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)

Clinical features of pregnancy in women with liver cirrhosis and/or portal hypertension have been reviewed. Termination of pregnancy is seldom indicated in a woman with compensated cirrhosis or a young woman with extrahepatic venous obstruction. However, the risk of spontaneous abortion is increased in cirrhotic women without shunt even if there is no deterioration of liver function. The risk of bleeding from esophageal varices or deterioration of liver function is usually unpredictable. Shunt surgery can be done with relatively little effect on both the mother and the fetus if conservative measurements fail to control the hematemesis. Vaginal delivery can be anticipated in most women, and cesarean section should be preserved for obstetric indications. The risk of postpartum hemorrhage is greatly increased, particularly in patients with previous shunt surgery. Perinatal loss is high because of the increased rate of premature delivery and stillbirth. Maternal prognosis is grave in women with cirrhosis.
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PMID:Pregnancy in liver cirrhosis and/or portal hypertension. 32 18

During the last 25 years, there have been important developments in visualising the portal vein, in examining its contents, and in measuring the pressure of blood flowing within it. Radiologists have set the scene and now is the time of the scanner. These technical advances have been applied to the diagnosis and treatment of patients with portal hypertension, and many ingenious surgical techniques have been proposed. The problem of successful treatment of the patient with bleeding oesophageal varices and cirrhosis of the liver, however, has not yet been solved. This report discusses the portal vein in terms of pressure, flow, and regeneration factors. Portal hypertension is classified and methods of relief are discussed.
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PMID:Portal circulation and portal hypertension. 34 61

The large number of chemical agents administered for therapeutic or diagnostic purposes can produce various types of hepatic injury by several mechanism. Acute injury may be cytotoxic, cholestatic or mixed. Cytotoxic injury may consist of necrosis or steatosis. Cholestatic injury may be cholangiolitic (hepatocanalicular) or bland (canalicular). Chronic hepatic lesions caused by medicinal agents include chronic active hepatitis, steatosis, cirrhosis, fibrosis, hepatoportal sclerosis (non-cirrhotic portal hypertension), hepatic vein thrombosis, peliosis hepatis, adenoma, carcinoma, and angiosarcoma. There is a useful relationship between the type of hepatic injury and the chemical setting in which the drugs are employed. Some agents produce the liver damage because they are intrinsic (true, predictable) hepatotoxins. Other (non-predictable "hepatotoxins"), produce hepatic injury only in the rare and unusually susceptible individual (idiosyncratic injury). Hepatotoxic agents can be recognised by their dose-dependent and experimental reproducibility, properties which are not shared by agents which produce hepatic injury only in idiosyncratic hosts. Intrinsic hepatotoxins may be categorised as direct or indirect. Direct hepatotoxins injure the hepatocyte by direct physiochemical alteration and as a consequence produce metabolic defects. Indirect hepatotoxins selectively block metabolic pathways and, by producing a precise biochemical lesion, lead to structural changes. They may lead to hepatic steatosis or necrosis (cytotoxic indirect hepatotoxins) or block bile flow (cholestatic indirect hepatotoxins). Direct hepatotoxins are rarely encountered as drugs. Overdoses of some drugs and antineoplastic agents appear to be indirect cytotoxic hepatotoxins, and the C-17 alkylated anabolic and contraceptive steroids are indirect, cholestatic hepatotoxins. Idiosyncracy of the host is the mechanism for most types of drug-induced hepatic injury. It may reflect allergy to the drug or a metabolic aberration of the host permitting the production of hepatotoxic metabolites.
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PMID:Drug-induced liver disease. 35 64

The uptake of (125)I albumin microaggregates (U-(125)I-AMA) from portal blood, during a single passage through the hepatic reticuloendothelial system, has been found to be generally decreased in cirrhosis. To investigate if a similar phenomenon occurs for the colloid flowing through the hepatic artery, the U-(125)I-AMA was first calculated in normal dogs after injection of a mixture of (51)Cr red blood cells ((51)Cr-RBC) and (125)I-AMA into the hepatic artery by comparing hepatic indicator dilution curves (IDC) obtained with both indicators. In nine dogs, the U-(125)I-AMA from hepatic artery blood was generally over 90%, as previously reported for the same colloid flowing through the portal vein in another group of normal dogs. This approach was then applied in nine patients with alcoholic cirrhosis who underwent combined umbilicoportal vein, hepatic vein, and hepatic artery catheterisation because of severe portal hypertension. Hepatic indicator dilution curves were obtained in the nine patients after injection of a mixture of (51)Cr-RBC and (125)I-AMA into the portal vein and the hepatic artery. The U-(125)I-AMA from portal and hepatic artery blood was measured by comparing (51)Cr-RBC and (125)I-AMA hepatic IDC. U-(125)I-AMA varied between 5.2 and 90.5% after portal vein injection and between 13.7 and 90.1% after hepatic artery injection; not difference was found between paired values. In all patients the extraction of indocyanine green (E-ICG) was calculated during a continuous infusion and significant correlations were found between E-ICG and U-(125)I-AMA from portal blood (r=0.931; p <0.001) or from hepatic artery blood (r=0.861; p <0.005). The decreased uptakes can be related to intrahepatic shunts or sinusoidal changes responsible for ineffective phagocytosis and restricted access of dye to parenchymal cells. These data indicate that in cirrhosis the hepatic artery and portal vein blood is cleared of colloid and ICG in a similar fashion and suggest nearly identical blood supply to the regenerative nodules by the hepatic artery and portal vein. Thus U-(125)I-AMA from hepatic artery or portal vein blood, as well as the E-ICG, may be used to estimate the functional hepatic blood supply in cirrhosis; this may prove to be useful in the prognosis of patients before portacaval shunts.
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PMID:Arterial and portal blood supply in cirrhosis: a functional evaluation. 38 41

Development of diabetes mellitus is a common complication of side to side porta-caval anastomosis (PCA). Five patients with liver cirrhosis and portal hypertension have been studied with intravehous (IVGTT, 0,5 g/Kg B.W.) and oral (OGTT, 1 g/Kg B.W.) glucose tolerance tests before and three weeks after PCA. Fasting plasma glucose was 84 +/- 7 before and 87 +/- 3 mg/dl after PCA. Fasting IRI increased from 17 +/- 3 to 31 +/- 6 microU/ml. The pattern of plasma glucose and IRI response to IVGTT did not change after PCA. Plasma glucose resonse to OGTT after PCA showed only an earlier rise at 60 instead of 90 minutes, whereas IRI resonse (area under the insulin curve) was significantly enhanced (from 12.4 to 19.8 U/l, p < 0.05). These data suggest a role of gut polipeptides in determining hyperinsulinemia and insulin resistence in PCA patients.
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PMID:[Glucose tolerance and insulinemia in patients with hepatic cirrhosis and portal hypertension treated by portacaval anastomosis]. 39 34

The generally held views that plasma renin activity (PRA) is increased in cirrhosis and that this is secondary to reductions in the "effective" blood or extracellular fluid (ECF) volumes, consequent on the effects of portal hypertension, were re-examined in the present study. Measurements of PRA in 67 patients representing different clinical stages of cirrhosis showed that the mean value in 15 patients without ascites was significantly reduced. In 21 of 35 with ascites, PRA was either reduced or within the normal range. A low plasma renin substrate concentration was not the cause for the low PRA. These findings are not in keeping with the concepts of reduced "effective" blood or ECF volumes at least for the majority of patients at these stages of cirrhosis under the conditions of the present study. The only group showing a significantly increased PRA had evidence of renal impairment. In these 17 patients the underlying reduction in renal perfusion may have been the stimulus to the kidney that led to an increase to renin secretion.
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PMID:Changes in plasma renin activity in cirrhosis: a reappraisal based on studies in 67 patients and "low-renin" cirrhosis. 39 38

Percutaneous transhepatic portography was performed in 22 patients with liver cirrhosis and portal hypertension. All patients had bled or were bleeding from presumed esophageal varices. One or more veins feeding esophageal varices were occluded with bucrylate. Follow-up examination in eight patients 1-12 months later showed recanalization of previously obliterated veins in six; however, these veins were markedly smaller than before the procedure. In patients where veins were still occluded, new veins had opened up and carried blood to the esophageal varices, which were filled to a lesser degree than before. In our experience, bucrylate is superior to Gelfoam, thrombin, and Etolein in producing venous occlusion.
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PMID:Isobutyl 2-cyanoacrylate (bucrylate) in obliteration of gastric coronary vein and esophageal varices. 41 93

A 55-year-old woman developed cirrhosis with portal hypertension while taking methyldopa. No other cause for the cirrhosis was evident. In view of the known hepatotoxic effects of methyldopa, a causal relationship is implied. Possible mechanisms of drug toxicity include both immunologic reactions and direct hepatocellular damage by the drug or its metabolites.
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PMID:Cryptogenic cirrhosis associated with methyldopa. 42 36

The increasing importance of physiological and functional surgical procedures in the surgical therapy of benign abdominal disease is implied. Positive results were achieved at the 2nd Department of Surgery of the University of Vienna following parietal cell vagotomy in hypersecretory gastroduodenal ulcer, latero-lateral pancreatico-jejunostomy according to Puestov-Mercadier in chronic relapsing pancreatitis, distal splenorenal shunt according to Warren in portal hypertension and following peritoneo-venous shunt according to Warren in portal hypertension and following peritoneo-venous shunt according to Le Veen in ascites and cirrhosis of the liver.
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PMID:[Modern functional and physiological techniques in abdominal surgery (author's transl)]. 42 27

A 68-year-old male underwent cholecystectomy with a normal operative wedge liver biopsy. Five months later he presented with secondary biliary cirrhosis and signs of portal hypertension and hepatocellular failure. At autopsy, a squamous cell carcinoma of the bile duct was found. This case represents an unusually rapid development of cirrhosis secondary to extrahepatic biliary obstruction with documentation of normal liver histology five months prior to his last admission.
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PMID:Rapid development of cirrhosis secondary to squamous cell carcinoma of the common bile duct. 42 5


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