Chae Kacey, Perlman Jordan, Fransman Ryan B, Wolfgang Christopher L, De Jesus-Acosta Ana, Mathioudakis Nestoras
Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Deparment of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
AACE Clin Case Rep. 2021 Jun 11;7(6):379-382. doi: 10.1016/j.aace.2021.06.001. eCollection 2021 Nov-Dec.
We describe a rare case of profound subcutaneous insulin resistance (SIR) presumed due to a paraneoplastic process caused by pancreatic adenocarcinoma that improved with intravenous insulin and tumor resection.
An 80-year-old man with previously well-controlled type 2 diabetes mellitus had worsening glycemic control (hemoglobin A1C increase of 6.5% to 8.6% over 4 months) following a recent diagnosis of pancreatic adenocarcinoma. His blood glucose was uncontrolled at 600 mg/dL despite rapid up-titration of a subcutaneous basal-bolus insulin regimen totaling 1000 units/d. Extensive evaluation of insulin resistance including insulin antibodies and anti-insulin receptor antibodies was negative. Due to clinical deterioration, the patient underwent pancreaticoduodenectomy before the completion of neoadjuvant chemotherapy. The patient received intravenous insulin before surgery, which resulted in rapid improvement in glycemic control. The patient's blood glucose normalized, and he was maintained on metformin monotherapy following pancreaticoduodenectomy.
This patient had evidence of SIR in the setting of pancreatic adenocarcinoma. SIR was likely a paraneoplastic process as glycemic control improved after tumor resection. Interestingly, the patient did not have hyperinsulinemia but rather evidence of β-cell dysfunction, which highlights the possibility of exogenous insulin resistance.
Paraneoplastic processes due to pancreatic adenocarcinoma can cause SIR, marked by profound hyperglycemia and deteriorating functional status. It is, therefore important to recognize this rare syndrome and appropriately escalate to a higher level of care and consider proceeding with tumor resection.
我们描述了一例罕见的严重皮下胰岛素抵抗(SIR)病例,推测是由胰腺腺癌引起的副肿瘤综合征所致,经静脉注射胰岛素和肿瘤切除后病情改善。
一名80岁男性,既往2型糖尿病控制良好,近期诊断为胰腺腺癌后血糖控制恶化(4个月内糖化血红蛋白从6.5%升至8.6%)。尽管将皮下基础 - 餐时胰岛素方案迅速上调至总计1000单位/天,其血糖仍高达600 mg/dL且未得到控制。对胰岛素抵抗进行的广泛评估,包括胰岛素抗体和抗胰岛素受体抗体检测均为阴性。由于临床病情恶化,患者在新辅助化疗完成前接受了胰十二指肠切除术。患者术前接受静脉胰岛素治疗,血糖控制迅速改善。患者血糖恢复正常,胰十二指肠切除术后维持二甲双胍单药治疗。
该患者在胰腺腺癌背景下存在SIR证据。SIR可能是一种副肿瘤综合征,因为肿瘤切除后血糖控制得到改善。有趣的是,患者没有高胰岛素血症,而是存在β细胞功能障碍的证据,这凸显了外源性胰岛素抵抗的可能性。
胰腺腺癌引起的副肿瘤综合征可导致SIR,表现为严重高血糖和功能状态恶化。因此,认识到这种罕见综合征并适当升级护理级别并考虑进行肿瘤切除非常重要。