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Clinical Specialist—Medicine Department of Pharmacy Services University Hospitals of Cleveland Wearn B16 11100 Euclid Avenue Cleveland, Ohio 44106-5000 fax 216/844-3152 anne.baciewicz{at}uhhs.com
Assistant Clinical Professor of Pharmacy in Medicine Case Western Reserve University Cleveland Assistant Professor of Medicine Department of Medicine Case Western Reserve University
Published Online, April 12, 2005. www.theannals.com, DOI 10.1345/aph.1E500
Case Report. An 18-year-old previously healthy female presented to her primary care physician with a 3-day history of headache, fatigue, sore throat, swollen neck glands, and sinus symptoms. Rapid ß-Streptococcus throat culture was negative. At this time, oral cefprozil 500 mg twice daily was prescribed for sinusitis and pharyngitis. Allergy history included procaine and aspirin/caffeine/salicylamide (Excedrin). The patient was on no other medications. Four days later, the woman returned to her physician with eyelid swelling and fatigue. At this time, laboratory values from the first visit showed a positive heterophile antibody (Monospot test) and atypical lymphocytosis suggestive of acute Epstein–Barr infection (Table 1). On day 7 of antibiotic therapy, cefprozil was discontinued due to development of a maculopapular, pruritic rash on her face and upper extremities. A tapering prednisone regimen was prescribed for the rash. Two days later, the patient presented to a community hospital emergency department with a worsening rash, hypotension (BP 79/24 mm Hg), tachycardia (HR 124 beats/min), periorbital edema, malaise, nausea, and vomiting. She received aggressive intravenous hydration and intravenous clindamycin, vancomycin, promethazine, and diphenhydramine. Prednisone was stopped. Laboratory values revealed leukocytosis with bandemia, atypical lymphocytes, and elevated liver transaminase levels (Table 1). Toxic shock syndrome (TSS) was suspected, and the patient was transferred from the community hospital to our facility's intensive care unit (ICU).
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Examination on ICU admission was remarkable for BP 100/60 mm Hg, HR 100 beats/min, and T 37.7 °C, along with periorbital edema, soft palate erythema, dry mucous membranes, and a generalized maculopapular rash. Over 24 hours, the patient was given 11 L of intravenous fluids and, for possible TSS, immunoglobulin 2 g/kg, vancomycin, and clindamycin. TSS was ruled out on the basis of negative blood cultures and absence of any bacterial source of infection. Three days after admission, the patient was discharged with a diagnosis of IM and a cefprozil-induced rash, which had significantly improved.
Discussion. To our knowledge, the literature contains only one case of cephalexin-induced rash in a patient with IM. Our patient had a similar presentation during treatment with a second-generation cephalosporin. The literature contains reports of other antibiotics, such as ampicillin, penicillin, azithromycin, and levofloxacin, causing a rash during IM.1-5 The pathogenesis of the rash is unknown, but it is postulated to be caused by an alteration in the host's immune status during the viral infection.2-5 Our patient's rash differed from the classic IM rash because it appeared about 10 days after her initial constitutional symptoms of IM and was more extensive, severe, and of longer duration than the classic IM rash that typically occurs after 4–6 days. A cephalosporin allergy may manifest with a dermatologic maculopapular or morbilliform rash, pruritus, exanthema, or urticaria (1–3%), eosinophilia (2.7–8.2%), positive antiglobulin or Coombs' test (1–2%), and/or drug fever (0.5–0.9%).6 The rash in our patient was possibly associated with cefprozil according to the Naranjo probability scale.7 We caution other practitioners to be aware of the possibility of drug-induced rash if antibiotics are prescribed in the setting of IM.
Footnotes
Dr. Baciewicz owns Bristol-Myers Squibb stock.
References
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