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

      case-report

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          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.

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          Most cited references15

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          Sarcoidosis and its neurological manifestations.

          Neurosarcoidosis is a disorder that is difficult to diagnose and manage. We assessed its neurological manifestations in 649 patients seen at The Johns Hopkins Hospital, Baltimore, from 1975 through 1980. Neurological problems could be attributed to neurosarcoidosis in 33 patients (5.1%). The presenting manifestation of sarcoidosis was neurological in 16 (48%) of them. Cranial neuropathy was the most frequent problem, and a peripheral facial nerve palsy was the single most common abnormality. Other manifestations were aseptic meningitis, hydrocephalus, parenchymatous disease of the central nervous system, peripheral neuropathy, and myopathy. Three-quarters of the patients were treated with steroids. The outcome was good in 27 (82%) of 33 episodes of neurological dysfunction in 25 patients with a well-documented clinical course. A thorough investigation of patients with suspected neurosarcoidosis is recommended to establish the diagnosis, delineate the extent of disease, and guide therapy.
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            Glucocorticoid inhibition of neurohypophysial vasopressin secretion.

            H Raff (1987)
            Several lines of evidence have suggested that neurohypophysial vasopressin secretion is under the influence of glucocorticoid negative feedback. Studies in clinical and experimental adrenal insufficiency have suggested that the impaired water excretion accompanying that syndrome may be due to elevated vasopressin levels. Furthermore, both the impaired water excretion and elevated vasopressin levels observed in adrenal insufficiency may be normalized by glucocorticoid treatment. This topic remains controversial, with a considerable body of evidence suggesting that vasopressin is elevated during adrenal insufficiency not because of a loss of central steroid negative feedback but because of alterations in plasma volume osmolality (renal mechanisms). Vasopressin responses to a variety of stimuli (hemorrhage, hypoxia, hypertonic saline) in normal humans and animals appear to be attenuated or eliminated by pretreatment with glucocorticoids. However, the vasopressinergic system appears to be considerably less sensitive to negative feedback than the corticotropin-releasing factor-adrenocorticotropic hormone (ACTH) system. There is evidence that the locus for this inhibitory effect is both directly at the posterior pituitary and within the hypothalamus. It is unlikely that corticosteroid negative feedback closes a direct hypothalamo-neurohypophysial-adrenocortical feedback loop. Since neurohypophysial vasopressin is involved in the control of ACTH secretion, it is more likely that the modulation of neurohypophysial vasopressin by glucocorticoid is an integral part of the overall negative-feedback control of ACTH secretion. The physiological role of glucocorticoid inhibition of vasopressin secretion remains speculative.
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              Neurosarcoidosis: clinical presentations and course in 50 patients.

              V Oksanen (1986)
              Fifty consecutive patients with neurosarcoidosis were evaluated retrospectively. Sarcoidosis presented first with neurologic signs in 24 patients (48%), but systemic symptoms developed later in all but five. Main neurologic involvements were central nervous system lesions in 33 patients (66%), cranial nerve paresis in 12 (24%), and peripheral nerve lesions in five patients (10%). Seventeen patients (34%) had more than one type of neurologic involvement. Routine cerebrospinal fluid (CSF) parameters showed unspecific abnormalities in 35 patients (70%). CSF angiotensin converting enzyme was elevated in 18 of 31 patients (58%). Brain computerized tomography was abnormal in 13 of 32 patients (41%). Visual and brainstem evoked potentials were abnormal in ten (43%) and eight (35%) of 23 patients, respectively, suggesting subclinical lesions in 13 patients. Neurologic signs improved in 24 patients (48%), were stable in 11 (22%), and progressed in 15 patients (30%). Six patients died. Cranial nerve lesions improved most often. Course of neurologic involvements was similar in acute or subacute and chronic sarcoidosis. The effect of steroid treatment was inconsistent.
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                Author and article information

                Journal
                Case Report Med
                CRIM
                Case Reports in Medicine
                Hindawi Publishing Corporation
                1687-9627
                1687-9635
                2011
                31 July 2011
                : 2011
                : 145856
                Affiliations
                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
                Author notes
                *Katsunobu Yoshioka: kmyoshi@ 123456rr.iij4u.or.jp

                Academic Editor: Masahiro Kohzuki

                Article
                10.1155/2011/145856
                3147132
                21811505
                2c4f8003-4a59-438e-8ccc-941810e062e9
                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.

                History
                : 13 February 2011
                : 7 June 2011
                Categories
                Case Report

                Medicine
                Medicine

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