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 months after non-A, non-B, non-C hepatitis. Aplastic anemia was diagnosed and therapy was begun with recombinant granulocyte colony-stimulating factor (G-CSF), methylprednisolone pulse therapy, antilymphocyte globulin and cyclosporin A. There was only an increase in the neutrophil counts. We continued G-CSF therapy of 300 micrograms/m2 on alternate days for 7 months. At this time the white blood cell count was 10,000/microliters and the patient developed high-grade fever and a painful, erythematous, tender plaque (3 X 3 cm) on the left thigh. We diagnosed the lesion as a skin infection and stopped G-CSF therapy and started antibiotics. Cultures were negative. The lesion slowly resolved, G-CSF was restarted after 2 months, and 1 month later disseminated lesions occurred. Antibiotic therapy was not effective. RESULTS: Biopsy of the lesion demonstrated infiltration of the dermis by sheets of neutrophils. We stopped G-CSF and began corticosteroid therapy. The skin lesions resolved rapidly. CONCLUSION: We postulated that Sweet syndrome was induced by G-CSF treatment.
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 months after non-A, non-B, non-C hepatitis. Aplastic anemia was diagnosed and therapy was begun with recombinant granulocyte colony-stimulating factor (G-CSF), methylprednisolone pulse therapy, antilymphocyte globulin and cyclosporin A. There was only an increase in the neutrophil counts. We continued G-CSF therapy of 300 micrograms/m2 on alternate days for 7 months. At this time the white blood cell count was 10,000/microliters and the patient developed high-grade fever and a painful, erythematous, tender plaque (3 X 3 cm) on the left thigh. We diagnosed the lesion as a skin infection and stopped G-CSF therapy and started antibiotics. Cultures were negative. The lesion slowly resolved, G-CSF was restarted after 2 months, and 1 month later disseminated lesions occurred. Antibiotic therapy was not effective. RESULTS: Biopsy of the lesion demonstrated infiltration of the dermis by sheets of neutrophils. We stopped G-CSF and began corticosteroid therapy. The skin lesions resolved rapidly. CONCLUSION: We postulated that Sweet syndrome was induced by G-CSF treatment.