Ballout Rami A, Arabi Asma
Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Calcium Metabolism and Osteoporosis Program, Department of Internal Medicine, Division of Endocrinology, American University of Beirut Medical Center, Beirut, Lebanon.
Front Endocrinol (Lausanne). 2017 Sep 25;8:243. doi: 10.3389/fendo.2017.00243. eCollection 2017.
A 56-year-old middle-eastern male with a long-standing history of poorly controlled type 2 diabetes mellitus presented to us complaining of severely painful bilateral upper and lower extremity cramps occurring shortly after his rapid-acting insulin analog injection(s). The cramps had started 6 months ago and have been occurring intermittently in non-predictable episodes since then. He had otherwise never experienced any insulin-related adverse reaction(s) before. His cramps are very painful and debilitating, interfering with his daily activities and placing him in a state of constant fear/anxiety of re-experiencing them. This caused him to become non-adherent with his prescribed treatment and poorly compliant with his follow-up regimens. Thorough examination showed a diffuse loss of sensation over the lower limbs. This was subsequently confirmed with a combined electromyography-nerve conduction study which indicated extensive diabetic axonal polyneuropathy. By contrast, lower extremity segmental arterial pressures were negative for peripheral vasculo-occlusive disease, ruling out vascular insufficiency as a possible etiology of the cramps. We then measured the levels of serum electrolytes right-before and 30 min right-after injecting the patient with his insulin. Potassium dropped by about 16% from its initial level, compared to a drop of only around 4% for calcium and none (0%) for magnesium. Thus, we speculated this insulin-induced sharp drop in serum potassium levels as potentiating the patient's already existing advanced diabetic neuropathy, thereby leading to muscle cramping. However, attempting potassium supplementation for a brief period of time led to a rapid resolution of cramps when they occurred and an overall reduction in their frequency of recurrence. This tilted our diagnosis toward the insulin-induced acute drop in serum potassium levels as the most likely etiology underlying the patient's cramps. Such an observation has been made only once previously within the literature, back in 1992, at the Duke University Medical Center.
一名56岁的中东男性,患有长期控制不佳的2型糖尿病,前来就诊,抱怨在注射速效胰岛素类似物后不久,双侧上下肢出现严重疼痛性痉挛。痉挛始于6个月前,从那时起间歇性发作,毫无规律。在此之前,他从未经历过任何与胰岛素相关的不良反应。他的痉挛非常疼痛且使人虚弱,干扰了他的日常活动,使他一直处于对再次发作的恐惧/焦虑状态。这导致他不遵守规定的治疗方案,也不配合后续的治疗计划。全面检查显示下肢感觉弥漫性丧失。随后的肌电图 - 神经传导联合研究证实了这一点,该研究表明存在广泛的糖尿病性轴索性多发神经病。相比之下,下肢节段性动脉压排除了外周血管闭塞性疾病,排除了血管功能不全作为痉挛可能病因的可能性。然后,我们在给患者注射胰岛素之前和之后30分钟测量了血清电解质水平。钾从初始水平下降了约16%,而钙仅下降了约4%,镁则没有下降(0%)。因此,我们推测胰岛素引起的血清钾水平急剧下降加剧了患者已有的晚期糖尿病神经病变,从而导致肌肉痉挛。然而,在痉挛发作时尝试短时间补充钾,导致痉挛迅速缓解,且复发频率总体降低。这使我们的诊断倾向于胰岛素引起的血清钾水平急性下降是患者痉挛最可能的病因。早在1992年,在杜克大学医学中心的文献中就曾有过一次这样的观察。