Curley Cameron, Kennedy Glen, Haughton Anne, Love Amanda, McCarthy Catherine, Boyd Andrew
Department of Haematology, Royal Brisbane and Women's Hospital, Brisbane, Queensland, Australia.
Asia Pac J Clin Oncol. 2010 Jun;6(2):77-9. doi: 10.1111/j.1743-7563.2010.01285.x.
Diabetes insipidus (DI) is a rare presenting complication of acute myeloid leukaemia (AML). Typically, the combination of DI and AML is associated with structural abnormalities of the neurohypophysis. We present a case of AML and DI presenting without any abnormalities of the neurohypophysis on radiological scanning and with normal cerebrospinal fluid examination. The AML karyotype at presentation was characterized by the presence of a t(3; 3)(q21; q26) translocation and monosomy 7. After treatment with induction chemotherapy, the patient achieved a complete remission and his DI resolved. At subsequent AML relapse, characterized by a complex karyotype without the t(3; 3)(q21; q26) translocation or monosomy 7, DI did not recur. Our case provides clinical support to the hypothesis that the t(3; 3)(q21; q26) translocation and/or monosomy 7 in AML may directly result in dysregulation of transcription factors resulting in development of DI in AML patients.
尿崩症(DI)是急性髓系白血病(AML)一种罕见的并发症。通常,尿崩症与急性髓系白血病的合并存在与神经垂体的结构异常有关。我们报告一例急性髓系白血病合并尿崩症患者,其放射学扫描未发现神经垂体有任何异常,脑脊液检查结果正常。初诊时急性髓系白血病的核型特征为存在t(3; 3)(q21; q26)易位和7号染色体单体。诱导化疗后,患者达到完全缓解,其尿崩症症状消失。在随后以复杂核型为特征的急性髓系白血病复发时(不存在t(3; 3)(q21; q26)易位或7号染色体单体),尿崩症未复发。我们的病例为以下假说提供了临床支持:急性髓系白血病中的t(3; 3)(q21; q26)易位和/或7号染色体单体可能直接导致转录因子失调,从而致使急性髓系白血病患者发生尿崩症。