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)

We describe here a patient with chronic hepatitis C and liver hemosiderosis whose serum ferritin level was notably reduced by long-term interferon-alpha (IFN alpha) therapy. The decrease of the elevated serum ferritin level was considered to have been mostly obtained by the improvement of liver dysfunction. However, at the beginning of the therapy, in spite of alanine aminotransferase (ALT) improvement, his serum ferritin level increased transiently, and after cessation of IFN alpha therapy, the serum ALT increased again, but the serum ferritin had not increased. This indicates that IFN alpha has an effect on the iron-related measurement, partly due to improvement of hepatic status.
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PMID:Decrease in serum ferritin level in a patient with HCV hepatitis and liver hemosiderosis by interferon-alpha. 776 77

1. Weanling male CD-1 mice were fed 120 (control), 5000 and 8000 mg of iron kg-1 for seven weeks. The haematocrit (P = 0.265), water consumption (P = 0.170) and percentage body weight ratios of kidney, spleen and heart were not affected by iron supplementation. 2. Iron supplementation reduced weight gain (P = 0.023), increased weight of liver (P = 0.0001), the iron deposition index and concentration of iron in the liver (P < 0.01). A strong correlation between liver iron concentration and level of iron in the diet (r = 0.989) was observed. Histologically, the deposition of iron was restricted to the hepatocytes, Kupffer cells and splenic macrophages. 3. Consumption of 5000 and 8000 mg of iron kg-1 resulted in hepatic damage, as judged by elevated serum alkaline phosphatase and alanine aminotransferase activities (P < 0.05). 4. This study indicates that prolonged feeding of excess dietary iron has the potential to cause hepatic accumulation of iron with resultant liver toxicity, and that mice may be a suitable model to study the mechanisms of dietary iron overload.
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PMID:Hepatotoxicity associated with dietary iron overload in mice. 790 62

Normal concentrations of some blood constituents were determined in young male Najdi (Saudi) camels. The mean values were as follows: total protein = 62.3 +/- 8.9 g/l, albumin = 33.5 +/- 8.9 g/l, bilirubin = 8.7 +/- 1.7 mumol/l, urea = 6.6 +/- 1 mumol/l, uric acid = 232 +/- 35.7 mumol/l, iron = 10.4 +/- 5.7 mumol/l, total iron binding capacity = 40.4 + 7.3 mumol/l, AST = 12 +/- 5 IU/l ALT = 9 +/- 4 IU/l and ALP = 42.6 + 21.3 IU/l. These values were compared with those reported by other investigators in camels with different ages, sexes and breeds as well as with blood constituents in true ruminants.
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PMID:Normal concentrations of some blood constituents in young Najdi camels (Camelus dromedarius). 791 62

Chronic hepatitis C has been demonstrated to be associated with hepatic iron overload, and the hypothesis that the disease activity of hepatitis C is associated with iron cytotoxicity was tested in male volunteer blood donors. Sera with either antibody to hepatitis C virus or hepatitis B surface antigen were selected for determination of ferritin concentration and alanine aminotransferase activity. A correlation between serum ferritin concentration (Y; microgram/l) and alanine aminotransferase activity (X; IU/l) was found in donors with antibody to hepatitis C (log Y = 0.65 x log X + 0.98, r = 0.53, and P < 0.01). The correlation was lower in donors with hepatitis B surface antigen (r = 0.37; P < 0.01). Hepatitis C virus infection probably induces time-dependent iron accumulation associated with the progression of disease activity, while hepatitis B virus infection results in a variety of iron loads with different clinical features. The high disease activity related to hyperferritinemia suggests the presence of iron-induced liver damage in donors with hepatitis C.
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PMID:Correlation between serum levels of alanine aminotransferase and ferritin in male blood donors with antibody to hepatitis C virus. 800 May 7

Proposed and interim European quality specifications for imprecision and inaccuracy have been compared with the US CLIA total error criteria for proficiency testing (PT). To assess the relative demands of separate imprecision and inaccuracy specifications vs total error criteria, we derived the imprecision and inaccuracy that would be allowable if a testing process were to provide 90% assurance of achieving the analytical quality required by CLIA PT criteria. Charts of operating specifications (OPSpecs charts) were prepared for commonly used single-rule and multi-rule quality control procedures with 2 and 4 control measurements per run. Of the 23 tests studied, the proposed European specifications for imprecision and inaccuracy were more demanding than the CLIA requirements for 12 tests (albumin, alkaline phosphatase, amylase, calcium, chloride, creatinine, lactate dehydrogenase, lithium, magnesium, total protein, sodium, and thyroxine). The CLIA total error criteria were more demanding than the proposed European specifications for nine tests (alanine aminotransferase, aspartate aminotransferase, total bilirubin, cholesterol, creatine kinase, iron, triglycerides, uric acid, and urea nitrogen). Two tests (glucose, potassium) showed different requirements at different decision levels. Manufacturers and laboratory analysts need to compare these different quality specifications on a test-by-test basis to guide the development, selection, evaluation, and control of laboratory measurement procedures.
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PMID:European specifications for imprecision and inaccuracy compared with operating specifications that assure the quality required by US CLIA proficiency-testing criteria. 781 63

Seventy-nine subjects (19 women and 60 men) with chronic viral hepatitis were studied to determine the role of hepatic iron and its biochemical correlates in determining response to interferon alpha therapy. Each subject was treated for 6 months with interferon alpha. A total of 45 (57%) subjects achieved either a full or partial response. No differences between responders and non-responders were evident for the type of hepatitis, age, initial alanine aminotransferase, serum iron, total iron binding capacity, %sat, or ferritin. In contrast, the hepatic iron content of non-responders was almost twice that of responders (1156 +/- 283 micrograms/g dry weight vs. 638 +/- 118; p < 0.05). Hepatic iron correlated with total iron binding capacity (r = 0.435) and ferritin (r = 0.585). This study showed that: 1) the hepatic iron content of responders is less than that of non-responders, 2) the relationships of hepatic iron with %sat and ferritin in patients with viral hepatitis are weak, and 3) hepatic iron content predicts a response to interferon therapy.
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PMID:Response to interferon alpha therapy is influenced by the iron content of the liver. 801 55

The purpose of this study was to determine whether interferon-alfa (IFN-alpha) therapy benefits patients with transfusion-dependent thalassemia and chronic active hepatitis C, and whether their iron burden modifies the response to this therapy. We conducted a controlled trial of recombinant IFN-alpha (3 million units per square meter of body surface area, three times a week for 15 months) in 65 patients with thalassaemia major and chronic active hepatitis C; 14 of them were untreated control subjects. In 21 of the 51 treated patients, alanine aminotransferase values returned to normal within 6 months, and hepatitis C virus ribonucleic acid was no longer detected in serum; no changes were detected among control subjects. The response to IFN-alpha therapy was inversely related (p < 0.002) to the liver iron burden as assessed by atomic absorption, the histologic semiquantitative method, or both methods. During 3 years of follow-up, two responder patients had relapses. We conclude that IFN-alpha represents a useful therapeutic option for children with transfusion-dependent thalassemia and chronic active hepatitis C with a mild to moderate iron burden.
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PMID:Effect of iron overload on the response to recombinant interferon-alfa treatment in transfusion-dependent patients with thalassemia major and chronic hepatitis C. 802 61

A 27-yr-old Jamaican male presented with a 2-month history of jaundice, pruritus, intermittent diarrhea, and right upper quadrant abdominal pain. Over the next month, his abdominal pain and diarrhea improved, but his jaundice and pruritus worsened. He was afebrile and profoundly jaundice, with a benign abdominal examination. Medical workup included a normal abdominal ultrasound, iron studies, ceruloplasm, and serum electrophoresis. Negative viral (Epstein-Barr virus, cytomegalovirus, mononucleosis, hepatitis A, B, C) studies, ANA, AMA, ASMA, RPR were noted. He denied any alcohol, drug, or toxin exposure. Liver tests revealed total bilirubin of 25.6 mg/dl, direct bilirubin of 13.9 mg/dl, alkaline phosphatase 278 IU/L, AST 45 IU/L, and ALT 71 IU/L. Liver biopsy demonstrated centrilobular zonal necrosis and cholestasis most consistent with a toxic reaction. The patient was again interviewed regarding potential toxins, and he admitted to the ingestion of ackee fruit, a native Jamaican fruit that is illegal in the United States. Shortly after he had ceased intake of the fruit, his symptoms resolved and his liver function tests returned to normal. We present a case of chronic ackee fruit ingestion that led to cholestatic jaundice, vomiting, and abdominal pain.
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PMID:Cholestatic jaundice due to ackee fruit poisoning. 807 44

The aim of this study was to determine the influence of aging on diquat-induced redox cycling in liver microsomes and diquat hepatotoxicity in rats. Diquat-stimulated production of superoxide anion radical and NADPH-cytochrome c (P-450) reductase activity were measured in liver microsomes prepared from male Fischer 344 rats at ages representing young adulthood (5-6 months), middle age (15-16 months), and old age (24-27 months). Both activities were decreased substantially (40%) in old rats. Diquat-induced liver damage was assessed 6 hr after the administration of diquat (0.1 mmol/kg, ip) on the basis of serum ALT and sorbitol dehydrogenase activities, hepatic microsomal cytochrome P-450 loss, and histological evaluation. The classical manifestations of hepatotoxicity in diquat-treated rats were as severe in old rats as in young-adult ones, despite the age-associated drop in redox cycling capacity. Diquat treatment also resulted in decreased concentrations of hepatic glutathione and ascorbic acid, increased concentrations of hepatic nonheme iron, and decreased liver weights. The changes in glutathione, nonheme iron, and liver weight were more pronounced in livers of middle-aged and old rats than in those of young-adult rats. These age-dependent differences could not be explained on the basis of plasma diquat concentrations, which were similar in the three age groups of rats. The absence of an effect of aging on the hepatotoxic effects of diquat indicates that redox cycling capacity is not limiting for the development of liver damage. Other effects of diquat were influenced by aging, but their relevancy to the hepatotoxicity is uncertain.
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PMID:Redox cycling and hepatotoxicity of diquat in aging male Fischer 344 rats. 810 18

Patients with the Hb beta + [IVS 1-5 (G-->C)] clinically presented as beta-thalassaemia intermedia and remained asymptomatic in the absence of blood transfusions. With or without blood transfusions the patients were short and had moderate to marked thalassaemia facies. Children who received blood transfusions showed progressive iron loading with age. The serum ferritin and serum alanine transaminase levels were significantly raised in the patients who were given blood transfusions. In the presence of blood transfusions, and absence of adequate iron chelation therapy, splenectomy became an inevitable event at some stage of the disease because of increasing transfusing requirements.
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PMID:Hb E beta +-thalassaemia in west Malaysia: clinical features in the most common beta-thalassaemia mutation of the Malays [IVS 1-5 (G-->C)]. 815 10


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