Gobaru Mizuki, Sakai Kentaro, Sugiyama Yuki, Kohara Chiaki, Yoshimizu Akiko, Matsui Rei, Sato Yuichi, Tsukamoto Tatsuo, Ashida Kenji, Higashi Harumichi
Department of Nephrology, Our Lady of the Snow Social Medical Corporation, St. Mary's Hospital, Kurume, Japan.
Department of Diabetes and Endocrinology, Our Lady of the Snow Social Medical Corporation, St. Mary's Hospital, Kurume, Japan.
AACE Clin Case Rep. 2021 Jun 18;7(6):372-375. doi: 10.1016/j.aace.2021.06.009. eCollection 2021 Nov-Dec.
The hyperosmolar hyperglycemic state (HHS), an acute complication of diabetes mellitus with plasma hyperosmolarity, promotes the secretion of anti-diuretic hormone (ADH) and reduces the storage of ADH. Magnetic resonance T1-weighted imaging reflects ADH storage in the posterior pituitary lobe, which disappears when the storage is depleted. Whether the HHS induces ADH depletion leading to clinical manifestations has been unclear.
A 55-year-old Japanese woman was admitted to our center because of mental disturbance and hypotension. She had received lithium carbonate for bipolar disorder and presented with polydipsia and polyuria from 15 years of age. On admission, she had mental disturbance (Glasgow Coma Scale, E4V1M1), hypotension (systolic blood pressure, 50 mmHg), and tachycardia (pulse rate, 123/min). Plasma glucose was 697 mg/dL osmolality was 476 mOsm/kg•HO, and bicarbonate was 23.7 mmol/L. The diagnoses of HHS and hypovolemic shock were made. During treatment with fluid replacement and insulin therapy, the urine volume continued to be approximately 3 to 4 L/day, and an endocrine examination revealed ADH insufficiency and nephrogenic diabetes insipidus. Desmopressin 10 μg/day and trichlormethiazide 2 mg/day were necessary and administered, and the endogenous ADH secretion improved gradually. The signal intensity of the pituitary posterior lobe, initially decreased on magnetic resonance T1 images, was also improved.
This patient had ADH insufficiency associated with ADH depletion due to hyperosmolarity and nephrogenic diabetes insipidus. Clinicians should be aware of the risk of the development of critical HHS and relative ADH insufficiency in patients being treated with lithium carbonate.
高渗高血糖状态（HHS）是糖尿病的一种急性并发症，伴有血浆高渗，可促进抗利尿激素（ADH）的分泌并减少其储存。磁共振T1加权成像反映ADH在后叶垂体的储存情况，当储存耗尽时该影像表现消失。HHS是否会导致ADH耗竭从而引发临床表现尚不清楚。
一名55岁的日本女性因精神障碍和低血压入住我院。她因双相情感障碍服用碳酸锂，自15岁起出现多饮和多尿症状。入院时，她有精神障碍（格拉斯哥昏迷量表评分E4V1M1）、低血压（收缩压50 mmHg）和心动过速（心率123次/分钟）。血浆葡萄糖为697 mg/dL，渗透压为476 mOsm/kg•H₂O，碳酸氢盐为23.7 mmol/L。诊断为HHS和低血容量性休克。在补液和胰岛素治疗过程中，尿量持续约为每天3至4升，内分泌检查显示ADH不足和肾性尿崩症。需要使用去氨加压素10 μg/天和三氯噻嗪2 mg/天，并逐渐改善了内源性ADH分泌。磁共振T1图像上最初降低的垂体后叶信号强度也有所改善。
该患者因高渗和肾性尿崩症导致ADH耗竭，伴有ADH不足。临床医生应意识到接受碳酸锂治疗的患者发生严重HHS和相对ADH不足的风险。
