Skalak Havird McLean, Haas Kaitlyn, Laub Melissa, Mulloy Laura L
Mercer University School of Medicine, Savannah, Georgia.
University of Georgia College of Pharmacy.
Am J Med Sci. 2025 May;369(5):630-633. doi: 10.1016/j.amjms.2024.08.023. Epub 2024 Aug 29.
Post-transplant diabetes mellitus (PTDM) is a well-known solid organ transplant complication, which can be related to immunosuppressants, particularly tacrolimus. We report an unusual presentation of PTDM with diabetic ketoacidosis (DKA). This is unique as PTDM typically resembles Type 2 DM, whereas DKA is associated with Type 1 DM and has rarely been reported as a complication of tacrolimus. A 38-year-old African American male on LCP-tacrolimus presented four months post kidney transplant with vomiting, weakness, poor appetite, and polyuria. Labs demonstrated hyperglycemia, ketonuria, and high anion gap metabolic acidosis. He was nonobese and had no personal or family history of Type 2 DM. DKA was suspected to be secondary to tacrolimus-induced pancreatic beta cell damage worsened by supratherapeutic tacrolimus levels. Latent autoimmune diabetes in adults (LADA) was diagnosed when further testing showed insulinopenia, low C-peptide, and anti-glutamic acid decarboxylase (GAD) autoantibodies. He required 120-units of subcutaneous insulin daily. Our literature review revealed only 16 other tacrolimus-induced DKA cases. No cases reported anti-GAD positivity and most showed beta cell toxicity reversibility with tacrolimus tapering or substitution. Our patient was early post-transplant with leukocytopenia, so tacrolimus was not exchanged. This unusual PTDM case may have resulted from both autoimmune and tacrolimus-induced beta cell destruction. Physicians should be aware of new onset LADA post-transplantation and tacrolimus toxicity leading to DKA, even in patients without traditional risk factors. Anti-GAD antibody screening in patients on tacrolimus who develop PTDM may identify patients less likely to recover beta cell function with immunosuppression augmentation which requires careful monitoring.
移植后糖尿病(PTDM)是一种众所周知的实体器官移植并发症,它可能与免疫抑制剂有关,尤其是他克莫司。我们报告了一例伴有糖尿病酮症酸中毒(DKA)的PTDM不寻常表现。这很独特,因为PTDM通常类似于2型糖尿病,而DKA与1型糖尿病相关,且很少被报道为他克莫司的并发症。一名38岁的非裔美国男性在接受肾移植并使用LCP-他克莫司治疗四个月后,出现呕吐、乏力、食欲减退和多尿症状。实验室检查显示血糖升高、酮尿和高阴离子间隙代谢性酸中毒。他并非肥胖,且无2型糖尿病的个人或家族史。怀疑DKA继发于他克莫司诱导的胰腺β细胞损伤,且治疗剂量以上的他克莫司水平使其病情恶化。进一步检查显示胰岛素缺乏、C肽水平低以及抗谷氨酸脱羧酶(GAD)自身抗体阳性,从而诊断为成人隐匿性自身免疫性糖尿病(LADA)。他每天需要皮下注射120单位胰岛素。我们的文献综述仅发现另外16例他克莫司诱导的DKA病例。没有病例报告抗GAD阳性,且大多数病例显示随着他克莫司减量或更换,β细胞毒性具有可逆性。我们的患者移植后早期出现白细胞减少,因此未更换他克莫司。这例不寻常的PTDM病例可能是自身免疫和他克莫司诱导的β细胞破坏共同导致的。医生应意识到移植后新发的LADA以及他克莫司毒性导致的DKA,即使在没有传统危险因素的患者中也应警惕。对于发生PTDM的他克莫司治疗患者,进行抗GAD抗体筛查可能有助于识别那些通过增加免疫抑制不太可能恢复β细胞功能的患者,这需要仔细监测。