SWEET SYNDROME IN A CHILD WITH APLASTIC-ANEMIA RECEIVING RECOMBINANT GRANULOCYTE-COLONY-STIMULATING FACTOR

Purpose: To elucidate the pathogenesis of Sweet syndrome, one patient with aplastic anemia was evaluated. Patient and Methods: A 15-year-old girl presented with intermittent fever and progressive pallor for 3 m onths after non-A, non-B, non-C hepatitis. Aplastic anemia was diagnos ed and therapy was begun with recombinant granulocyte colony-stimulati ng factor (G-CSF), methylprednisolone pulse therapy, antilymphocyte gl obulin and cyclosporin A. There was only an increase in the neutrophil counts. We continued G-CSF therapy of 300 mu g/m(2) on alternate days for 7 months. At this time the white blood cell count was 10,000/mu l , and the patient developed high-grade fever and a painful, erythemato us, tender plaque (3 x 3 cm) on the left thigh. We diagnosed the lesio n as a skin infection and stopped G-CSF therapy and started antibiotic s. Cultures were negative. The lesion slowly resolved, G-CSF was resta rted after 2 months, and 1 month later disseminated lesions occurred. Antibiotic therapy was not effective. Results: Biopsy of the lesion de monstrated infiltration of the dermis by sheets of neutrophils. We sto pped G-CSF and began corticosteroid therapy. The skin lesions resolved rapidly. Conclusion: We postulated that Sweet syndrome was induced by G-CSF treatment.