Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus

Background: 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...

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Autores principales:	Mizuki Gobaru, MD, Kentaro Sakai, MD, Yuki Sugiyama, MD, Chiaki Kohara, MD, Akiko Yoshimizu, MD, Rei Matsui, MD, Yuichi Sato, MD, Tatsuo Tsukamoto, MD, Kenji Ashida, MD, Harumichi Higashi, MD
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	nephrogenic diabetes insipidus central diabetes insipidus hyperglycemic hyperosmolar syndrome Diseases of the endocrine glands. Clinical endocrinology RC648-665
Acceso en línea:	https://doaj.org/article/f6a3a05038e54422a3bce5902a8fbdea
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spelling	oai:doaj.org-article:f6a3a05038e54422a3bce5902a8fbdea2021-11-06T04:32:54ZTransient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus2376-060510.1016/j.aace.2021.06.009https://doaj.org/article/f6a3a05038e54422a3bce5902a8fbdea2021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2376060521000821https://doaj.org/toc/2376-0605Background: 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. Case Report: 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•H2O, 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. Conclusion: 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.Mizuki Gobaru, MDKentaro Sakai, MDYuki Sugiyama, MDChiaki Kohara, MDAkiko Yoshimizu, MDRei Matsui, MDYuichi Sato, MDTatsuo Tsukamoto, MDKenji Ashida, MDHarumichi Higashi, MDElsevierarticlenephrogenic diabetes insipiduscentral diabetes insipidushyperglycemic hyperosmolar syndromeDiseases of the endocrine glands. Clinical endocrinologyRC648-665ENAACE Clinical Case Reports, Vol 7, Iss 6, Pp 372-375 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	nephrogenic diabetes insipidus central diabetes insipidus hyperglycemic hyperosmolar syndrome Diseases of the endocrine glands. Clinical endocrinology RC648-665
spellingShingle	nephrogenic diabetes insipidus central diabetes insipidus hyperglycemic hyperosmolar syndrome Diseases of the endocrine glands. Clinical endocrinology RC648-665 Mizuki Gobaru, MD Kentaro Sakai, MD Yuki Sugiyama, MD Chiaki Kohara, MD Akiko Yoshimizu, MD Rei Matsui, MD Yuichi Sato, MD Tatsuo Tsukamoto, MD Kenji Ashida, MD Harumichi Higashi, MD Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus
description	Background: 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. Case Report: 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•H2O, 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. Conclusion: 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.
format	article
author	Mizuki Gobaru, MD Kentaro Sakai, MD Yuki Sugiyama, MD Chiaki Kohara, MD Akiko Yoshimizu, MD Rei Matsui, MD Yuichi Sato, MD Tatsuo Tsukamoto, MD Kenji Ashida, MD Harumichi Higashi, MD
author_facet	Mizuki Gobaru, MD Kentaro Sakai, MD Yuki Sugiyama, MD Chiaki Kohara, MD Akiko Yoshimizu, MD Rei Matsui, MD Yuichi Sato, MD Tatsuo Tsukamoto, MD Kenji Ashida, MD Harumichi Higashi, MD
author_sort	Mizuki Gobaru, MD
title	Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus
title_short	Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus
title_full	Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus
title_fullStr	Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus
title_full_unstemmed	Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus
title_sort	transient antidiuretic hormone insufficiency caused by severe hyperosmolar hyperglycemic syndrome based on nephrogenic diabetes insipidus
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/f6a3a05038e54422a3bce5902a8fbdea
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Transient Antidiuretic Hormone Insufficiency Caused by Severe Hyperosmolar Hyperglycemic Syndrome Based on Nephrogenic Diabetes Insipidus

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