Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A 62-year-old man with refractory leukemia transformed from myelodysplastic syndrome was placed on hydroxyurea (hydroxycarbamide) at a daily dose of 500 mg. Because of insufficient cytoreductive efficacy, the dose was increased to 1,500 mg five days later. Eight days after the initiation of hydroxyurea, the patient started complaining of chills, fever, and vomiting. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were markedly elevated to 5,098 and 3,880 IU/l from 44 and 59 IU/l in one day, respectively. Tests for hepatitis viruses were all negative. With the discontinuation of hydroxyurea, AST and ALT returned to their former levels within two weeks. A drug-induced lymphocyte stimulation test for hydroxyurea was positive with a stimulating index of 2.0. Hepatic dysfunction has been recognized as one of the side effects of hydroxyurea. However, there have been only a limited number of reports demonstrating drug allergy to have a role in hepatic dysfunction accompanied by fever and gastrointestinal symptoms. The findings of our case strongly suggest that all presentations could be explained by drug allergy. Physicians should be mindful of the potential for acute and severe hepatic dysfunction due to allergic reaction against hydroxyurea.
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PMID:[Hydroxyurea (hydroxycarbamide)-induced hepatic dysfunction confirmed by drug-induced lymphocyte stimulation test]. 2449 45

Extrapulmonary tuberculosis is the reactivation of the remaining latent organism which spreads during primary infection by the lymphohematogenous way. It should be considered in the differential diagnosis especially in endemic countries for tuberculosis. Tuberculosis (TB) treatment is based on the principle of the combined use of several drugs. As a result of the combination therapy there can be life threatening side effects which can lead to improper use of medications and may also cause drug resistance. In this report, we present an 85-year-old male patient desensitized due to the development of allergy against multi-drugs with rib tuberculosis and chest wall abscess to whom, culture, drug susceptibility and genotypical tests were applied. In November 2012, the patient applied to a medical center with complaints of swelling and pain under the right rib, underwent rib resection and eventually diagnosed as rib TB by histopathological examination. However, the anti-TB treatment was discontinued due to the hypersensitivity reactions in the skin and in addition to the hepatic and renal dysfunction side effects. The patient had widespread redness, rash and pruritus on the body and the laboratory findings were as follows; ALT: 114 U/L, AST: 152 U/L, ALP: 93 U/L, GGT: 26U/L, blood urea nitrogen (BUN): 26 mg/dL and creatinine: 1.7 mg/dL. After the disapperance of the complaints within 3 days of drug discontinuation, isoniazid treatment was initiated. However, the new treatment was also discontinued when the reactions reoccurred. Afterwards, the patient developed hypersensitivity reactions against the combination of streptomycin and ethambutol. The patient refused any further treatment and was discharged from the hospital. The patient was untreated for the last 5 months and admitted to our clinic with a fistulized swelling and abscess in the right chest wall. Bacteria was not detected in the acid-fast staining of the abscess material, however Mycobacterium tuberculosis was isolated from culture by MGIT (Mycobacteria Growth Incubator Tube; BBL MGIT, BD, USA) system. The spoligotyping revealed that the genotype was Haarlem 1. Major drug susceptibility testing against rifampin, streptomycin, ethambutol, isoniazid, and pyrazinamide yielded sensitivity to those drugs. Minor drug susceptibility testing against paraaminosalicylic acid, ethionamide, kanamycin, capreomycin and ofloxacin was found to be sensitive. A regimen of isoniazid 300 mg/day, ethambutol 1000 mg/day and moxifloxacin 400 mg/day was initiated. Rapid oral desensitization against isoniazid and ethambutol were repeated on two consecutive days. The patient continued antituberculosis therapy for 12 months without adverse reactions. The chest wall fistula was closed. Abscess was drained surgically. Clinical and radiological improvements were achieved. The patient remains clinically disease free and continues his regular follow ups. This case is presented to emphasize about the importance of culture and susceptibility testing in extrapulmonary tuberculosis cases and desensitization in drug hypersensitivity reactions.
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PMID:[A case of rib tuberculosis and chest wall abscess with multi-drug hypersensitivity reactions]. 2631 87