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)

Hepatotoxic reactions to antibacterials are rare, occurring with an estimated frequency of between 1 and 10 per 100,000 drug prescriptions for most antibacterials. Although many antibacterial-induced hepatotoxic reactions have a characteristic clinical and biochemical pattern e.g. cholestatic hepatitis (flucloxacillin) or fatty liver (tetracycline), many can also present with a variety of clinicopathological patterns e.g. nitrofurantoin is associated with the development of acute hepatitis, granulomatous hepatitis and chronic active hepatitis. Almost all reactions are idiosyncratic, with no diagnostic laboratory tests to aid the diagnosis. Early diagnosis is essential and requires a vigilant physician to elicit a detailed drug history. Although the outcome is usually good when the offending antibacterial is withdrawn, morbidity may persist for years and fatalities have occurred, particularly when there is a delay in recognising the hepatotoxic antibacterial. There is no specific treatment for antibacterial-induced hepatotoxicity other than withdrawing the implicated drug. For severe disease, however, liver transplantation should be considered.
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PMID:Antibacterial-induced hepatotoxicity. Incidence, prevention and management. 886 66

Alcoholic liver disease encompasses three main forms of liver injury: fatty change, alcoholic hepatitis and cirrhosis. However, there are many other types of injury, including perivenular fibrosis, venous occlusive lesions, microscopic cholangitis and chronic active hepatitis. The pathological spectrum is reviewed in this paper, and the contribution of other injurious agents to the pathological features is identified. Alcoholic liver disease can be mimicked by a variety of non-alcoholic liver diseases. However, features such as fatty liver with perivenular fibrosis, giant mitochondria, spotty hepatocyte necrosis, Mallory bodies, a micronodular pattern of cirrhosis, and iron deposition are strongly suggestive of an alcoholic aetiology. Correlation of clinical findings, and especially the alcohol history, and histopathological factors is necessary for the definitive diagnosis.
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PMID:Pathological spectrum of alcoholic liver disease. 897 50

In hematoxylin and eosin (H and E) stained sections from liver biopsies, the destruction of bile ducts in the portal triads is regarded as an important histologic parameter in the diagnosis of primary biliary cirrhosis (PBC). In contrast, the bile ducts are not destroyed by chronic inflammation in chronic active hepatitis (CAH). Nevertheless, the differential histologic diagnosis between PBC and virus or autoinmune-induced chronic active hepatitis (CAH), is very difficult in 15% of cases. That difficulty is mainly due to the impossibility of identifying bile ducts in the portal triads with marked lymphocytic infiltration. In this investigation we report that bile ducts may be specifically stained by anti-human cytokeratin 7 (CK7). Sections from 16 liver biopsies (PBC = 6, CAH = 6 and fatty liver (FL) = 4) were stained with H and E and CK7. The results in H and E stained sections indicated that the mean number of bile ducts found in PBC was was 0.56 (range 0-2), in CAH 0.67 (range 1-3), and in FL 0.56 (range 1-3). In parallel CK7 stained sections, the mean number of bile ducts in PBC was 5.33 (range 2-35), in CAH 3.44 (range 4-18), and in FL 1.39 (range 2-6). The difference between H and E and CK7 stained sections was significant (p < 0.001) in all 3 groups. In the light of these preliminary results, it would appear that Cytokeratin 7 may be the stain of choice to detect bile ducts, an important parameter to histologically differentiate between PBC and CAH, as well as to classify PBC into its different stages.
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PMID:The detection of bile ducts in liver biopsies by cytokeratin 7. 962

In distinguishing normal from abnormal hepatic changes, the author described the expected changes in liver tests that occur during complicated pregnancy. This article reviews the forms of pre-existing liver disease that may affect or be affected by pregnancy, as well as liver diseases that tend to arise during pregnancy. Among the pre-existing liver diseases are autoimmune chronic active hepatitis, which may be activated by pregnancy and tends to be associated with an increased risk of still and premature births. Worsening of chronic hepatitis B and C has occasionally been observed. While some women with cirrhosis can sustain a normal pregnancy without any worsening of hepatic function, others develop liver failure; plus, women with cirrhosis are less fertile and have higher rates of both stillbirths and premature infants. Other liver disorders that may or may not be affected by pregnancy include Dubin-Johnson syndrome, Gilbert syndrome, benign recurrent intrahepatic cholestasis, Wilson's disease, hepatic adenomas, and focal nodular hyperplasia. Among the hepatic disorders that occur during pregnancy in normally healthy women and then resolve after delivery is intrahepatic cholestasis of pregnancy (also known as pruritus gravidarum, recurrent intrahepatic cholestasis of pregnancy, and obstetric hepatosis). Others include acute fatty liver of pregnancy and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), which may be part of the spectrum of disorders associated with pre-eclampsia/eclampsia. Pregnancy may also trigger the dissemination of herpes infection to the liver.
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PMID:Liver problems in pregnancy: part 2--managing pre-existing and pregnancy-induced liver disease. 973 96

In clinical trials, all lipid-lowering agents have been associated with mild, asymptomatic elevations of alanine aminotransferase (ALT) and asparate aminotransferase enzymes. This, along with the fact that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors are hepatotoxic in some animals, led the US Food and Drug Administration (FDA) to recommend monitoring of liver enzymes for all lipid-lowering agents, except the bile acid sequestrants. Because the drugs act by different mechanisms, ALT elevations may be a pharmacodynamic effect related to lipid lowering, rather than a direct effect of the drug. Animal studies support this assumption. ALT elevations of 3 times the upper limit of normal occur in <3% of patients in clinical trials of lipid-lowering drugs. The elevations are transient and often dose-related, and they usually revert to normal while continuing therapy and have never been associated with hepatotoxicity. Confounding factors include alcohol, acetaminophen, and pre-existing liver disease, such as chronic hepatitis C and type II diabetes with fatty liver, which are both associated with mild, intermittent elevations of ALT. The more important issue is whether or not lipid-lowering agents are hepatotoxic. There are case reports of hepatotoxicity (cholestasis, jaundice, hepatitis, chronic active hepatitis, fatty liver, cirrhosis and acute liver failure) with all of the drugs, except cholestyramine. To date there are just 5 cases of documented liver failure linked to lovastatin. There is no evidence that monitoring reduces the rate of hepatotoxicity. Mild elevations of ALT that occur with many drugs, including HMG-CoA reductase inhibitors, do not predict hepatotoxicity. Liver enzyme elevations appear to be a class characteristic of lipid-lowering agents. Hepatotoxicity is a rare idiosyncratic reaction, occurring only with sustained released nicotinic acid.
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PMID:Defining patient risks from expanded preventive therapies. 1085 89

Liver steatosis, diabetes mellitus and hepatitis C virus (HCV) genotype have been implicated in liver fibrosis in HCV-related chronic active hepatitis (CAH). The aim of this study was to evaluate whether steatosis and diabetes were associated with more severe liver fibrosis in patients with genotype 1b HCV-related CAH. One-hundred and eighty patients (98 men, 82 women; age range 17-68 years; median 51) infected with genotype 1b HCV underwent ultrasound examination and liver biopsy because of elevated levels of serum alanine transaminase. Based on liver histology, patients were divided into three steatosis classes: 1 (involving <33% of hepatocytes), 2 (34-66%) and 3 (>66%). Fibrosis was graded with the Ishak score (range: 0-6). Virological and epidemiologic characteristics, biochemical data, body mass index, and apparent duration of disease were recorded. Diabetes was identified according to American Diabetes Association criteria. The median fibrosis grade was 2 (23 patients had liver cirrhosis) in the three steatosis classes, with no significant differences between classes. At multivariate analysis, fibrosis was significantly related to age, alanine transaminase, diabetes, hepatitis B core antibody, steatohepatitis and grading. At binary logistic regression analysis, only diabetes and fibrosis stage were significantly associated with steatohepatitis. Steatosis was not an independent risk factor for liver disease severity in our CAH/genotype 1b HCV-infected patients. Steatohepatitis was associated as well as diabetes and affected the severity of liver fibrosis.
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PMID:Steatohepatitis is associated with diabetes and fibrosis in genotype 1b HCV-related chronic liver disease. 1787 6

Acute fatty liver of pregnancy is a heterogeneous disorder which may occur in the absence of a detectable gene mutation for the enzyme long-chain L-3-hydroxyacyl-CoA dehydrogenase. Acute fatty liver of pregnancy has been reported to complicate several gastrointestinal disorders including viral hepatitis, chronic active hepatitis and intrahepatic cholestasis of pregnancy. A case of acute fatty liver of pregnancy in a woman with ulcerative colitis and familial hidradenitis suppurativa without a detectable gene mutation is presented. The potential role of inflammatory cytokines in precipitating acute fatty liver of pregnancy is discussed.
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PMID:Acute fatty liver of pregnancy in a woman with ulcerative colitis and familial hidradenitis suppurativa. 3021 81

CD98 is a multifunctional glycoprotein that is involved in various biological processes such as amino acid transport, cell adhesion, diffusion, adhesion, and proliferation. The role of CD98 in liver disease has not thoroughly been examined and is limited reports in the literature. Among these reports, direct association for CD98 in nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC) have been reported. Our lab has reported that targeting CD98 in high fat diet mice reduced steatosis and inflammation in NAFLD. Other reports associate CD98 in HCC due in part to the role of CD98 in activating integrin signaling. Herein, we present CD98 staining on liver biopsies from NAFLD, chronic active hepatitis, cirrhosis, and 3 stages of HCC to demonstrate the upregulation of CD98 expression throughout liver disease progression. In addition, we analyze current literature to elucidate roles and potential roles of CD98 with each stage of liver disease.
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PMID:Role of CD98 in liver disease. 3205


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