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LETTER
Acute Hepatitis, Interstitial Nephritis, and Eosinophilia
Manfred Hauben and
Carl Adler
1 April 1995 | Volume 122 Issue 7 | Pages 555-556
TO THE EDITOR:
Saliba and Herbert [1] observed an increased incidence of oxacillin-associated hepatotoxicity in patients with human immunodeficiency virus (HIV infection); however, this study did not account for intergroup differences in variables relevant to causality assessment of adverse drug reactions, such as concomitant medications, coexisting pathologic abnormalities, and treatment indication. We also found that patients with HIV infection may be at increased risk for drug-induced hepatotoxicity [2-4].
A 35-year-old female inpatient with HIV infection who previously had adverse reactions (rash) to penicillin and trimethoprim-sulfamethoxazole developed striking aminotransferase elevations, acute interstitial nephritis, and eosinophilia shortly after the initiation of intravenous aztreonam and vancomycin. On admission, the patient was receiving zidovudine, methadone, fluconazole, and diphenhydramine. Therapy with oral erythromycin, 1 g every 6 hours, was discontinued after one dose because of nausea and vomiting. Pretreatment laboratory tests included alanine aminotransferase (47 U/L), aspartate aminotransferase (51 U/L), alkaline phosphatase (64 U/L), bilirubin (0.5 mg/dL), prothrombin time (12.2 seconds), blood urea nitrogen/creatinine ratio (20/0.8), negative serologic tests for hepatitis B, and an anticytomegalovirus titer of 1:32. Ultrasound showed increased echogenicity of the hepatic parenchyma, pericholecystic edema without focal lesions or cholelithiasis, and normal-sized kidneys with increased cortical echogenicity. The abnormalities regressed after antibiotic therapy was withdrawn (Table 1).
The clinical setting, temporal evolution, and laboratory test results indicate an adverse drug reaction or reactions. The pattern and level of aminotransferase elevation would be unusual for either drug [5]. Immunologic abnormalities associated with HIV infection may have contributed to the occurrence of these events and to previous dermatologic reactions to trimethoprim-sulfamethoxazole and penicillin. Infection with HIV has been associated with an increased risk for and severity of adverse drug reactions, particularly hypersensitivity reactions. Mechanisms reported to explain this increased risk include slow acetylation or glutathione deficiency (or both) and drug-specific IgE antibodies [2-4]. Physicians should watch for the development of adverse drug reactions in HIV-infected patients so that therapy with the responsible drugs can be quickly discontinued.
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Author and Article Information
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Pfizer, New York, NY 10017-5755. Jamaica Hospital, New York, NY 11418.
1. Saliba B, Herbert PN. Oxacillin hepatoxicity in HIV-infected patients (Letter). Ann Intern Med. 1994; 120:1048.
2. Ackerman Z, Levy M. Hypersensitivity reactions to drugs in acquired immune deficiency syndrome. Postgraduate Medical Journal. 1989; 63:55-6.
3. Harb GE, Jacobsen MA. Immunodeficiency virus (HIV) infection. Does it increase susceptibility to adverse drug reactions. Drug Safety. 1993; 9:1-8.
4. Harb G, Alldredge G, Coleman E, Jacobsen M. Pharmacoepidemiology of adverse drug reactions in hospitalized patients with human immunodeficiency virus (HIV) disease. J Acquir Immune Defic Syndr. 1993; 6:919-26.
5. Stricker BH. Antimicrobial agents. In: Stricker, BH. Drug Induced Hepatic Injury. 2d ed. New York: Elsevier; 1992:194,213.
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