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)

New evidence is obtained for inhibitory effect of isoniazid on activity of transaminases in prolonged application of the drug. Increase in the isoniazid inhibitory effect on alanine aminotransferase activity was shown to correlate with elevated concentration of Cu2+ in blood serum arising in experimental tuberculosis. Cu2+ and Co2+ caused the increase in the inhibitory effect of isoniazid due to their incorporation into structure of the preparation. The microelements, combined with pyridoxine, inhibited alanine aminotransferase and vice versa activated aspartate aminotransferase.
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PMID:[New aspects of the effect of isoniazid on transaminase activity in tuberculosis]. 66 79

In a retrospective study the following was found: Out of 111 patients suffering from tuberculosis and receiving a combined INH-therapy without Rifampicin 23% showed an increase of serum-transmainase activities, on the other hand out of 105 patients, treated with a combination including Rifampicin 74% did so. A pathological De Ritis ratio GOT/GPT was found in 31 among 59 comparable cases of Rifampicin-treated patients, and a pathological ratio GOT + GPT/AP in 22 among 37 cases before the transaminase-activities rose above normal. Development of a distinct toxic hepatic damage has to be anticipated in those cases, which show a De Ritis ratio below 0,5 or a GOT + GPT/AP ratio above 1,0 while transaminase-activity still is only slightly elevated. Liver biopsies taken from 10 patients showed no regular relation to the biochemical data.
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PMID:[Frequency, diagnosis, and course of hepatotoxic side effects of Rifampicin (author's transl)]. 99 24

A 42-year-old woman was admitted because of cough, sputum, and fever. A chest roentgenogram revealed a nodular density in the left upper lung field with satellite lesions compatible with tuberculoma. Mycobacterium tuberculosis was detected from sputum. Five weeks after starting the treatment with 0.4 g/day of isoniazid, 0.45 g/day of rifampicin, and 0.75 g/day of streptomycin, she showed itching erythema in the trunk. The white blood cell count was 4,500/mm3 with 14% eosinophils, and serum transaminases were slightly increased (GOT 101 U/L, GPT 74 U/L). Although isoniazid and rifampicin were stopped, the erythema with exfoliation spread to her extremities, suggesting exfoliative dermatitis. The white blood cell count reached 15,990/mm3 with 68% eosinophils (10,810/mm3). Stimulation indices measured with the lymphocyte stimulation test (LST) were 109% with rifampicin, 140% with isoniazid, and 275% with streptomycin, suggesting streptomycin-induced allergy. After cessation of streptomycin, the symptoms gradually improved. After the reaction had subsided, the treatment with isoniazid, rifampicin, and ethambutol was resumed, but she showed no further adverse reactions. LST seems to be very useful to identify the drug or drugs responsible for the reactions occurred during the treatment by antituberculosis drugs.
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PMID:[A case of pulmonary tuberculosis associated with severe skin eruption, prominent eosinophilia, and liver dysfunction induced by streptomycin]. 153 89

A retrospective study on the evaluation of antituberculous drugs for patients with hepatic dysfunction was undertaken to clarify treatment regimens. The values of GOT, GPT and T. Bil were used as indicators of liver function, and the "deterioration" in the liver function was defined as a level greater than 1.5 times the initial value. Of total 538 cases of active pulmonary tuberculosis, 103 cases (19.1%) had abnormalities in liver functions before chemotherapy, and 21 of 103 cases showed the deterioration in their liver functions during chemotherapy. There was little relationship between the initial status of liver functions and the incidence of their deteriorations after chemotherapy. Nine of 21 cases did not exceed the 3 times of normal ranges of liver functions. These nine cases could tolerate the same regimens of chemotherapy, and showed satisfactory clinical responses to chemotherapy with two exceptions: one died of tuberculosis and the other cerebrovascular disease. On the other hand, of 12 cases with elevated values of hepatic function greater than 3 times the normal limits, 6 cases discontinued chemotherapy. One case, however, died of hepatic failure related to chronic active hepatitis. Eight of 12 cases showed the rapid improvement of liver dysfunctions. These results suggest that antituberculous drugs are acceptable to patients with hepatic dysfunction as long as the elevations of GOT, GPT and T. Bil stay within 3 times of normal limits. Further chemotherapy could be continued under careful monitoring of liver functions even if the cases exhibit elevated levels of liver functions greater than 3 times the normal ranges.
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PMID:[Chemotherapeutic evaluation of pulmonary tuberculosis patients with a complication of hepatic dysfunction]. 205 6

A 33-year-old heterosexual white man underwent a liver biopsy for determination of mild elevation of aminotransferase levels (aspartate aminotransferase, two times; alanine aminotransferase, three times). The patient had acquired immunodeficiency syndrome (stage IVC2) with tuberculosis of the lymph nodes. Antibody to hepatitis B surface antigen and antibody to hepatitis B core antigen were positive. Syphillis tests were positive. Liver architecture was normal; sinusoids were dilated with perisinusoidal, centrilobular, and portal fibrosis. On a 1-micron-thick section and under electron microscopy, perisinusoidal cells appeared to be massively loaded with lipids, while endothelial cells contained numerous dense bodies. Some hepatocytes presented evidence of cell damage. Sinusoids were infiltrated by an increased number of lymphocytes and macrophages. This patient who had recently been treated for tuberculosis was not taking extra vitamin A. He had no disease so far reported as being associated with perisinusoidal cell hypertrophy. This case and others are evidence that acquired immunodeficiency syndrome represents another cause of perisinusoidal cell hypertrophy in which there is no documented hypervitaminosis A.
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PMID:Perisinusoidal cell hypertrophy in a patient with acquired immunodeficiency syndrome. 237 62

Cyclopiazonic acid (CPA) was given daily to groups of guinea pigs at doses of 0.00625, 0.0125, 0.025, 0.05, 0.1, 0.2, 0.4, 0.8, 1.6, and 1.95 mg/day for 30 days. All guinea pigs were sensitized and survivors were skin tested twenty-five days later with Mycobacterium tuberculosis. Mortalities occurred only in the two greatest dose groups. Signs of disease included anorexia, roughened hair coat, diarrhea and incoordination. The major histopathologic changes occurring in these two groups included hepatocellular vacuolar degeneration and necrosis of the gastric mucosa with infiltration of neutrophils in the deep gastric mucosa. CPA did not affect cutaneous hypersensitivity to M. tuberculosis, complement activity, serum glycocholic acid concentrations or weight gains. There were increases in aspartate aminotransferase, alanine aminotransferase, and sorbitol dehydrogenase concentrations in the serum of guinea pigs in the two greater dose groups, but no changes were found in serum concentrations of SAP. There was a slight increase in the serum bilirubin concentrations in the greater dose groups.
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PMID:Effect of cyclopiazonic acid on delayed hypersensitivity to Mycobacterium tuberculosis, complement activity, serum enzymes, and bilirubin in guinea pigs. 309 99

The paper investigates the relationships between hydrophobic parameters and antituberculotic activity of 2-alkylthio-6-benzamidobenzothiazoles, tested on INH-resistant strain of Mycobacterium tuberculosis. In the group of compounds with linear alkyl substituents in position 2, the tuberculostatic effect is increasing with decrease of lipophility of alkyls. Branching of the alkyls strongly increases the activity. The hepatotoxicity of compounds under study was investigated by means of the activity of serum aminotransferases (ALT, AST) in Wistar type rats. The hepatotoxicity of compounds seemed to be smaller than that of the thiobenzamides.
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PMID:[Relation between chemical structure, antitubercular activity and hepatotoxicity of 2-alkylthio-6-benzamidobenzothiazoles]. 312 40

Enzyme levels of lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured in the cytosol of renal cortex samples from either normal and pathologic kidney tissue. The mean enzyme activity values, expressed in Units per gram of cytosolic protein decreased in the following order: normal cortex (LDH = 4,299 +/- 654; AST = 522 +/- 101; ALT = 197 +/- 44). chronic pyelonephritis (LDH = 2,360 +/- 876; AST = 297 +/- 117; ALT = 90 +/- 48), hydronephrosis (LDH = 2,208 +/- 1,264; AST = 279 +/- 165; ALT = 82 +/- 61), pyonephrosis (LDH = 1,410 +/- 596; AST = 158 +/- 69; ALT = 23.4 +/- 16.4) and renal tuberculosis (LDH = 1,149 +/- 481; AST = 93 +/- 34; ALT = 5.6 +/- 2.8). The decrease in the enzyme activities paralleled tissue damage and it was shown to affect cellular functionality in relation with energy and amino acid metabolism.
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PMID:Cytoplasmic enzyme activities involved in energy and amino acid metabolism in pathological human renal cortex. 324 90

Both tuberculosis and hepatitis B are endemic in southeast Asia and are common among refugees to the United States from that region. Isoniazid, used for the prophylactic treatment of tuberculosis, is a potentially hepatotoxic drug. Carriers of the hepatitis B virus are likely to have some degree of liver damage due to their chronic infection. We hypothesized that prophylactic treatment of carriers with isoniazid would cause greater liver damage, as measured by serum alanine aminotransferase (ALT) levels, than would such therapy of noncarriers. Cross-sectional and longitudinal studies of the southeast Asian refugee population in Philadelphia failed to support this hypothesis. Isoniazid did not cause greater hepatotoxicity in hepatitis B carriers than in noncarriers. Although carriers had higher ALT levels than noncarriers, both groups experienced transient ALT elevations during the first 2 months of isoniazid prophylactic therapy. Therefore, we concluded that chronic infection with hepatitis B virus is not a contraindication to the prophylactic use of isoniazid.
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PMID:Isoniazid prophylaxis in hepatitis B carriers. 376 21

The incidence and degree of liver injury was prospectively evaluated in 44 children, ages between 4 months and 14 years (mean age, 4.5 years) treated for tuberculosis with 15 to 20 mg isoniazid/kg/day and 15 mg rifampin/kg/day (INH-RIF). None of the patients had hepatic dysfunction before initiation of treatment. Elevation of the serum alanine aminotransferase (ALT) concentration (greater than 100 units) occurred in 36 patients (82%). One patient with an increase in the ALT value had coincidental infection with hepatitis B. The incidence of hepatotoxicity did not correlate with the patients' age or sex. Fifteen of the 36 patients developed clinical hepatitis with jaundice. In 7 patients liver enlargement and prolongation of the prothrombin time were also observed. In all but one patient liver dysfunction was recognized 6 to 30 days (mean, 14 days) after start of treatment. Biochemical signs of hepatic injury in the 35 surviving patients regressed completely without alteration of the INH-RIF regimen in 22 patients. These facts suggest the possibility that hepatocellular damage may be due to the effect of tubercle bacilli products liberated in the liver after their destruction by antituberculous drugs. However, the high rate of hepatotoxic reactions warns that the dose of 10 mg INH/kg/day should not be exceeded when that drug is combined with RIF.
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PMID:Hepatotoxic reactions in children with severe tuberculosis treated with isoniazid-rifampin. 400 Sep 89


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