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Long Island Jewish Medical Center New Hyde Park, NY 11042
Drug-induced eosinophilic lung disease is a known complication of a wide variety of agents [1]. A typical radiographic appearance is that of bilateral nonsegmental homogeneous consolidation in the lung periphery, which is frequently referred to as a reversed pulmonary edema pattern [2]. Mesalamine (5-aminosalicylic acid), a drug used in the treatment of patients with ulcerative colitis, has rarely been reported as a cause of eosinophilic pulmonary disease [3, 4]. We report a unique case of "unilateral reversed pulmonary edema" or "photonegative" pattern of eosinophilic pneumonia that complicated treatment with mesalamine.
A 53-year-old woman who was a lifelong nonsmoker and had a history of ulcerative colitis and dementia presented with a 1-week history of new-onset dry cough, fever, and malaise. Initially, her vital signs and the laboratory findings were normal except for a fever of 102°F (38.9° C) orally. An initial chest radiograph (Fig. 3) revealed peripheral homogeneous nonsegmental consolidation on the right side only with no evidence of a pleural effusion. The patient was admitted with the diagnosis of community-acquired/aspiration pneumonia and was started on IV antibiotics. She remained febrile, prompting a change in the antibiotic regimen, and within 24 hr a chest radiograph revealed an increasing infiltrate in the same distribution. Her eosinophilia increased to a peak of 27.9% (2200/mm3) by day 3. Her cough and eosinophilia persisted, a new maculopapular rash developed, and a repeated radiograph revealed consolidation of virtually the entire right lung with no infiltrates detectable on the left. On day 9 all antibiotics were discontinued because of the possibility of a drug reaction, and sputum, urine, stool, and blood were cultured. Fiberoptic bronchoscopy was performed with bronchoalveolar lavage and transbronchial biopsies. Bronchoalveolar lavage revealed 79% eosinophils, and pathology was consistent with eosinophilic pneumonia without evidence of vasculitis, parasitic infestation, or infection. All cultures, including stool cultures for ova and parasites, were negative. Despite the discontinuation of antibiotics, the elevated eosinophil count and the unilateral radiographic abnormalities persisted. At that point, mesalamine, which the patient had been using continuously for 4 months, was discontinued and 60 mg of prednisone was started. Within 24 hr of the discontinuation of mesalamine, defervescence occurred, the eosinophilia rapidly remitted (0.7%), and radiography showed that her condition had stabilized with the infiltrate resolving almost completely by day 18. After the steroid taper, the infiltrate did not recur.
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In summary, an increasing number of drugs have been implicated in eosinophilic lung disease, which can vary from largely asymptomatic radiographic infiltrates to, as in this patient, acute eosinophilic pneumonias. Mesalamine was almost certainly the cause of pulmonary disease in our patient, although this finding has been rarely reported [3, 4]. Although there are extensive anecdotal reports of pulmonary infiltrations associated with inflammatory bowel disease, the timing of rapid and sustained clinical and radiographic improvement after discontinuation of the drug and the failure to recur after the steroid taper make this unlikely in our patient. Furthermore, her bowel disease was quiescent throughout the course of this illness.
We conclude that drug-induced eosinophilic pneumonia should be considered in patients at risk for drug toxicity even in cases of a unilateral radiographic infiltration, particularly if the pattern is that of reversed pulmonary edema.
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