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)

Sequential standard (1.0 U./kg.) and augmented (4.0-5.0 U./kg.) secretin response to the pancreas has been briefly compared in normal subjects and in patients with combinations of alcoholism, cirrhosis and alcoholic pancreatitis. The results of sequential testing led to the conclusion that, for clinical purposes, the standard test is adequate for the diagnosis of well established pancreatic pathologies causing gross destruction of the parenchyma. The augmented test is of particular value when the response to 1 U./kg. produced equivocal results, inasmuch as augmented stimulation enhances the masked secretory deficiency. The administration of the augmented stimulus to alcoholic patients yielded data which suggest a new hypothesis of pathogenesis for alcoholic pancreatitis, e.g., the postsecretin response pattern of minimal pancreatic inflammatory pathology is hypersecretion. Alcohol is thought to induce fatty degeneration of the pancreatic cell initially. Continued injury leads to necrosis and fibrosis.
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PMID:Standard and augmented secretin testing in chronic pancreatic alcoholic disease. 118 15

Rats were given 36 per cent of calories as ethanol, gin, brandy, whisky or red wine together with hypocaloric (25 per cent of normal), hypocaloric--low-protein--highfat, or hypocaloric--low vitamin diets for several months and compared with rats given isocaloric amounts of glucose instead of alcohol. In spite of high mortality rate no severe liver lesions occurred, especially no cirrhosis. Congeners present in different alcoholic beverages therefore seem to lack important hepatotoxic effects at least in the rat.
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PMID:The effect on the rat liver of long-term administration of different alcoholic beverages together with inadequate diets. 118 21

Rats drank ethanol, on the average 1.20 g/100 g body weight, for various periods up to nearly 300 days. Experimental variables included a high-fat, low-protein diet, administration of additional ethanol by stomach tube, and CCl4 injections instead of ethanol. Growth was retarded by all the variables, especially by the high-fat, low-protein diet. The specific histological finding in the ethanol groups was the presence of Mallory bodies. Significant increase in total liver lipids was caused by ethanol, and rapid fat accumulation, inflammatory changes, and even fibrosis and cirrhosis by the high-fat, low-protein diet and the CCl4 injections. Ethanol raised the concentrations of collagen and soluble protein in the liver; the collagen content was increased also by the high-fat, low-protein diet and the CCl4 injections. The incorporation of proline to collagen was stimulated in incubated liver slices from both ethanol-treated and high-fat, low-protein-fed rats. These treatments also increased the concentration of free proline in the liver, thus augmenting the protein synthesis in fibroblasts.
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PMID:Effect of long-term administration of ethanol to the rat: lipids, collagen and other proteins, and Mallory bodies in the liver. 120 62

Ethanol metabolism and its influence on serum lactate/pyruvate ratio was studied after intravenous infusion of ethanol in 17 patients: 4 controls, 5 alcoholics with cirrhosis, 4 non-alcoholic cirrhotics and 4 alcoholics without liver disease. All refrained from the use of alcohol and drugs 4 weeks prior to the experiment. After maximal ethanol blood levels were achieved at the end of the infusion, ethanol removal occurred at two different rates. This was probably due to the fact that different volumes of ethanol were distributed with time: a fast period (30 to 60 min) and a slow period (60 to 180 min). The rates of disappearence in the two periods were similar in all groups which suggests that liver cirrhosis, independent of clinical severity and/or chronic alcoholism with previous abstinence from alcohol, does not modify ethanol metabolic rates in the liver. The relation lactate/pyruvate doubled in all cases but it occurred within 30 minutes in the groups without liver disease and within 60 minutes in the cirrhotics. This could account for the decreased liability of cirrhotic patients to alcohol hypoglycemia.
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PMID:Ethanol metabolism in liver cirrhosis and chronic alcoholism. 121 Oct 63

A model has been developed for the administration to rats and baboons of ethanol as part of a nutritionally adequate liquid diet. With this regimen, ethanol intake was much higher than with conventional procedures. All animals gained or maintained their body weight, and liver morphology was normal in the controls. Isocaloric substitution of carbohydrate by ethanol (36% of total calories in rats and 50% in baboons) resulted in the production of fatty liver in all animals, while the baboons also developed alcoholic hepatitis and cirrhosis with increased activities of serum glutamic oxaloacetic transaminase. Inebriation and manifestation of dependence upon withdrawal of the diet were observed in baboons and quantitated in the rat. Chemical alterations produced by ethanol at the fatty liver stage were characterized by hyperlipemia, striking triglyceride accumulation in the liver and enhanced activities of microsomal drug metabolizing enzymes, including the microsomal ethanol oxidizing system (MEOS). Ultrastructural changes of the mitochondria and the endoplasmic reticulum were already present at the fatty liver stage and persisted throughout the hepatitis and cirrhosis. The lesions were similar to those observed in alcoholics (including the inflammation and the central sclerosis), and differed strikingly from the alterations produced by other models of liver injury. In showing that all aspects of liver injury observed in alcoholics can be reproduced in animals by the feeding of pure ethanol with an adequate diet, this study incriminates ethanol itself as a cause for the hepatic complications. This new experimental model is proposed as a tool for the study of the pathogenesis and treatment of alcoholic liver injury and dependence.
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PMID:Alcoholic liver injury: experimental models in rats and baboons. 123 25

Alcoholic subjects differ in the incidence of cardiomyopathy. Of potential variables, sex may be important since few females are seen with cardiomyopathy, even adjusting for the lower incidence of alcoholism. To examine this question, noninvasive systolic time intervals were measured in 22 males and 14 females of similar age, heart rate, and arterial pressure, without clinical evidence of heart disease or hypertrophy. Duration and intensity of ethanol intake and the interval from last drinking episode were apparently equivalent. In male alcoholics, the left ventricular preejection period and ejection time (PEP/LVET) ratio of 0.410 +/- 0.020 was significantly higher than in the 11 normal males (0.316 +/- 0.007) (P less than 0.001). In female alcoholics, the ratio was 0.322 +/- 0.015, compared to 0.310 +/- 0.01 for 11 normal females, and was significantly less than in the male patients (P +/- 0.001). In addition prolonged intraventricular conduction by high-frequency ECG was more prevalent in the male group. To further ensure equivalency of alcoholism, patients with biopsy-proved cirrhosis were selected. In nine males, PEP/LVET was significantly higher than in the 10 females. Thus, abnormal myocardial function was evident in males but not in females, suggesting that sex is a determinant of the toxic effects of ethanol on myocardium.
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PMID:Preclinical cardiomyopathy in chronic alcoholics: a sex difference. 125 24

A total of 42 biopsy specimens of the liver (blind and spot) in 32 patients with alcoholic cirrhosis of the liver were investigated. Morphological, portal, postnecrotic, and mixed types of cirrhosis were established. The portal type of cirrhosis is most common. On the basis of repeated analyses of biopsy materials of the liver it may be assumed that the development of cirrhosis of the liver of alcoholic etiology is connected with multiple attacks of acute alcoholic hepatitis. Abstention from alcohol consumption resulted in stifestations of exacerbation of cirrhosis. On the other hand, continuation of alcohol consumption contributed to progressing of cirrhosis, which following several attacks of alcoholic hepatitis, may change its morphological type: portal cirrhosis "transforms" into the postnecrotic or mixed type. The data obtained clarified the role of ethanol in progressing alcoholic cirrhosis of the liver, which according to the initial mecranisms of its development in postnecrotic, since every attack of acute alcoholic hepatitis is accompanied by coagulative (fields of alcoholic hyaline, or Mallory's bodies), or by colliquative (balloon dystrophy) necrosis of hepacytes.
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PMID:[The morphology and morphogenesis of alcoholic cirrhosis of the liver]. 127 77

To investigate the prevalence of antibody to hepatitis C virus (anti-HCV) in heavy drinkers with liver disease in Japan, we tested serum samples from 113 heavy drinkers with liver disease and 121 without liver disease. All were negative for HBsAg with no history of blood transfusion. These subjects had consumed more than 80 g of ethanol daily for 5 years or more. Findings for anti-HCV determined by recombinant immunoblot assay testing were positive in 14 (35.9%) of the 39 patients with liver cirrhosis, 14 (58.3%) of the 24 patients with hepatocellular carcinoma and in 8 (53.3%) of the 15 patients with chronic hepatitis. The anti-HCV positive rate in the drinkers with these liver diseases was significantly higher than in those with such disorders as fatty liver (0/10), hepatic fibrosis (0/22), and alcoholic hepatitis (0/3), as well as in the alcoholics without liver disease (5/121, 4.2%). Considering histologic findings in the anti-HCV positive cirrhotics, the occurrence of lymph follicle formation (71.4%), piecemeal necrosis (78.6%) and loose fibrosis (64.3%) were observed to a significantly higher extent than in cirrhotics who were negative for anti-HCV. These findings suggest that advanced chronic liver disease among heavy drinkers in Japan, especially of hepatocellular carcinoma, is closely associated with HCV infection. In the livers of heavy drinkers who were positive for anti-HCV, histologic findings indicated the possibility of viral infection.
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PMID:High prevalence of antibody to hepatitis C virus in heavy drinkers with chronic liver diseases in Japan. 131 67

The authors describe a case of subcutaneous neoplastic seeding in the abdominal wall in a 67-year-old man with posthepatitic liver cirrhosis complicated by a single nodule of well-differentiated hepatocellular carcinoma. He was treated with percutaneous ethanol injection (PEI) performed under ultrasound guidance. The neoplastic seeding developed along the needle track used to carry out fine-needle biopsy and PEI and was diagnosed 6 months after the beginning of treatment.
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PMID:Neoplastic seeding complicating percutaneous ethanol injection for treatment of hepatocellular carcinoma. 131 21

A Nigerian series of 890 patients with primary liver cell carcinoma, seen during the recent three years, has been examined with a view to establishing the natural history of the tumour in untreated cases. There were 60 males and the mean age of all the patients was 50 years. Hepatitis B surface antigen was positive in 70 pc of tested patients and there were higher pathologic levels of aflatoxins in these patients when compared to normal controls. Liver cirrhosis was associated with 81 pc of patients. Alcohol and smoking were unlikely to be aetiologically important in these patients. The macroscopic type of tumour was mainly diffusely nodular and the commonest microscopic pattern was the characteristic trabecular pattern. Metastases were present in 52 pc of the patients and were mainly to the lungs. Due to late presentation and underlying cirrhosis, most patients were critically ill with high incidence of ascites, jaundice and hepatic precoma. The mean survival time of all patients was six months after onset of the initial symptoms to death and only three weeks after admission to death. The major causes of death were advanced cancer in 78 pc, hepatic failure in 48 pc and rupture of tumour, 39 pc. These observations clearly show that the prognosis of liver cancer is dismal in this environment, as elsewhere. Medical education on earlier presentation in hospital and early operative removal of the tumour should be emphasised. It is suggested that an attempt through immunisation should be employed to reduce the incidence of liver cancer in the population.
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PMID:The natural history of primary liver cell carcinoma: a study of 89 untreated adult Nigerians. 132 87


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