Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Series of total bile acid levels in blood plasma of definite time intervals before and after administration of three different stimulants, i.e. caerulein, egg yolk and fatty meal, were investigated in 10 normal subjects as a control group, in three patients in the florid stage of acute viral hepatitis, in 15 patients in the convalescent stage of acute viral hepatitis, in 10 patients with chronic persistent hepatitis, in 15 patients with chronic aggressive hepatitis, in 20 patients with cirrhosis of the liver and in 15 patients with fatty liver. This procedure can be regarded as an endogenous bile acid tolerance test and can be utilized as a differential diagnostic tool for chronic liver diseases.
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PMID:Endogenous bile acid tolerance test and its clinical significance--series of total bile acid levels in plasma before and after contraction of the gallbladder in patients with chronic liver diseases. 738 59

Fourteen patients, aged 18 to 38 years, presented in the last trimester of pregnancy, or immediately post partum, with severe acute hepatic dysfunction. Liver biopsy confirmed the presence of acute fatty liver in six patients; the cause of hepatic dysfunction was presumed viral hepatitis in five patients, pre-eclampsia in two, and gram-negative septicaemia in one. There was one set of twins and the perinatal mortality was 33 per cent; there were three maternal deaths (21 per cent). Two survivors with acute fatty liver subsequently had successful pregnancies without evidence of hepatic dysfunction.
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PMID:Acute liver disease with encephalopathy and renal failure in late pregnancy and the early puerperium -- a study of fourteen patients. 743 58

A common reason for referring patients to hepatologists is persistently abnormal serum transaminase levels with vague constitutional symptoms. In the United Kingdom, these abnormalities are most often caused by a fatty liver either related to obesity or alcohol abuse; they are less commonly caused by chronic liver disease, particularly chronic viral hepatitis, autoimmune hepatitis, or chronic biliary disease. Endocrine disease is rarely a cause of these abnormalities, although hypothyroidism and hyperthyroidism are well-recognized causes. Addison's disease has been only reported once in the literature by R. G. Olsson as a cause of increased transaminase levels associated with constitutional symptoms; it is not mentioned in textbooks on hepatology. Three patients with Addison's disease are reported here, all of whom had increased serum transaminase levels for more than 6 months before the recognition of the hypoadrenalism with resolution to normal after steroid replacement. Hepatologists should consider subclinical Addison's disease as a cause of persistently increased transaminase levels with constitutional symptoms in the absence of evidence for fatty liver as well as viral and autoimmune markers.
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PMID:Subclinical Addison's disease: a cause of persistent abnormalities in transaminase values. 755 2

Autoimmune hepatitis (AIH) runs a variable clinical course. Slow disease progression or even spontaneous remissions can be observed and suggest that the autoimmune process can, at least to a certain extent, be controlled by regulatory elements of the patient's own immune system. In experimental autoimmune hepatitis (EAH) spontaneous recovery is regularly observed and associated with antigen-specific and antigen-nonspecific suppression. The aim of the current study was to search for similar immunoregulatory phenomena in patients with AIH. We examined T-cell reactivity to soluble human liver antigens in 11 patients with active autoimmune hepatitis and 30 patients with other liver diseases (chronic viral hepatitis, primary biliary cirrhosis, fatty liver). T-cell reactivity to liver antigens was almost exclusively confined to the AIH patients. In 9 of these 11 patients we were able to compare the T-cell response in active untreated disease, directly after initiation of immunosuppressive therapy and in remission, at which point T-cell reactivity was found to be markedly reduced. Addition of irradiated peripheral blood cells from the active disease phase or the remission phase to the responding cells taken before treatment showed that in eight of the nine patients there was marked suppression of the liver-specific T-cell response by cells from the remission phase. Study of the in vivo immune responsiveness by giving a tetanus toxoid booster immunization to nine patients with active untreated AIH as well as healthy controls and patients with other liver diseases showed that none of the patients with AIH showed a response to the tetanus immunization, whereas almost all the other patients showed marked responses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for spontaneous immunosuppression in autoimmune hepatitis. 763 4

Increased activation of lymphocytes in inflammatory bowel disease is reflected by alterations of various immunological functions including enhanced spontaneous secretion of rheumatoid factor by mononuclear cells. since in rheumatic diseases increased secretion of rheumatoid factor is associated with decreased levels of beta-endorphin in circulating blood mononuclear leukocytes, we investigated levels of leukocyte beta-endorphin in inflammatory bowel disease and compared them with those in hepatobiliary disorders and in healthy subjects. Levels of beta-endorphin were measured in extracts from peripheral blood mononuclear leukocytes by radioimmunoassay. beta-Endorphin levels ranged from 0 to 67 pg/10(6) cells. Mononuclear leukocytes from ulcerative colitis patients contained as much beta-endorphin as those from healthy control subjects. In patients with Crohn's disease, levels of beta-endorphin were reduced by as much as roughly 50%. An inverse relationship was found between leukocyte beta-endorphin on the one hand and erythrocyte sedimentation rate, blood granulocyte or thrombocyte counts, and C-reactive protein levels in plasma on the other. In patients with various hepatobiliary disorders including fatty liver disease, viral hepatitis, primary biliary cirrhosis, and cryptogenic or alcoholic cirrhosis, beta-endorphin levels were not significantly different from the normal range values. Data indicate that leukocyte beta-endorphin may be involved in regulation of the systemic inflammatory activity of Crohn's disease.
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PMID:Decreased beta-endorphin content in peripheral blood mononuclear leukocytes from patients with Crohn's disease. 786 97

In heavy drinkers with clinical evidence of liver disease, routine investigations should exclude the possibility of other chronic liver diseases of non-alcoholic aetiology requiring specific therapy--these include chronic viral hepatitis, autoimmune diseases of the liver, Wilson's disease and genetic haemochromatosis. If abnormalities in liver biochemistry persist despite abstinence, or if the diagnosis of alcoholic liver disease is in doubt, a liver biopsy should be carried out. Studies evaluating the role of liver biopsy in alcoholic liver disease suggest that without histological confirmation the diagnosis will be inaccurate in 10-20% of patients. Serum biochemistry and the currently available imaging modalities have severe limitations in determining the relative contributions of fatty liver, alcoholic hepatitis and cirrhosis to the overall picture in alcoholic liver disease. Histological examination is therefore of additional value in determining the prognosis, which is worst in patients with a combination of alcoholic hepatitis and cirrhosis. There are a number of indices available, based on clinical and laboratory information, for evaluating the short-term prognosis, but these can only be used with accuracy if the histological pattern of damage has initially been evaluated.
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PMID:Investigation of alcoholic liver disease. 821 5

Although liver disease during pregnancy is a rare event, it can have devastating effects on the mother and the child. This article reviews diseases uniquely associated to pregnancy, such as fatty liver of pregnancy, toxemia, and others. It also details new advances in diseases such as viral hepatitis and pregnancy and intrahepatic cholestasis of pregnancy.
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PMID:Hepatic emergencies in pregnancy. 837 18

In a retrospective study of 1101 patients (302 men, 799 women; mean age 56,7 [19-88] years) with symptomatic cholelithiasis who had undergone elective cholecystectomy and intraoperative liver biopsy, histological examination revealed inflammatory changes in the gallbladder in 96.7%, chronic fibrotic cholecystitis in 94.5% and a severe form of cholecystitis in 8.8%. Clinically relevant changes in the liver parenchyma were present in 27.9%, most frequently intrahepatic cholangitis (21.8%). The latter was significantly more common in choledocholithiasis than in isolated cholecystolithiasis. 27 patients had signs of severe liver disease, namely viral hepatitis, cirrhosis or fatty liver. Since the gall-bladder in cholelithiasis is almost always inflamed, cholecystectomy is the treatment of choice. Not uncommonly liver biopsy will reveal clinically relevant changes in the liver parenchyma. This will be useful information, especially in the management of symptoms which persist postoperatively.
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PMID:[Histopathological changes of gallbladder and liver parenchyma in symptomatic cholelithiasis]. 850 22

Asymptomatic patients with abnormal results on liver function test pose a diagnostic challenge. In general, determinations of routinely ordered tests of liver function are neither sensitive nor specific for liver disease. Fatty liver, alcohol-related liver damage and chronic viral hepatitis are the most common causes of abnormal liver function test results in asymptomatic patients. Causes of asymptomatic liver disease include hemochromatosis, Wilson's disease, drug toxicity, chronic autoimmune hepatitis, biliary cirrhosis, sclerosing cholangitis, alpha1-antitrypsin deficiency and sarcoidosis. The most efficient screening tests for liver damage are alanine transaminase, alkaline phosphatase and bilirubin. Repeat testing when results are abnormal, and use of ancillary tests, such as creatine phosphokinase or gamma-glutamyl-transferase, may confirm liver damage. Imaging studies help exclude biliary obstruction or neoplasm. Treatable illnesses should be ruled out. Three to six months of observation for progressive symptoms and liver dysfunction may follow. After the period of observation, further laboratory tests, a diagnostic liver biopsy and/or referral to gastroenterologist may be needed.
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PMID:Evaluating asymptomatic patients with abnormal liver function test results. 862 23

Medicinal agents can produce various types of hepatic injury by several mechanisms. Hepatic injury may lead to acute syndromes that resemble viral hepatitis, fatty liver of pregnancy, and obstructive jaundice, as well as to a number of chronic syndromes. Acute liver damage relates, at least in part, to the apparent mechanism of injury. Hepatic injury induced by large single overdose of intrinsically toxic drugs (e.g., acetaminophen, ferrous salts) develops within 24 to 72 hours of intake and usually is accompanied by renal failure. Regular intake of some toxic drugs, (e.g., methotrexate) leads to slowly evolving chronic disease. Liver damage due to hypersensitivity-type idiosyncrasy usually appears after 1 to 5 weeks of taking the drug unless there has been previous exposure and is preceded or accompanied by systemic features that are hallmarks of hypersensitivity. Hepatic injury attributable to metabolic idiosyncrasy may appear after weeks to months of taking the drug and usually presents without the systemic features. Organs other than the liver may be involved in the syndrome of drug-induced injury as the result of selective injury or as part of a hypersensitivity reaction.
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PMID:General aspects of drug-induced liver disease. 874 97


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