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)

Chemopreventive agents benzyl selenocyanate (BSC) and 1,4-phenylenebis(methylene)selenocyanate (p-XSC) were fed in NIH-07 diet to male and female F344 rats (4, 2, and 0.5 mg/kg/day for BSC and 20, 10, and 5 mg/kg/day for p-XSC) for 13 weeks. Weight gains were depressed for male and female rats fed 4 and 2 mg/kg/day BSC, females fed 0.5 mg/kg/day BSC, and male rats fed 20 and 10 mg/kg/day p-XSC. At necropsy, no clear treatment-related lesions were noted, but dose-dependent hepatomegaly was observed in both sexes of BSC and p-XSC groups. Plasma transaminases AST and ALT were elevated in the higher dose groups, while hemoglobin, HCT, and RBC were reduced in most BSC and some p-XSC treatment groups. Plasma glucose was reduced in BSC-treated males. Significant histologic findings included moderate to severe hepatic centrilobular hypertrophy with fatty change in all males and females in the 4 mg/kg/day BSC groups and in 9/15 males and 3/15 females in the 2 mg/kg/day BSC groups. Dose-dependent, mild centrilobular hypertrophy with minimal fatty change was observed in the mid- and low-dose BSC groups and in all p-XSC groups. Mild to moderate renal tubular and interstitial nephritis occurred in the 4 mg/kg/day male BSC group. Dietary maximum tolerated dose levels for chemoprevention studies are 0.5 mg/kg/day (3.0 ppm Se) for BSC and 5 mg/kg/day (32.5 ppm Se) for p-XSC, compared to literature values of 2-3 ppm Se for Na2SeO3.
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PMID:Subchronic toxicity of benzyl selenocyanate and 1,4-phenylenebis(methylene)selenocyanate in F344 rats. 142 15

A fatal case of acute fulminant hepatitis following exposure to dichloropropanols is reported. A 59-year-old male worker in a chemical plant developed general malaise, nausea and vomiting several hours after cleaning a tank that had contained dichloropropanols. He had no previous history of hepatic dysfunction. On admission, hepatomegaly was prominent. Because of highly elevated levels of GOT and GPT in the serum, reduced prothrombin time and a lowered consciousness level, a diagnosis of fulminant hepatitis was made. Significant decreases of leukocytes and platelets were also observed. Serum creatinine and BUN were slightly elevated. Although plasma exchanges were conducted on the third and fourth day, the liver functions continued to deteriorate. The patient died on the fifth day. Because dichloropropanols could be detected in the blood specimens obtained at the time of admission, we considered that fulminant hepatitis in this case was attributed to dichloropropanols exposure. To our knowledge, this is the first case of fulminant hepatitis after dichloropropanols-exposure.
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PMID:[Fulminant hepatitis after the inhalation of dichloropropanols]. 150 13

During the twenty-nine-year period from June 1959 to October 1988, 32 infants and children with histology-proved hepatoblastoma were seen at the Department of Pediatrics, National Taiwan University Hospital (NTUH). The age at diagnosis ranged from four days to six years, with a mean of one year and eight months. Most of the patients (87.5%) were under the age of three. There was no sex predilection (16 males, 16 females). The most common presenting signs were an upper abdominal mass (71.9%) and/or abdominal distention (62.5%). Physically, all the patients revealed hepatomegaly, with or without mass. Laboratory abnormalities included primarily thrombocytosis (64.3%), elevated serum aspartate aminotransferase (75.0%), serum alanine aminotransferase (62.5%), cholesterol (78.3%) and alphafetoprotein (92.3%). According to the classification of Ishak and Glunz, 56.3% of these belonged to the epithelial type; the others belonged to the mixed type. During the follow-up period, 6 patients with complete resection of the tumor remained alive from 2 years to 17 years and 4 months. Twenty-two patients died from 8 days to 16 months after diagnosis. Four patients were lost to follow-up. The two-year survival rate was 21.4% (6/28). Complete resection of the tumor was the key treatment for achieving survival.
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PMID:Hepatoblastoma in infancy and childhood: a clinical and pathological study of 32 cases. 164 97

The characteristics of liver damage associated with the use of diclofenac, a popular nonsteroidal anti-inflammatory drug, were investigated by reviewing adverse drug reaction reports for Australia. Twenty six patients were reported for whom diclofenac was the sole suspected drug cause of their liver damage. The average age of the patients was 64 years (range 37-84 years); 19 (70%) were women. The most common clinical features were jaundice, hepatomegaly, anorexia, and nausea. Features of drug hypersensitivity were not reported. Duration of treatment with diclofenac before the onset of the illness ranged from 6-417 days (median 76 days). The most prominent biochemical abnormalities were raised serum aspartate transaminase and alanine transaminase activity of up to 30 to 40 times the upper limit of the normal range. Recovery generally started soon after withdrawal of diclofenac and the decrease in aspartate transaminase and alanine transaminase for the group was exponential, with half lives of around 13 days. The average total dose taken by 18 patients for whom accurate data were available was 8.7 g (range 1.4-63.5 g) and, unexpectedly, there was a significant relation between the logarithm of the dose of diclofenac and the logarithms of the peak and mean transaminase levels. Hepatocellular damage during treatment with diclofenac seems to be a rare event. From this analysis of Australian reports it seems that in a small subgroup of patients liver injury may be a direct toxic effect of diclofenac or a metabolite.
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PMID:Diclofenac hepatitis. 175 73

Among 203 patients with high altitude erythrocythemia (HAE), 89% had various kinds of alimentary canal symptoms, while these were present only in 31% of a control group (P less than 0.01). 49% of the HAE group had stomach, while only 8% of the control group had it. Endoscopic examination revealed 44% of the HAE group had peptic ulcer, being much higher than 6% of the control group. The ratio of gastric to duodenal ulcer in the HAE group was 2 to 1. The HAE patients had higher values of ALT, total bilirubin, LDH activity, LDH1 and LDHs, but lower values of AKP, LDH2, LDH4 and gamma-GT than the controls. The difference was, however, of no statistical significance. B mode ultrasonography showed that the incidence of hepatomegaly and splenomegaly was 24% and 11% respectively in the HAE group, while it was only 4% and 2% in the control group. HAE patients usually had symptoms of digestive system two years after the onset and the incidence at that time was 67%. With the extended course of the disease, the incidence gradually came down. The mechanism of digestive system impairment in HAE was probed and it was shown that treatment of digestive system impairment would promote the healing of HAE.
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PMID:[Impairment of the digestive system in high altitude erythrocythemia]. 179 46

It has been generally accepted that congestive heart failure does not lead to fulminant hepatic failure, unless it is associated with cardiac shock or low cardiac output. Only three cases have been reported, in which liver congestion is followed by fulminant hepatic failure without a history of shock or low cardiac output. Here we present a case of a 48-year-old man with dilated cardiomyopathy and pulmonary infarction, who developed fulminant hepatic failure from congestion. When he was admitted for the control of diabetes mellitus, hepatomegaly of 3-finger breadth and marked cardiomegaly without pulmonary congestion was noted. Diabetes was controlled using insulin. But 3 weeks after admission, he sometimes complained of back dullness because of pulmonary infarction. His heart gradually increased in size, and Jugular venous dilatation and pretibial pitting edema also worsened. Jaundice was noted and serum GOT and GPT increased. A large liver of 6-finger breath below the right costal margin was able to be felt. But within one week, the size of the liver markedly decreased and the signs of hepatic failure such as jaundice, hepatic encephalopathy and numerous petechiae appeared. Blood pressure was maintained and no hypotension or cardiac shock was noted. The patient died of fulminant hepatic failure on the 20th days after onset of the hepatic failure. The autopsy revealed liver atrophy with severe central lobular necrosis, and thrombus in the right main pulmonary artery which caused severe pulmonary infarction. The mechanism of fulminant hepatic failure not accompanied with low cardiac output is discussed.
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PMID:[A case of fulminant hepatic failure secondary to congestive heart failure]. 187 44

The course of liver involvement during the first three weeks of typhoid fever was studied in 20 patients. Previous studies of liver involvement in typhoid fever have not considered the time course of changes. In this study, hepatomegaly was found during the 2nd or 3rd wk more often than in the 1st wk (36% vs. 11%), whereas jaundice was detectable in 9% of patients after the 1st wk, but never before. Alkaline phosphatase, AST, and ALT were raised in 100%, 100%, and 91% of cases, respectively, during the 2nd and 3rd wk but during the 1st wk, only 11%, 89%, and 56% had mild increases. This study shows that, although the clinical picture of hepatitis is unusual, liver involvement is invariably present after the 1st wk, and should not be considered as a complication, but as a feature of the disease.
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PMID:The liver in typhoid fever: always affected, not just a complication. 188 3

Forty-two with hepatosplenic patients treated with praziquantel and followed up for 5 years. One half of the patients received a single 30 mg/kg dose and the other half, two doses of 25 mg/kg given 4 hrs apart. According to Hoffman and Kato-Katz stool exams, an 83.3% cure rate, was observed after twelve months. Stool egg counts in cases of incomplete cure were greatly reduced. Liver function, as assessed by serum levels of aspartate aminotransferase, alanine aminotransferase, gamma glutamyltransferase and alkaline phosphatase activities as well as albumin and gamma globulin showed marked improvement after one year. Hepatomegaly was reduced in 81.0% of patients and splenomegaly in 78.8%. Spleen regression was complete in 15.1% of the total, and in 18.5% of those with compensated hepatosplenic disease. As a result of these observations, the authors recommend early treatment with anti-schistosomal medication, either oxamniquine or praziquantel, to halt progression of disease and reduce splenomegaly.
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PMID:Reduction of morbidity in hepatosplenic schistosomiasis mansoni after treatment with praziquantel: a long term study. 212 17

Fifteen Thai children, diagnosed with dengue hemorrhagic fever and admitted to the Children's Hospital in Bangkok, were studied. All cases were serologically proved to be secondary dengue infections. The clinical signs and symptoms in the first few days of the acute febrile phase were similar to those observed in cases with classical dengue fever, and included continuously high fever, headache, muscle pain, nausea, vomiting and abdominal pain, etc. In the laboratory findings we noted hypoalbuminemia and mild elevation of the GOT and GPT. The hemogram showed an increasing atypical lymphocyte count during the acute febrile period. Prolongations of the partial thromboplastin time and thrombin time were also found, especially in the severe shock cases. All patients had varying degrees of hepatomegaly and pleural effusion from their chest x-rays accompanied by a rapid increase in the hematocrit of more than 20% and a fall in the platelet count to less than 100000/microliters. During the plasma leakage period the patients easily developed shock, even leading to death, unless adequate fluid supplies were given. This is also the major pathophysiological difference between dengue hemorrhagic fever and classical dengue fever. Although some studies concerning the pathogenesis of dengue hemorrhagic fever have been reported, but the exact mechanisms need further investigation.
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PMID:[Clinical observation of 15 Thai children with dengue hemorrhagic fever]. 234 55

A retrospective analysis was made of 78 patients presenting breast neoplasm with hepatic metastases confirmed by ultrasound. Clinical hepatomegaly was present in 61%. The serum glutamic-oxaloacetic transaminase (SGOT) was elevated in 72%, the serum glutamic-pyruvic transaminase (SGPT) in 56%, the serum alkaline phosphatase (Aph) in 86%, and the gamma-glutamil transpeptidase (GGT) in 76%. A hypoechogenic multiple nodular pattern (HMN) was observed in 69%, a diffuse hypoechogenic pattern (DH) in 15%, and a mixed multiple nodular pattern (MMN) in 11%. No single nodular pattern was presented in any patient. The univariate analysis showed a better survival rate in patients with a mixed pattern (mean 11 months, range 1-29 months) (p = 0.027). No significant differences were observed regarding the remaining patterns, age, presence or not of hepatomegaly, or altered enzymatic values.
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PMID:Ultrasonic patterns observed in hepatic metastases from breast carcinoma: diagnosis and evolution. 256 48


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