Sisam D A, Sheehan J P
Regional Diabetes Management Center, Amherst, Ohio.
J Am Osteopath Assoc. 1990 Jan;90(1):83-6.
We describe the first case of chronic neutropenia of 17 years' duration following gold therapy in a 53-year-old woman given a 1-g course of gold therapy in 1965 for treatment of seropositive rheumatoid arthritis. Although she had a good response to the gold therapy, her originally normal leukocyte count fell to 1.2 x 10(9)/L. Over the subsequent 17 years, she required multiple hospitalizations for recurrent skin, mouth, and respiratory tract infections. Serial leukocyte counts failed to show a cyclical nature to the chronic neutropenia. Normal results of a technetium Tc 99m spleen scan and lack of increased bone marrow leukocyte precursors rendered a diagnosis of Felty's syndrome unlikely. A bone marrow biopsy specimen revealed an isolated reduction in the number of myeloid precursors, which is consistent with gold-induced bone marrow toxicity. This patient's relative freedom from serious life-threatening infections remains enigmatic, but is undoubtedly related to her ability to augment another phagocytic cell line, and the remarkable phagocytic activity of her monocytes appears to have well compensated for her neutropenia. This activity was most likely responsible for her long-term survival.
我们描述了首例因金制剂治疗导致慢性中性粒细胞减少症长达17年的病例。该患者为一名53岁女性,1965年接受了1克疗程的金制剂治疗以治疗血清学阳性的类风湿性关节炎。尽管她对金制剂治疗反应良好,但她原本正常的白细胞计数降至1.2×10⁹/L。在随后的17年里,她因反复出现皮肤、口腔和呼吸道感染而多次住院。连续的白细胞计数未显示慢性中性粒细胞减少症具有周期性。锝Tc 99m脾扫描结果正常且骨髓白细胞前体未增加,使得费尔蒂综合征的诊断不太可能。骨髓活检标本显示髓系前体细胞数量单独减少,这与金制剂诱导的骨髓毒性一致。该患者相对免于严重威胁生命的感染,其原因仍不明确,但无疑与她增强另一种吞噬细胞系的能力有关,并且她单核细胞显著的吞噬活性似乎很好地弥补了她的中性粒细胞减少症。这种活性很可能是她长期存活的原因。