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Case Reports in Medicine
Volume 2011, Article ID 145856, 5 pages
http://dx.doi.org/10.1155/2011/145856
Case Report

Arginine Vasopressin-Independent Mechanism of Impaired Water Excretion in a Patient with Sarcoidosis Complicated by Central Diabetes Insipidus and Glucocorticoid Deficiency

1Department of Internal Medicine, Osaka City Sumiyoshi Hospital, 1-2-16, Higashikagaya, Suminoeku, Osaka City, Osaka 559-0012, Japan
2Department of Internal Medicine, Osaka City Juso Hospital, Osaka 532-0034, Japan
3Department of Endocrinology and Metabolism, Osaka City General Hospital, Osaka 534-0021, Japan
4Department of Pathology, Osaka City General Hospital, Osaka 534-0021, Japan

Received 13 February 2011; Accepted 7 June 2011

Academic Editor: Masahiro Kohzuki

Copyright © 2011 Katsunobu Yoshioka et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.5–4.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels during the hypertonic saline test. In conclusion, we showed in human study that masked diabetes insipidus could be mediated by AVP-independent mechanisms.