Oh Hye Jin, Yun Myung Jae, Lee Seong Tae, Lee Seung June, Oh So Yeon, Sohn In
Department of Internal Medicine, Seoul Medical Center, Seoul, Korea.
Korean J Hematol. 2011 Dec;46(4):279-82. doi: 10.5045/kjh.2011.46.4.279. Epub 2011 Dec 27.
We report a case of a 51-year-old woman with Evans syndrome (autoimmune hemolytic anemia and primary immune thrombocytopenia) and hypothyroidism. She was previously diagnosed with Hashimoto's thyroiditis in 1994 (age, 35) and autoimmune hemolytic anemia (AIHA) 3 years ago. She was treated with oral prednisolone. After a period, in which the anemia waxed and waned, there was an abrupt development of thrombocytopenia (nadir 15×10(9)/L) that coincided with the tapering off of prednisolone after 3 years of administration. Because her thrombocytopenia was refractory to prednisolone, we administered rituximab (375 mg/m(2) weekly) for 4 weeks. Two weeks after the completion of the rituximab treatment, her platelet count was up to 92×10(9)/L. No intermittent peaking of thyroid stimulating hormone occurred after rituximab treatment was initiated. Evans syndrome and autoimmune thyroiditis might share common pathophysiological mechanisms. This notion supports the use of rituximab in a patient suffering from these disorders.
我们报告一例51岁女性，患有伊文氏综合征（自身免疫性溶血性贫血和原发性免疫性血小板减少症）及甲状腺功能减退症。她曾在1994年（35岁时）被诊断为桥本甲状腺炎，3年前被诊断为自身免疫性溶血性贫血（AIHA）。她接受了口服泼尼松龙治疗。经过一段时间贫血病情反复后，在服用泼尼松龙3年后逐渐减量时，突然出现血小板减少（最低点为15×10⁹/L）。由于她的血小板减少对泼尼松龙治疗无效，我们给予利妥昔单抗（375mg/m²，每周一次）治疗4周。利妥昔单抗治疗结束后两周，她的血小板计数升至92×10⁹/L。开始利妥昔单抗治疗后，促甲状腺激素未出现间歇性峰值。伊文氏综合征和自身免疫性甲状腺炎可能具有共同的病理生理机制。这一观点支持在患有这些疾病的患者中使用利妥昔单抗。
