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November 2001

Churg-Strauss Syndrome Associated With Fluticasone Therapy

Arch Dermatol. 2001;137(11):1527-1528. doi:

In the February issue of the ARCHIVES,1 we reported a case of Churg-Strauss syndrome (CSS) with prominent skin involvement that was successfully treated with a combination of low-dose interferon alfa-2a (Roferon-A), 9 × 106to 13 × 106 IU/wk, and prednisolone, 20 mg/d. The patient presented initially in April 1999 with a half-year history of recurrent bronchial infections and airway obstruction. He had no history of asthma or other allergic diseases. Four weeks before admission he was prescribed prednisolone, 10 mg, and a combination of fluticasone propionate and salmeterol xinafoate (Viani forte Discus) for inhalation. The interferon alfa therapy was well tolerated by the patient and all laboratory parameters and the eosinophil counts returned to values slightly above the normal range. However, when the interferon alfa dose was tapered below 9 × 106 IU/wk, the rash instantly reappeared within 1 week and the eosinophil counts increased. In August 1999 the patient had a bronchial infection with fever and rhinopharyngitis, which led to a strong increase of the eosinophil counts combined with eosinophilic pulmonary infiltration and rash, and the interferon alfa dose had to be increased to 18 × 106 IU/wk. In December 1999 we found a letter on the Food and Drug Administration homepage discussing a connection between CSS development and treatment with inhaled fluticasone (http://www.fda.gov/medwatch/safety/1999/floven.htm). This prompted us to substitute the fluticasone treatment with budesonide (Pulmicort). Pulmonary eruptions improved spontaneously, and there was a complete resolution of the vasculitic rash. All blood parameters including eosinophil counts returned to normal values within 4 weeks, enabling us to discontinue the interferon alfa therapy and to keep the patient on a regimen of 20 mg/d of prednisolone and inhalation of albuterol and budesonide for the treatment of his bronchitis. When the patient was seen 2 months later in February 2000 with another bronchial infection, the white blood cell counts showed a leukocytosis with elevated neutrophil counts, and eosinophil counts in the normal range. We consider this finding as strong evidence that the CSS was no longer active. The patient remained well without any symptoms of CSS or vasculitis during the year 2000 and is currently treated with 20 mg/d of prednisolone and inhaled budesonide, showing only minor airway obstruction and a peakflow of 300 to 400 mL/min.

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