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)

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

Rifampicin pharmacokinetics in rats with acute affection of the liver with carbon tetrachloride did not alter. Chronic affection with carbon tetrachloride resulted in retarded elimination of the antibiotic from blood. There was observed no relationship between increased activities of transamination enzymes such as alanine aminotransferase and aspartate aminotransferase in blood serum of animals and changes in rifampicin pharmacokinetics.
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PMID:[Rifampicin pharmacokinetics in experimental hepatitis]. 343 92

Thirty four children with tuberculous meningitis were treated with rifampicin (mean, 17 mg/kg/day) and isoniazid (mean, 18 mg/kg/day). Fifteen (44%) showed rise in transaminase GOT and GPT values and four cases (11.7%) developed jaundice, hepatomegaly and low prothrombin levels. Rifampicin was removed in only nine of these 15 cases with signs of liver disfunction, but complete normalization of liver function and disappearance of symptoms occurred in all cases even when the treatment was not interrupted. Children are more sensitive to hepatic injury during rifampicin and isoniazid combination therapy than adults. Our results indicate very good prognosis for this hepatopathy and suggest that rifampicin need not be withdrawn in the benign situations. Removal of the rifampicin treatment may delay recovery of serious cases of tuberculous meningitis.
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PMID:[Hepatotoxicity of rifampicin and isoniazid in the treatment of tuberculous meningitis (author's transl)]. 733 8

Seven patients with primary biliary cirrhosis were treated with rifampicin administered for 2 weeks in a daily dose 450-600 mg. Due to the treatment the itch disappeared completely in 4 and decreased significantly in 3 patients. As shown by the antipyrine test, half-life and clearance of antipyrine returned to normal suggesting cytochrome P-450 induction as a result of hydroxylation activity. There was a tendency to lowering of bilirubin, cholesterol, alkaline phosphatase, asparagine--and alanine aminotransferase against an increase in gammaglobulins. The differences were, however, insignificant. Rifampicin tolerance was satisfactory.
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PMID:[The treatment of primary biliary liver cirrhosis with rifampicin]. 821 5

Rifampicin conferred significant protection against carbon tetrachloride (CCl4)-induced liver injury. Serum alanine transaminase (ALT) and aspartate transaminase (AST) activities were not markedly altered and only hepatocellular fatty degeneration was found in mice pretreated with rifampicin (200 mg/kg), whereas severe centrilobular necrosis was observed and serum ALT and AST activities were as high as 281 and 271 I.U./l, respectively, in the control group following administration of CCl4 (400 microliters/kg). The contents and activities of microsomal drug-metabolizing enzymes in rifampicin-pretreated animals were also much higher than those of the controls. CCl4-mediated malondialdehyde (MDA) formation was increased in rifampicin-treated liver microsomes, demonstrating that rifampicin was capable of increasing the NADPH-dependent metabolism of CCl4 catalyzed by P-450 2E1 to produce free radicals. However, MDA formation was obviously depressed by rifampicin at varying concentrations from 2 to 32 x 10(-6) M in an in vitro cytochrome P-450 (P-450) enzyme system. On the other hand, NADPH oxidation in the metabolism of CCl4 and aniline hydroxylation were not suppressed in the presence of rifampicin in this systems, suggesting that rifampicin did not influence the biotransformation of CCl4 by P-450 2E1 in vitro. Therefore, the protective effect of rifampicin against CCl4 hepatotoxicity appeared to result from the direct inhibition of lipid peroxidation generated by CCl4-derived free radicals.
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PMID:Protective effect of rifampicin against acute liver injury induced by carbon tetrachloride in mice. 878 35

A case of a 73-year-old woman with acute renal failure due to toxic shock syndrome (TSS) is reported. The patient was admitted to our hospital with the complaints of high fever, disturbance of consciousness and shock. Laboratory findings on admission were; CRP 25.11 mg/dl, WBC 35000/ microl, Plt 1.6 x 10(4)/ microl, GOT 155 U/l, GPT 65 U/l, CPK 4202 U/l (CPK-MM 96%), BUN 123 mg/dl and SCr 7.0 mg/dl. Because of anuria, hemodialysis was performed. This patient was treated with dopamine, methyl prednisolone (MP), frozen fresh plasma, AT III, antibiotics, and platelet transfusion. The bacterial cultures of blood and cerebrospinal fluid were negative, but MRSA was isolated subsequently from the pharynx and vagina. We investigated the production of toxic shock syndrome toxin 1 (TSST-1) and staphylococcal enterotoxins (SE). The isolated MRSA produced TSST-1, SEB and SEC. Accordingly, we made the diagnosis of TSS. After improvement of acute renal failure and the patient's general condition, MRSA persisted and TSST-1 was still found in the patient's blood. Finally we eradicated the MRSA and TSST-1 after administration of ciprofloxacin hydrochloride (CPFX) and Rifampicin (RFP).
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PMID:[A case of toxic shock syndrome (TSS) induced by methicillin-resistant staphylococcus aureus (MRSA) presenting as acute renal failure with disseminated intravascular coagulation]. 885 34

Mycobacterium tuberculosis is a concern in patients with human immunodeficiency virus (HIV) infection. Rifampin (RIF), an agent used against M. tuberculosis, is contraindicated with most HIV protease inhibitors. Atazanavir (ATV) has clinical efficacy comparable to a standard of care regimen in naive patients and, when dosed with low-dose ritonavir (RTV), also in treatment-experienced patients. We evaluated here the safety and pharmacokinetics of ATV, resulting from three regimens of ATV, RTV, and RIF in 71 healthy subjects. The pharmacokinetics for ATV and RTV were assessed after 6 and 10 days of dosing with ATV 400 mg (n = 53) and with ATV-RTV at 300 and 100 mg (ATV/RTV 300/100; n = 52), respectively. Steady-state pharmacokinetics for ATV, RTV, RIF, and desacetyl-rifampin (des-RIF) were measured after 10 days of dosing of ATV/RTV/RIF 300/100/600 (n = 17), ATV/RTV/RIF 300/200/600 (n = 17), or ATV/RTV/RIF 400/200/600 (n = 14). An RIF 600-alone arm was enrolled as a control group (n = 18). With ATV/RTV/RIF 400/200/600, ATV area under the concentration-time curve values were comparable, but the C(min) values were lower relative to ATV 400 alone. ATV exposures were substantially reduced for the other RIF-containing regimens relative to ATV 400 alone and for all regimens relative to ATV/RTV 300/100 alone. RIF and des-RIF exposures were 1.6- to 2.5-fold higher than with RIF 600 alone. The incidence of grade 3/4 alanine aminotransferase/aspartate aminotransferase values was limited to 1 subject each in both the ATV/RTV/RIF 300/200/600 and the ATV/RTV/RIF 400/200/600 treatments. Coadministration of ATV with RIF was safe and generally well tolerated. Since ATV exposures were reduced in all regimens, ATV and RIF should not be coadministered at the dosing regimens studied.
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PMID:Effect of rifampin on steady-state pharmacokinetics of atazanavir with ritonavir in healthy volunteers. 1700 14

We report active tuberculosis in a pregnant physician caused by TB-transmission at the workplace. Because of increased liver enzymes, therapy with Rifampicin was temporarily interrupted. During pregnancy and the first seven month of the 12 month lactation period, the mother was treated for tuberculosis. The healthy newborn showed elevated GOT for the following two years after birth. Moderately elevated GPT was observed during the first months. A normal liver was seen in pre- and post-natal sonography. Therefore it is likely that the increased liver enzymes were caused by the chemotherapy of the mother.
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PMID:[Case report--tuberculosis in a health care worker during pregnancy]. 1885 9

The World Health Organization (WHO) has shown concern about the burden of tuberculosis in the developing countries. Even though rifampicin is an effective drug in the management of tuberculosis, it has been documented to have some toxic effects in humans. Therefore, this study intends to investigate the modulatory effect of vitamins C and E on the hepatotoxicity, sperm quality and brain toxicity of Rifampicin. Forty Wistar albino rats were used, 10 animals per group. Group 1 animals received 0.3 mL of distilled water, the Group 2 animals received the therapeutic dose of rifampicin, Group 3 animals received therapeutic doses of rifampicin plus vitamin E, while Group 4 received therapeutic doses of rifampicin and vitamin C. The administration was performed orally during three months; the animals were sacrificed by cervical dislocation at the end of that period. Blood samples were collected and liver function and lipid profile was analyzed using fully automated clinical chemistry device. The liver, brain and reproductive organs underwent histopathological examination. Sperm samples were collected from the epididymis to achieve count and motility and morphological analysis. Results showed rifampicin alone to raise (p < 0.05) liver function enzymes (Aspartate amino transferase [AST], Serum alanine amino transferase [ALT] and Total Bilirubin) when compared with controls. While the vitamin E treated group showed remarkable protection, the vitamin C treated group showed questionable protection against the rifampicin induced liver damage. Sperm count results showed an important (p < 0.05) increase in the sperm quality in vitamin E and C treated groups. However, the vitamin E plus Rifampicin treated group showed increased lipid peroxidation. The histopathological findings revealed structural damages by rifampicin in liver, brain and epididymis while some remarkable architectural integrity was observed in the antioxidant-treated groups. It can be concluded that vitamin E or C improved sperm quality and protected against the brain damage caused by rifampicin. Moreover, vitamin E demonstrated remarkable hepatoprotection against rifampicin induced damage while vitamin C shows a questionable hepatoprotection.
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PMID:Modulatory activity of antioxidants against the toxicity of Rifampicin in vivo. 2030 54

This study examined the effects and possible mechanisms of rifampin against acetaminophen-induced hepatotoxicity in mice. Rifampin significantly enhanced the biotransformation of acetaminophen, evidenced by the increase in p-aminophenol formation in rifampin-treated microsomes and the increase in plasma clearance rate of acetaminophen. Pretreatment with rifampin significantly decreased serum alanine transaminase (ALT) activities, aspartate transaminase (AST) activities and prevented severe liver necrosis following acetaminophen overdose. The contents and activities of microsomal drug-metabolizing enzyme were less affected in rifampin-pretreated mice in comparison to the animals treated with acetaminophen alone. Rifampin was capable of increasing glutathione (GSH) level and GSH reductase activity and reducing GSH depletion and the decrease in GSH reductase activity by acetaminophen in mice. In addition, it was found that the microsomal Ca(2+)-ATPase activity was not directly related to acetaminophen toxic species generated in the P450 enzyme system in vitro. These findings suggest that rifampin has species-specific effects on the liver against acetaminophen-induced hepatotoxicity in mice, which increase the level of GSH by promoting GSH regeneration.
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PMID:Effects and mechanisms of rifampin on hepatotoxicity of acetaminophen in mice. 2272 60


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