TY - JOUR
T1 - Syndrome of inappropriate secretion of antidiuretic hormone associated with angiotensin-converting enzyme inhibitor therapy in the perioperative period
AU - Nakayama, Takashin
AU - Fujisaki, Hiroto
AU - Hirai, Shintaro
AU - Kawauchi, Ruri
AU - Ogawa, Kyohei
AU - Mitsui, Ayaka
AU - Hirano, Keita
AU - Isozumi, Kazuo
AU - Takahashi, Takayuki
AU - Komatsumoto, Satoru
N1 - Publisher Copyright:
© The Author(s) 2019.
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Introduction: Angiotensin-converting enzyme (ACE) inhibitors are one of the most commonly used medications for hypertension. Rarely, ACE inhibitors have the potential to cause a syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Case presentation: A 70-year-old woman with > 10 years ACE inhibitor therapy with normonatremia suddenly developed severe SIADH when she took a liquid diet in the uneventful perioperative period, with hemodynamic stability and no surgical complications. She promptly recovered from SIADH subsequent to discontinuing the ACE inhibitor therapy and changing her diet. Therefore, it was assumed that excess antidiuretic hormone secretion due to an ACE inhibitor and free water load from the liquid diet contributed to hyponatremia in our patient. Conclusion: Patients treated with an ACE inhibitor can latently experience inappropriate secretion of antidiuretic hormone, and rapidly develop severe hyponatremia together with additional factors affecting water or salt homeostasis regardless of the length of the administration duration. Clinicians should monitor serum sodium levels in such patients not only just after the initiation of ACE inhibitors but also upon the appearance of those factors.
AB - Introduction: Angiotensin-converting enzyme (ACE) inhibitors are one of the most commonly used medications for hypertension. Rarely, ACE inhibitors have the potential to cause a syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Case presentation: A 70-year-old woman with > 10 years ACE inhibitor therapy with normonatremia suddenly developed severe SIADH when she took a liquid diet in the uneventful perioperative period, with hemodynamic stability and no surgical complications. She promptly recovered from SIADH subsequent to discontinuing the ACE inhibitor therapy and changing her diet. Therefore, it was assumed that excess antidiuretic hormone secretion due to an ACE inhibitor and free water load from the liquid diet contributed to hyponatremia in our patient. Conclusion: Patients treated with an ACE inhibitor can latently experience inappropriate secretion of antidiuretic hormone, and rapidly develop severe hyponatremia together with additional factors affecting water or salt homeostasis regardless of the length of the administration duration. Clinicians should monitor serum sodium levels in such patients not only just after the initiation of ACE inhibitors but also upon the appearance of those factors.
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U2 - 10.1177/1470320319834409
DO - 10.1177/1470320319834409
M3 - Article
C2 - 30843458
AN - SCOPUS:85062636061
SN - 1470-3203
VL - 20
JO - JRAAS - Journal of the Renin-Angiotensin-Aldosterone System
JF - JRAAS - Journal of the Renin-Angiotensin-Aldosterone System
IS - 1
ER -