Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxicological correlation between blood biochemical parameters and liver histopathological findings was summarized mainly in rats and dogs on the basis of our experiments and published papers. In rats and dogs with hepatocytic necrosis, GPT and GOT increased with a good correlation to necrotic severity. In dogs with cholestasis, ALP, gamma-GTP, T.BIL and BSP retention rates increased. In mixed types of hepatitis or cholestasis and hepatic necrosis, GPT, GOT and ALP increased in rats and dogs and additionally gamma-GTP and BSP retention rates increased in dogs. In hepatic steatosis, CHOL and TRIG decreased in rats and dogs. In hepatic injury due to accumulation of foreign materials or cell components and sinusoidal cell injury, no specific correlation with biochemical parameters was noted.
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PMID:Toxicological correlation between changes in blood biochemical parameters and liver histopathological findings. 927 20

A 34-year-old man had asymptomatic hepatomegaly, slightly increased serum alanine aminotransferase and gamma-glutamyl transpeptidase levels, and a sonographic pattern suggesting diffuse hepatic steatosis. Liver biopsy revealed fatty change in 25% to 50% of hepatocytes. The patient also had low serum levels of cholesterol and triglycerides and met clinical, biochemical, and familial diagnostic criteria of heterozygous hypobetalipoproteinemia. We could not relate his hepatic steatosis to any already known cause of fatty liver and could only attribute it to heterozygous hypobetalipoproteinemia. Familial heterozygous hypobetalipoproteinemia should be ruled out in patients with unexplained hepatic steatosis.
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PMID:Diffuse fatty liver in familial heterozygous hypobetalipoproteinemia. 941 28

Nonalcoholic steatohepatitis (NASH) is the term used for a common form of fatty liver presenting in adults with varied clinical manifestations. The most common presentation is asymptomatic elevation of liver enzymes (AST or SGOT and ALT or SGPT), which can be discovered incidentally in the course of an annual checkup, life insurance examination, or as part of surrogate screening before blood donation. At the other end of the clinical spectrum is the patient with complications from cryptogenic cirrhosis, who also shows a lack of evidence of alcohol as an etiological factor in pathogenesis. Clinical associations of probable relevance include gender (female), obesity, diabetes, and hyperlipidemia, but many patients do not conform to any of these stereotypes (e.g., young men of normal weight with normal fasting glucose and lipid levels). Liver biopsy confirms the diagnosis of NASH, the association of steatosis with an inflammatory response being the sine qua non for the condition and "creeping fibrosis" being a variable but possibly sinister feature. Newer imaging techniques may provide convincing evidence of steatosis, but they give little insight into ongoing fibrosis, and liver biopsy therefore remains the gold standard. The mainstay of treatment remains judicious weight loss coupled with positive dietary advice, including the ingestion of adequate but not excessive vitamins. After initial encouraging data. the assessment of ursodeoxycholic acid currently being studied under randomized controlled conditions is eagerly awaited.
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PMID:Nonalcoholic fatty liver (NASH syndrome). 943 7

Recently, hepatitis GB virus C (HGBV-C) has been recovered from patients with non-A-E hepatitis. However, it has been unclear whether HGBV-C may be related to the development of alcoholic liver disease (ALD) or not. In this study, we determined HGBV-C RNA in sera from alcoholic patients without markers for hepatitis C and B viruses to evaluate the role of HGBV-C in ALD. Serum samples were obtained from 68 patients with ALD and 40 nonalcoholic patients with chronic type C liver disease. HGBV-C RNA was detected in only 3 of 68 (4.4%) patients with ALD, in 2 of 27 patients with hepatic fibrosis, and in 1 of 5 patients with chronic hepatitis. There was no HGBV-C RNA in sera from patients with fatty liver, alcoholic hepatitis, or cirrhosis. Serum levels of AST, ALT, and gamma-glutamyltranspeptidase in alcoholic patients with, as well as without, HGBV-C RNA decreased to normal levels after abstinence. In addition, an inflammatory change was not observed in liver biopsy specimens obtained from two HGBV-C-positive patients with alcoholic hepatic fibrosis. Our results clearly suggest that the prevalence of HGBV-C infection in patients with ALD is rare and that HGBV-C may not play an important role in the development of liver disease in alcoholics.
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PMID:Clinical significance of hepatitis GB virus C infection in alcoholic liver disease. 943 37

The role of T-cell activation in alcoholic liver disease was investigated in rats fed alcohol and subsequently exposed to concanavalin A (Con A). Following Con A injection (20 mg/kg body weight), greater increases in liver-to-body weight ratio and ALT levels were observed at 12 and 24 hr in rats fed ethanol, compared with control rats fed sucrose. Furthermore, increases in serum interleukin-6 and tumor necrosis factor-alpha levels were noted in ethanol-fed rats, with maximal levels detected at 4 hr declining thereafter, but remaining above control levels at 24 hr. Analysis of T-cell subpopulations showed an increased percentage of CD4+, CD5+, and CD8+ T cells in blood from all groups, but not in liver perfusate. In contrast, a significant increase in the percentage of activated CD25+ T cells was detected in both blood and liver perfusate from rats fed ethanol even 24 hr after Con A injection. When CD4+ and CD8+ T cells from liver perfusate were cultured in the absence or presence of Con A, an increase in interleukin-6 and tumor necrosis factor-alpha production in supernatants was observed in ethanol-fed rats. In cultures stimulated with Con A, a 2- to 8-fold increase in cytokine production was detected, with intrahepatic CD4+ T cells being the major source. Immunohistological analysis revealed infiltration of CD4+ T cells around portal vein and central vein areas associated with fatty liver and severe hepatic necrosis. The results suggest that alcohol consumption induced a dysregulated T-cell population that mediated hepatic necrosis following polyclonal activation with Con A.
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PMID:Altered T-lymphocyte responsiveness to polyclonal cell activators is responsible for liver cell necrosis in alcohol-fed rats. 962 56

Among 380 bone marrow transplant (BMT) recipients, five cases (1.3%) of clonorchiasis were observed from 1991 to 1996. Clonorchis sinensis infection was evident in the results of stool examinations performed for screening purposes 7 days before bone marrow transplantation. Salmonella species were isolated concomitantly from the stools of two of the five patients. None of the patients had symptoms due to clonorchiasis. Ultrasonography did not show dilated hepatobiliary ducts, stones, or periportal fibrosis. Fatty liver changes were detected in one patient. All five patients received praziquantel (25 mg/kg po t.i.d. for 1 day) before bone marrow transplantation. Only two patients who underwent allogeneic transplantation had mild venoocclusive disease of the liver with transient hyperbilirubinemia and mildly elevated liver enzyme levels, whereas hyperbilirubinemia or elevated serum alanine aminotransferase levels, related to conditioning toxicity, occurred in two other patients. After treatment with praziquantel, stool examination for all five patients were negative for C. sinensis ova. In addition, Salmonella species were not detected after ciprofloxacin prophylaxis. All five patients survived for > 300 days. Given the availability of effective therapy and in the absence of excessive complications, clonorchiasis is not a contraindication to bone marrow transplantation.
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PMID:Clonorchiasis in bone marrow transplant recipients. 970 91

Carbon tetrachloride-injected rats were given liquid diets with and without betaine for 7 d. Hepatic lipidosis was induced by 4 daily injections of carbon tetrachloride (CCl4). Animals were killed and their livers and blood taken for analysis of betaine, S-adenosylmethionine (SAM), betaine homocysteine methyltransferase (BHMT), triglyceride, alanine aminotransferase and aspartate aminotransferase. Liver samples were also processed and stained for histological examination. Supplemental betaine reduced triglyceride in the liver and centrilobular hepatic lipidosis induced by the CCl4 injections. In both the control and experimental groups receiving betaine, liver betaine, BHMT and SAM were significantly higher than in their respective groups not receiving betaine. This study provides evidence that betaine protects the liver against CCl4-induced lipidosis and may be a useful therapeutic and prophylactic agent in ameliorating the harmful effects of CCl4.
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PMID:Betaine reduces hepatic lipidosis induced by carbon tetrachloride in Sprague-Dawley rats. 977 59

We studied the association of fatty liver with subcutaneous and visceral obesity in 46 male and 36 female patients with body mass index (BMI) over 22 kg/m2. The correlation coefficient between the ratio of the visceral adipose tissue to the subcutaneous adipose tissue (V/S) and the computed tomography (CT) number of the liver was -0.299 (P < 0.05) and that between the V/S ratio and the ratio of the CT number of the liver to that of the spleen (CT-L/CT-S) was -0.335 (P < 0.05) in the males. Partial correlation analysis after making correction for BMI showed an increased correlation coefficient of -0.485 (P < 0.05) between the V/S ratio and the CT-L/CT-S ratio in the males. The odds ratio in the males for CT-L/CT-S below 1.0 and V/S above 1.0 was 3.25 with a 95% confidence interval of 1.02 to 9.39. No such association between the V/S ratio and the CT-L/CT-S ratio was present in the female patients. Multiple regression analysis with serum level of alanine aminotransferase, a marker of fatty liver, as an independent variable revealed a partial regression coefficient of -17.7 for CT-L/CT-S (P < 0.05) in the males and -21.7 (P < 0.05) in the females, validating the CT-L/CT-S ratio as an index of fatty liver. The results indicate the association of fatty liver as determined by the CT-L/CT-S ratio with visceral obesity in males.
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PMID:Association of fatty liver with increased ratio of visceral to subcutaneous adipose tissue in obese men. 978 Dec 73

To determine the clinical manifestations and histopathologic features of serum TTV DNA-positive chronic liver disease, we investigated eleven patients who showed serum TTV DNA alone, as detected by the polymerase chain reaction using first generation primer sets (RD primer series). Clinical manifestations were as follows: (1) biochemical abnormalities of the ALT-dominant and gamma-GTP-dominant types; (2) persistently elevated gamma-GTP despite normalization of ALT in gamma-GTP-dominant type patients; (3) association of TTV with pathogenesis of fatty liver or alcoholic liver dysfunction; and (4) response to liver-protective medicines. Histopathologic features were as follows: (1) inflammation-related cell infiltration scattered within the portal area, with distinguishable necroinflammation in the lobular region; (2) pathologic findings on biliary epithelium; (3) high incidence of steato-metamorphosis involvement; and (4) histologic characteristics undistinguishable from "viral" chronic hepatitis in some liver specimens.
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PMID:[Clinical manifestations and histopathologic features of chronic liver disease with serum TT virus (TTV) DNA positive alone as measured by first generation primer sets]. 1039 Sep 96

Hepatic steatosis has been reported as one of the characteristics which discriminates hepatitis C from other forms of hepatitis, besides lymphoid follicles and bile duct damage. However, it is unclear whether or not the presence of hepatitis C virus (HCV) itself is associated with the development of steatosis. The possibility that the HCV itself is directly related to the development of steatosis was examined. The intrahepatic core protein levels, as a marker of the HCV load, were correlated with the presence of steatosis in 43 patients with chronic hepatitis C. Among 43 patients studied by Western blotting, the core protein was detected in the liver in 27 (62.8%). On the other hand, hepatic steatosis was observed in 21 (48.8%) of the 43 patients. Importantly, the core protein was detectable in 19 (90.4%) of the 21 patients with steatosis, while it was detected in only 8 (36.4%) of the 22 patients without steatosis (P = 0.008). However, serum HCV-RNA levels as determined by the Amplicor monitor were not significantly different between patients with and without steatosis. Multivariate analysis showed that the serum alanine aminotransferase level (P = 0. 013), body mass index (P = 0.038), and intrahepatic HCV core protein positivity (P = 0.038) were the independent parameters best predictive of steatosis. These results indicate a close relationship between intrahepatic HCV and the development of steatosis, and suggest a possible role of the HCV itself or core protein in the pathogenesis of steatosis in human chronic hepatitis C.
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PMID:Steatosis and intrahepatic hepatitis C virus in chronic hepatitis. 1045 47


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