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)

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55

Over the past 20 years we have moved from a situation in which we had no therapy for alcoholic liver disease, through a period when any therapy we had was purely empirical, to an era where we have specific therapies for different aspects of this disease based upon sound pathogenic principles. In this short review, an attempt has been made to summarize these advances in the understanding of the pathogenesis of alcoholic liver disease. In particular, they explain why patients with severe acute alcoholic hepatitis continue to deteriorate in hospital despite withdrawal from alcohol, why they respond to corticosteroids, why only a small percentage of patients develop cirrhosis, and why propylthiouracil may offer protection.
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PMID:Review article: the treatment of alcoholic liver disease. 142 Jul 46

The work deals with a group of 212 patients suffering from various forms of precirrhotic alcoholic liver disease and includes a period of 8.5 years (January 1981-June 1989). At least two liver biopsies were performed in all patients. according to the histological diagnosis, the patients were distributed into 6 subgroups: simple hepatic steatosis--24 cases (11.3%), hepatic fibrosis--40 cases (18.8%), hepatic steatofibrosis--69 cases (32.5%), acute alcoholic hepatitis--18 cases (8.5%), chronic active hepatitis--43 cases (20.3%) and chronic persisting hepatitis--18 cases (8.5%). The assessed histological parameters included: fatty transformation, hepatic fibrosis, inflammatory infiltrate within the lobules and in the portal spaces, hepatocellular necrosis, cholestasis, proliferation of the bile ductules and modification of the lobular architectonic. The work is aimed at pointing out the precirrhotic hepatic histological lesions induced by alcohol and fraught with an increased risk of progression towards liver cirrhosis. The histological sequential examination of alcoholic hepatic lesions confirm the possibility of progression and installation of the cirrhotic stage for a number of these lesions. Liver cirrhosis developed in 44 patients (20.7%) within a period of 3-7 years, on an average 5.5 years. The progression toward cirrhosis occurred in 12 patients (5.7%) with steatofibrosis, in 11 (5.2%) with hepatic fibrosis, in 14 (6.6%) with an intralobular inflammatory infiltrate, in 17 (8%) with hepatocellular necrosis, in 3 (1.4%) with cholestasis, in 5 (2.3%) with proliferation of the bile ductules and in 10 patients (4.7%) with a modification of the lobular architectonic. In addition, cirrhosis was detected in 8 patients (3.8%) with alcoholic hepatitis and in 13 patients (6.1%) with chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The criteria of histological activity and the prognosis in precirrhotic alcoholic hepatopathies]. 167 Jan 14

Two hundred eighty-one alcoholic patients were prospectively evaluated by clinical, biochemical, and histologic parameters during a 4-yr period to assess their prognosis. They were stratified into four categories of injury: 1) fatty liver (26 patients), 2) acute alcoholic hepatitis (106), 3) cirrhosis (39), and 4) cirrhosis with superimposed alcoholic hepatitis (111). The rate of survival and variables correlating with survival varied according to the group. At 48 months, 70% of the patients with fatty liver were alive, 58% in the alcoholic hepatitis group, 49% in cirrhosis, and 35% in alcoholic hepatitis superimposed upon cirrhosis. Within group one, deaths were due to causes unrelated to liver disease. In the alcoholic hepatitis group, factors significantly correlating with survival were ascites, alanine amino-transferase levels, grams of alcohol consumed, continuation of alcohol intake, and clinical severity of disease. Survival in patients of group three correlated significantly with prothrombin time and histologic severity score. Patients with combined cirrhosis and alcoholic hepatitis exhibited the worst prognosis, with the most significant predictors of survival being age, grams of alcohol consumed, the ratio of serum aminotransferases (AST:ALT) and the histologic and clinical severity of the disease. Although a different pattern of correlates was observed for each pathologic level of injury, knowledge of the various correlates aids in prognostic assessment.
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PMID:Prognostic factors in alcoholic liver disease. VA Cooperative Study Group. 199 35

Although altered cytokine homeostasis has been implicated in the pathogenesis of alcoholic liver disease, the relationship between cytokines and metabolic consequences of alcoholic liver disease is unknown. We, therefore, sought to correlate circulating concentrations of tumor necrosis factor-alpha, interleukin-1 and interleukin-6 to clinical and biochemical parameters of liver disease in chronic alcoholic patients. We used an enzyme-linked immunosorbent assay to measure plasma tumor necrosis factor and interleukin-1 and a bioassay to measure serum interleukin-6 in three groups of alcoholic men as follows: (a) actively drinking alcoholic men without evidence of chronic liver disease, (b) nondrinking alcoholic men with stable cirrhosis and (c) patients with acute alcoholic hepatitis. Mean cytokine concentrations were elevated in cirrhotic patients and alcoholic hepatitis patients compared with controls and alcoholic patients without liver disease. Tumor necrosis factor-alpha and interleukin-1 alpha concentrations remained elevated for up to 6 mo after diagnosis of alcoholic hepatitis, whereas interleukin-6 normalized in parallel with clinical recovery. Concentrations of all three cytokines were correlated with biochemical parameters of liver injury and hepatic protein synthesis plus serum immunoglobulin concentrations. We could not demonstrate a relationship between cytokine concentrations and peripheral endotoxemia. Percentages of peripheral blood monocytes that reacted with monoclonal antibodies to CD25 (interleukin-2 receptor) and human lymphocyte antigen-DR were similar for alcoholic patients and controls. These data suggest that tumor necrosis factor-alpha and interleukin-1 alpha are related to some of the metabolic consequences of both acute and chronic alcohol-induced liver disease, whereas interleukin-6 is related to abnormalities seen in acute liver injury.
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PMID:Circulating tumor necrosis factor, interleukin-1 and interleukin-6 concentrations in chronic alcoholic patients. 199 37

The poor prognosis of severe acute alcoholic hepatitis has stimulated interest in specific forms of treatment aimed at reducing the short term mortality as well as preventing progression to cirrhosis. Several controlled trials of steroid therapy have suggested an improvement in short-term survival, but the benefit seems to apply to highly selected cases only. Treatment with propylthiouracil and insulin and glucagon infusions has also shown promising results in controlled studies but there is still no general agreement on their value. Despite recent interest in the use of colchicine to prevent progression of cirrhosis in chronic liver disease of other aetiologies, its role in alcoholic liver disease is not yet clear. In end-stage alcoholic cirrhosis, excellent results are now being achieved with liver transplantation, although this is limited to patients who are not alcohol dependent and in whom there is no alcohol-induced extrahepatic disease.
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PMID:Treatment of advanced alcoholic liver disease. 187 84

Esophagogastrectomy for carcinoma of the esophagus or cardia has been performed in 32 patients with histologically proven hepatic cirrhosis. Thirty-one esophagogastrectomies were performed through a separate abdominal and right thoracic approach in 25 patients, a left thoracoabdominal approach in five patients, and without thoracotomy in two patients. One patient had a colon interposition. Seven patients died after operation (21%) as a result of anastomotic leakage in two patients, hepatorenal in four patients and portal thrombosis in one patient. The type of procedure did not influence mortality. The most common postoperative complication was the development of ascites (68%), and when associated with hepatorenal syndrome (in four patients) there was significant mortality (p less than 0.05). Sepsis was present in the terminal stages of all nonsurvivors. A prothrombin time less than or equal to 60% of normal values was the only significant preoperative predictive factor of mortality, with none of the three patients surviving below this level (p less than 0.05). It is concluded that the presence of cirrhosis is not a contraindication to esophagogastrectomy for carcinoma when curative resection can be undertaken. Hepatic reserve is the determinant factor of operative prognosis. Operative risk is acceptable if patients are classified as Child's class A, and prothrombin time is over 60% of normal values. Operation should be delayed when acute alcoholic hepatitis is present. Intraoperative discovery of cirrhosis is not a contraindication to resection when the above criteria are met.
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PMID:Esophagogastrectomy for carcinoma in cirrhotic patients. 221 Jun 5

In a group of 1,025 cases of alcoholic liver the authors detected 28 cases (2.73%) of acute alcoholic hepatitis on the basis of the morphologic examination, 75% were males, mean age 45 +/- 18 years. The mean amount of alcohol consumed daily was 106.7 g for a mean duration of 19.78 years. The hepatic lesional substrate was hepatic steatosis and cirrhosis in 7 cases (25%) and steatofibrosis in the other 14 cases (50%). The triggering factors were the abuse of alcohol in 27 cases and a pneumonia in the last case. The disease was characterized by fever, encephalopathy, hepatomegaly, hepatocytolytic-cholestatic syndrome. The evolution was dictated by the gravity of the background hepatic lesional substrate.
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PMID:[Acute alcoholic hepatitis]. 257 74

To investigate whether disordered immune function, as shown by abnormalities in lymphokine production, is present in alcoholic liver disease, interleukin-1 and interleukin-2 activity were assayed in a group of patients with acute alcoholic hepatitis in the absence of underlying cirrhosis, and a group of patients with inactive alcoholic cirrhosis. Activities of both IL-1 and IL-2 in alcoholic hepatitis were similar to those of normal individuals, although in abstinent patients with alcoholic cirrhosis, IL-1 activity was increased and IL-2 activity decreased. Lymphocyte transformation in response to PHA in patients with alcoholic hepatitis was significantly impaired when compared with normal controls, and addition of exogenous IL-2 did not correct this impaired response over a wide range of concentrations of both PHA and IL-2. These observations suggest the underlying defects in cell mediated immunity in acute alcoholic hepatitis, as assessed by blast transformation, could be fundamentally different from those of alcoholic cirrhosis and could be secondary to the metabolic effects of acetaldehyde or altered redox potentials on the behaviour of proliferating cells.
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PMID:Contrasts in interleukin-1 and interleukin-2 activity in alcoholic hepatitis and cirrhosis. 262 42

Plasma noradrenaline and adrenaline concentrations were measured in 75 patients with cirrhosis in order to attempt to correlate these concentrations and liver failure and hemodynamic changes. The increased noradrenaline concentration was not correlated with the degree of liver failure estimated by Pugh's classification, with the cause of cirrhosis, with the presence of acute alcoholic hepatitis or with the presence of ascites. Adrenaline concentration was higher in cirrhotic patients with acute alcoholic hepatitis than in those without these lesions. Noradrenaline concentration was significantly correlated with heart rate, wedged hepatic venous pressure and renal blood flow. Noradrenaline concentration was also negatively correlated with stroke volume and adrenaline concentration was negatively correlated with cardiac output and stroke volume. These findings confirm the relationships between portal hypertension, sympathetic hyperactivity and renal function in patients with cirrhosis.
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PMID:[Relation between plasma catecholamines, the severity of the liver disease and hemodynamics in patients with cirrhosis]. 268 Jul 27


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