis from alcoholic cirrhosis.
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PMID:[Diagnostic and prognostic value of the assessment of selected indicators of humoral immunity in alcoholism-related pathology of the liver]. 144 22

Bile acid concentrations in serum, and urinary and faecal excretion of bile acids have been studied in ten patients with liver cirrhosis as a consequence of alcohol abuse. Eight of the patients were categorized as Child group A, whereas the remaining two patients comprised Child group C. Individual bile acids were isolated and identified by gas chromatography coupled to mass spectrometry. Total fasting serum bile acid concentrations were elevated in all patients, but not correlated to conventional tests of liver function. Eight of the patients had increased urinary excretion of bile acids. Faecal bile acid-excretion was highly variable between patients, and also between Child's group A and C patients. Total fasting serum bile acid concentrations were not correlated to either urinary, faecal, or total bile acid excretion (= synthesis of bile acids) or to the ratio between urinary and faecal excretion of bile acids. The daily synthesis of bile acids showed a large overlap between Child's group A and C patients. The percentage of chenodeoxycholic acid and its metabolites relative to total daily excretion of bile acids did not correlate, indicating that the synthesis pathways for the primary bile acids does not systematically change in relation to the rate of synthesis. We conclude that even in mild cirrhosis, serum bile acid concentrations are elevated. However, no consistent changes in synthesis of bile acids or synthesis pathways was observed in such patients.
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PMID:Serum concentrations and excretion of bile acids in cirrhosis. 145 51

A total of 164 patients with alcoholism-induced osteonecrosis were seen over a 22-year period, from 1962 to 1984. Twenty-three percent of patients were female and 30.5% were black. The average duration of alcohol abuse was 9.5 years, ranging from 8 to 20 years. The presence of femoral head necrosis was diagnosed in patients aged 21-67 years; 28% of patients were under 40 years of age and 76% were under 50 years. Bilateral hip necrosis was present in 44.5% of patients and, within three years of the diagnosis of FHN, the presence of multifocal necrosis became evident in 23 cases at sites away from the hip (shoulders and knees). Hyperlipidemia was found in 38.4% of cases, involving both cholesterol and triglycerides. Serum amylase was elevated in 33 patients; liver dysfunction was present in 50; hepatomegaly was found in 32; and biopsy-confirmed cirrhosis was present in 22 cases. Hyperuricemia was found in 22 patients, some of whom had received steroids. Disabling hip pain was the first manifestation of disability related to alcohol abuse in 158 patients, most of whom required total hip joint replacement. This study supports the hypothesis that alcoholism-induced bone necrosis is caused by fat embolism linked to co-existent hyperlipidemia. The treatment of hyperlipidemia by dietary means or lipotropic medication and the cessation of alcohol abuse is advised. Multi-center studies employing such treatment should provide evidence of its effect on the evolution of necrosis as well as the incidence of bilateral hip femoral head necrosis and multifocal lesions.
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PMID:Alcoholism-induced bone necrosis. 151 11


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