Shimizu T, Yoshida I, Eguchi H, Takahashi K, Inada H, Kato H
Department of Pediatrics and Child Health, Kurume University, School of Medicine, Kurume, Japan.
J Pediatr Hematol Oncol. 1996 Aug;18(3):282-4. doi: 10.1097/00043426-199608000-00009.
To elucidate the pathogenesis of Sweet syndrome, one patient with aplastic anemia was evaluated.
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.
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.
We postulated that Sweet syndrome was induced by G-CSF treatment.
为阐明Sweet综合征的发病机制，对1例再生障碍性贫血患者进行了评估。
一名15岁女孩在患非甲、非乙、非丙型肝炎3个月后出现间歇性发热和进行性面色苍白。诊断为再生障碍性贫血，并开始用重组粒细胞集落刺激因子（G-CSF）、甲泼尼龙冲击疗法、抗淋巴细胞球蛋白和环孢素A进行治疗。仅中性粒细胞计数有所增加。我们每隔一天继续给予300微克/平方米的G-CSF治疗，持续7个月。此时白细胞计数为10,000/微升，患者出现高热，左大腿出现一个疼痛、红斑、触痛的斑块（3×3厘米）。我们将该病变诊断为皮肤感染，停用G-CSF治疗并开始使用抗生素。培养结果为阴性。病变逐渐消退，2个月后重新开始使用G-CSF，1个月后出现播散性病变。抗生素治疗无效。
病变活检显示真皮有大量中性粒细胞浸润。我们停用G-CSF并开始使用皮质类固醇治疗。皮肤病变迅速消退。
我们推测Sweet综合征是由G-CSF治疗诱发的。
