Tomoyasu Masako, Mori Yusaku, Fukase Ayako, Kushima Hideki, Hirano Tsutomu
Division of Diabetes, Metabolism, and Endocrinology, Department of Internal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa, Tokyo, 142-8555, Japan.
J Med Case Rep. 2019 Jan 5;13(1):3. doi: 10.1186/s13256-018-1945-z.
There are several reports of pheochromocytoma crisis triggered by systemic glucocorticoid administration. However, pheochromocytoma crisis after intra-articular glucocorticoid administration has been rarely reported.
A 45-year-old Japanese man presented to our hospital with a sudden, severe headache. He had no history of diabetes. He had received an intra-articular injection of betamethasone (2 mg) for joint pain, 2 days prior to his admission. On examination, his blood pressure was 240/126 mmHg and pulse was 120 beats/minute. The possibility of cerebrovascular events was ruled out by imaging studies and lumbar puncture. Blood tests revealed severe hyperglycemia (523 mg/dL) and metabolic acidosis (pH 7.21, anion gap 26.2 mEq/L, lactate 11.75 mmol/L) with a glycosylated hemoglobin level of 5.7%. Although a urine sample could not be obtained, fulminant type 1 diabetes mellitus and diabetic ketoacidosis were suspected based on these findings. However, after the initial treatment for diabetic ketoacidosis, his insulin secretion was found to be normal and the plasma levels of ketones were not elevated. This excluded the possibility of fulminant type 1 diabetes mellitus and diabetic ketoacidosis. Subsequently, a left adrenal gland tumor and elevated levels of serum catecholamine and urinary catecholamine metabolites were detected, while his other hormone levels were normal. Serum catecholamine levels did not decrease following the clonidine test, and a functional scintigraphy using iodine-131 metaiodobenzylguanidine showed strong uptake in the region of the left adrenal gland. Although no signs of pheochromocytoma crisis, such as paroxysmal hyperglycemia and hypertension, had been observed since admission, a pheochromocytoma was diagnosed based on the investigations. After controlling his blood pressure, a left adrenalectomy was performed.
This case illustrates that intra-articular glucocorticoid administration can induce a pheochromocytoma crisis and an increase in hyperglycemia, and that pheochromocytoma crisis can resemble the clinical picture of fulminant type 1 diabetes mellitus owing to severe hyperglycemia with metabolic acidosis and normal glycosylated hemoglobin levels, especially under the influence of glucocorticoid.
有几篇关于全身应用糖皮质激素引发嗜铬细胞瘤危象的报道。然而,关节腔内注射糖皮质激素后发生嗜铬细胞瘤危象的情况鲜有报道。
一名45岁的日本男性因突发剧烈头痛前来我院就诊。他无糖尿病病史。入院前两天,他因关节疼痛接受了关节腔内注射倍他米松(2毫克)治疗。检查时,他的血压为240/126毫米汞柱,脉搏为120次/分钟。影像学检查和腰椎穿刺排除了脑血管事件的可能性。血液检查显示严重高血糖(523毫克/分升)和代谢性酸中毒(pH值7.21,阴离子间隙26.2毫当量/升,乳酸11.75毫摩尔/升),糖化血红蛋白水平为5.7%。尽管未能获取尿液样本,但基于这些发现怀疑为暴发性1型糖尿病和糖尿病酮症酸中毒。然而,在对糖尿病酮症酸中毒进行初始治疗后,发现他的胰岛素分泌正常且血浆酮水平未升高。这排除了暴发性1型糖尿病和糖尿病酮症酸中毒的可能性。随后,检测到左侧肾上腺肿瘤以及血清儿茶酚胺和尿儿茶酚胺代谢产物水平升高,而他的其他激素水平正常。可乐定试验后血清儿茶酚胺水平未降低,使用碘-131间碘苄胍的功能闪烁显像显示左侧肾上腺区域有强烈摄取。尽管自入院以来未观察到嗜铬细胞瘤危象的迹象,如阵发性高血糖和高血压,但根据检查诊断为嗜铬细胞瘤。控制血压后,进行了左侧肾上腺切除术。
该病例表明关节腔内注射糖皮质激素可诱发嗜铬细胞瘤危象并导致高血糖升高,且嗜铬细胞瘤危象可能类似于暴发性1型糖尿病的临床表现,原因是严重高血糖伴代谢性酸中毒且糖化血红蛋白水平正常,尤其是在糖皮质激素的影响下。