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 existence of a relationship between HLA and the possibility of the development of an alcoholic cirrhosis is researched in this paper. This work was done from 1982 to 1984, by the staff of four clinics of the Medicine School of the University of Uruguay. We studied 47 alcoholics with portal cirrhosis, 19 non-cirrhotic alcoholics and 250 healthy nonalcoholic controls. We confirmed with liver biopsy the cirrhosis in the first group and in the second, liver biopsy was performed in order to assure that they had no cirrhosis. Table I shows the histocompatibility antigens which were tested in the 3 groups. Levels of significance were obtained from exact Fisher test with Yates correction for discontinuity; Pc (corrected P) and RR (relative risk) were also determined. In the alcoholics with portal cirrhosis, the HLABW40 showed a Pc less than 0,005 (RR = 3,93). In the non-cirrhotic alcoholics no significative association was found. We conclude that the carrier of the genetic marker HLABW40, has almost 4 times more chances to develop a cirrhosis as consequence of chronic alcoholic abuse. The presence of this marker, in our patients, has no association with the possibility that an individual becomes an alcoholic abuser. We think that if this data are confirmed in a wider study, some guidelines for the prevention of alcoholic cirrhosis may be established.
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PMID:[The importance of HLA antigens in alcoholic cirrhosis]. 386 71

Trichosporon is a common cause of superficial mycotic infection but has rarely been associated with endocarditis. The case of a patient who had a peritoneovenous shunt for chronic intractable ascites due to Laennec liver cirrhosis is described. The shunt was revised on several occasions, and the last procedure was complicated by a draining skin sinus wound. To the authors' knowledge, this is the first reported case of Trichosporon endocarditis complicating a peritoneovenous shunt.
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PMID:Trichosporon beigelii endocarditis as a complication of peritoneovenous shunt. 401 85

Halothane, enflurane, isoflurane, and fentanyl were examined for their potential to exacerbate liver dysfunction in rats with preexisting cirrhosis. Male Wistar rats given sodium phenobarbital for 2 weeks are assigned randomly to two groups. One group (cirrhotic) was exposed by inhalation to carbon tetrachloride (CCl4) in air at weekly intervals for 12 weeks to induce cirrhosis. The other group (noncirrhotic) was handled similarly but received air only. Five weeks after the last exposure to CCl4, cirrhotic and noncirrhotic rats were given three hours of 1 MAC halothane, enflurane, or isoflurane in 50% oxygen, or 350 micrograms fentanyl per kg of body weight and 50% oxygen, or 50% oxygen only. Blood gas tensions and blood glucose levels were measured before, during, and at the end of exposure. Forty-eight hours after exposure, serum chemistries were measured in each rat for comparison with preexposure values. Rats were then killed by CO2 overdose, and liver, kidney, and testis were prepared for microscopic examination. Enflurane, isoflurane, and halothane, but not fentanyl, produced mild respiratory acidosis and no change in serum glucose levels. All anesthetics resulted in a mild but similar degree of acute liver dysfunction as indicated by small increases in SGOT or SGPT in both cirrhotic and noncirrhotic rats. Liver histology revealed mild to moderate portal cirrhosis with fibrosis and well-developed micronodules in rats exposed to CCl4, but no superimposed acute hepatocellular damage was noted. It is concluded that all the anesthetics used in this study were associated with the same minimal degree of postanesthetic hepatic dysfunction and that the dysfunction was similar in both cirrhotic and noncirrhotic rats.
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PMID:Effects of volatile anesthetics or fentanyl on hepatic function in cirrhotic rats. 406

Iron absorption is under delicate control and the level of absorption is adjusted to comply with the body's need for iron. To measure the intestinal setting for iron absorption, and thereby indirectly assess body iron requirements, cobaltous chloride labelled with (57)Co or (60)Co was given by mouth and the percentage of the test dose excreted in the urine in 24 hours was measured in a gamma counter. Seventeen control subjects with normal iron stores excreted 18% (9-23%) of the dose. Increased excretion, 31% (23-42%), was found in 10 patients with iron deficiency anemia and in 15 patients with depleted iron stores in the absence of anemia. In contrast, 12 patients with anemia due to causes other than iron deficiency excreted amounts of radiocobalt within the normal control range. In patients with iron deficiency, replenishment of iron stores by either oral or parenteral iron caused the previously high results to return to normal.Excretion of the test dose was normal in portal cirrhosis with normal iron stores but it was markedly increased in patients with cirrhosis complicated by either iron deficiency or endogenous iron overload. It was also raised in primary hemochromatosis. Excretion of the dose was reduced in gluten-sensitive enteropathy. Gastrointestinal surgery and inflammatory disease of the lower small intestine had no effect on the results except that some patients with steatorrhea had diminished excretion.The cobalt excretion test provides the clinician with a tool for the assessment of iron absorption, the detection of a reduction in body iron stores below the level that is normal for the subject in question, the differentiation of iron deficiency anemia from anemia due to other causes, and the investigation of patients with iron-loading disorders.
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PMID:Cobalt excretion test for the assessment of body iron stores. 557 25

Records were reviewed of 160 patients who underwent transjugular liver biopsy (TJLB) during a five-year period. Percutaneous transperitoneal needle biopsy was contraindicated in 95% of these patients because of coagulation abnormalities or massive ascites. Moderate complications occurred in two patients. Diagnostic biopsy material was obtained in 129 (81%). TJLB provided useful information in 44 of 58 patients without documented alcohol abuse (clinical Groups III and IV). TJLB disclosed additional diagnoses aside from Laennec cirrhosis in 15 of 48 alcoholic patients with sudden clinical deterioration (Group II), including 11 cases with other stages of alcholic liver disease and four cases of primary or metastatic neoplasm. TJLB revealed diagnoses other than Laennec cirrhosis, including three neoplasms, in six of 54 clinically stable alcoholics (Group I). TJLB frequently yielded important data relative to clinical management or prognosis in Group II, III, and IV patients; it was less useful in Group I patients.
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PMID:Transjugular liver biopsy in high-risk patients with hepatic disease. 647 6

Dogs with portal cirrhosis but without portal hypertension (end-to-side portacaval anastomosis) retain sodium and expand plasma volume before ascites formation. In our study, dogs were subjected to bile duct ligation and simultaneous side-to-side portacaval anastomosis (PCA) in order to create a canine model of hepatic cirrhosis without intrahepatic or portal hypertension. The effect of normalizing intrahepatic pressures in the face of venous outflow block on sodium handling was studied. 13 dogs survived the surgical procedures and were followed. Two dogs developed sodium retention and ascites at 5-6 wk (livers were cirrhotic) when the PCA spontaneously closed. 11 dogs were free of sodium retention and ascites for as long as 12 wks after surgery, while ingesting 35 meq/d of sodium. In this group glomerular filtration rate remained normal throughout the period of observation and there was no expansion of plasma volume. Nine of these dogs were then fed 85 meq/d of sodium; eight remained in sodium balance and one retained sodium and went on to develop ascites. When 10-15 mg i.m. of desoxycorticosterone acetate (DOCA) was given daily, five dogs developed sodium retention and ascites, while four escaped from DOCA. Dogs who developed ascites had either a partially occluded PCA (4/5) or a patent PCA, but with a significant portacaval pressure gradient of 9.5 cm H2O (1/5). In all four dogs who escaped from DOCA, the PCA was widely patent and the mean pressure gradient was only 1.6 cm H2O. Both groups were equally cirrhotic, as judged by histological and biochemical parameters. We conclude that normalizing intrahepatic pressure by providing an outflow tract for the cirrhotic liver will abolish that component of early renal tubular sodium retention not due to portal venous hypertension or ascites sequestration.
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PMID:Dogs with experimental cirrhosis of the liver but without intrahepatic hypertension do not retain sodium or form ascites. 663 May 20

In 12 patients with Laennec's cirrhosis conjugated cholic acid was measured by radioimmunoassay simultaneously in the portal vein, the aorta, and the hepatic vein. Furthermore, the concentration was measured for 90 minutes after i. v. injection of cholecystokinin. In the fasting patient the porto-venous extraction ratio was 0.45 (SD 0.23) and the arterio-venous extraction ratio was 0.24 (SD 0,21). 15-30 minutes after cholecystokinin the bile acid concentration significantly increased. In this time the porto-venous extraction ratio rose to 0.71 while the aorto-venous extraction ratio was different. These results agree with the hemodynamics found in cirrhosis. After cholecystokinin the increase in the extraction ratio account for the blood loss by porto venous shunts which corresponds to an increase of the portal compartment.
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PMID:[Conjugated cholic acid in the portal vein, aorta and hepatic vein in patients with alcohol toxic liver cirrhosis]. 664 39

Although much is known about the neuropsychological functioning of cirrhotic individuals with Laennec's (alcohol associated) cirrhosis, little is known about the neuropsychological functioning of individuals with nonalcoholic cirrhosis. In the present investigation, we have determined that individuals suffering from chronic nonalcoholic cirrhosis, despite the absence of clinical signs of hepatic encephalopathy, are impaired on neuropsychological tests that measure visuopractic capacity, visual scanning, and perceptual-motor speed. In contrast, intellectual, language, memory, attentional, motor, and learning abilities are intact. In comparison with a chronically ill control group of patients suffering from Crohn's disease, individuals with advanced nonalcoholic cirrhosis exhibit less emotional disturbance, but are more impaired in their daily activities. These findings indicate that individuals with nonalcoholic cirrhosis, even in the absence of overt clinical signs of encephalopathy, manifest neuropsychological impairments and experience significant disruption in the routines of everyday living.
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PMID:Nonalcoholic cirrhosis associated with neuropsychological dysfunction in the absence of overt evidence of hepatic encephalopathy. 671 71

Comparative studies on a total of 41628 autopsies from the Institutes of Pathology of Wuppertal and Tuebingen revealed a 2,97 fold increase of liver cirrhosis in Wuppertal and 2,29 fold rise of prevalence in Tuebingen between 1946 and 1975. In Tuebingen this increasing prevalence preponderates in men, in Wuppertal in women. Thus, between 1964-1975 in Tuebingen the prevalence of liver cirrhosis in men exceeds liver cirrhosis in women 2,1 fold, in Wuppertal 1,1 fold only. After World War II a considerable increase was observed in both Institutes within 25 years, which reached a maximum with 8,2% of all adults in Tuebingen in 1969 and 11,8% in 1972 in Wuppertal, especially owing to an increase of portal cirrhosis. Since then no further rise has been noticed.
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PMID:[Liver cirrhosis in autopsy material within 48 years. I. Changes of prevalence, regional differences (author's transl)]. 708 May 72

Post mortems of 2289 patients with liver cirrhosis revealed that 37% died of causes related directly to cirrhosis i.e. liver failure or hemorrhage from oesophageal varices. Patients who died of ruptured oesophageal varices in 82% have splenomegaly and most frequently hepatomegaly. Livercell carcinomas were recognized in 7,5% of cirrhotic livers, increasing to 10% in 1976-1978. This rise particularly is conspicuous in women. Liver carcinoma is 4,5 times more frequent in postnecrotic than in portal cirrhosis.
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PMID:[Liver cirrhosis in autopsy material within 48 years. II. Causes of death, liver cell carcinoma, weights of liver and spleen (author's transl)]. 708 May 73


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