Journal of Postgraduate Medicine
 Open access journal indexed with Index Medicus & ISI's SCI  
Users online: 1904  
Home | Subscribe | Feedback | Login 
About Latest Articles Back-Issues Articlesmenu-bullet Search Instructions Online Submission Subscribe Etcetera Contact
 :: Next article
 :: Previous article 
 :: Table of Contents
 ::  Similar in PUBMED
 ::  Search Pubmed for
 ::  Search in Google Scholar for
 ::Related articles
 ::  [PDF Not available] *
 ::  Citation Manager
 ::  Access Statistics
 ::  Reader Comments
 ::  Email Alert *
 ::  Add to My List *
* Registration required (free) 

  IN THIS Article
 ::  Introduction
 ::  Case report
 ::  Discussion
 ::  Acknowledgement
 ::  References

 Article Access Statistics
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal

Year : 1981  |  Volume : 27  |  Issue : 1  |  Page : 40-1

Spontaneous transient inappropriate secretion of antidiuretic hormone.

How to cite this article:
Agarwal M B, Anjaria P D, Mehta B C. Spontaneous transient inappropriate secretion of antidiuretic hormone. J Postgrad Med 1981;27:40

How to cite this URL:
Agarwal M B, Anjaria P D, Mehta B C. Spontaneous transient inappropriate secretion of antidiuretic hormone. J Postgrad Med [serial online] 1981 [cited 2023 Sep 23];27:40. Available from:

  ::   Introduction Top

Systemic diseases of many types have been associated with the syndrome of inappropriate secretion of Antidiuretic hormone (SIADH). We recently observed a patient in whom SIADH developed transiently but no primary disorder could be isolated which could have caused excessive Antidiuretic hormone (ADH) release or production.

  ::   Case report Top

P.K., a 60 year old woman was admitted for progressive drowsiness over two days. Her previous history was unremarkable. She was neither a diabetic nor hypertensive and denied smoking or drinking alcohol. There was no evidence of head injury and she had not taken any drugs. Her examination was normal with blood pressure of 140/90 mm. of Hg. There was no evidence of dehydration and CNS was normal except for the altered sensorium. No focal deficit could be detected and meningeal signs were absent. Laboratory studies included a WBC count of 9600/c. mm. with P-60%, L.-38% and E.-2%; hemoglobin was 13.0 g.%; platelets were adequate; ESR was 10 mm. at the end of one hour; serum sodium was 112 mEq/liter; serum potassium--3.0 mEq/liter; serum chloride, 74 mEq/liter; and serum carbon dioxide 35 mEq/liter. BUN was 10 mg./dI; serum creatinine, 0.8 mg/dI; blood glucose, 125 mg/dI; and serum calcium, 10.0 mg/dI; urinalysis showed no protein or glucose; and sediment was unremarkable. Radiological studies of the skull and chest were normal. Electrocardiogram was normal.
The serum osmolality was 248 mosm/kg. and urinary osmolality was 452 mosm/kg. Twenty four hour urine collection showed the following levels; sodium 75 mEq/24 hours; potassium 25 mEq/24 hours; Chloride 52 mEq/24 hours, creatinine 540 mg/24 hours; and total volume, 800 ml. over 24 hours. CSF examination, liver function tests, brain scan, electroencephalogram and tri-Iodothyronine-charcoal uptake study were normal.
The patient was treated with water restriction to 700 ml/day and was given hypertonic saline (300 ml. of 5% saline every 24 hours for two days). She regained consciousness in three days. By one week, serum sodium had risen to 134 mEq/1. Water loading test carried out 10 days later, with one liter of water given orally during a four hour period was normal. The clinical picture continuously improved and the patient regained a normal sensorium in about two weeks. A repeat CSF examination was normal. She could not recollect any precipitating factor for her illness and has remained normal one year later. Mean while her barium study of the whole gut, intravenous pyelography, bronchoscopy, urinary ketogenic and keto-steroid estimations and a bone marrow study were carried out. They were all normal.

  ::   Discussion Top

The criteria laid down by Bartter and Schwartz[1] for diagnosis of SIADH were fulfilled in this patient. At the time of her severe and symptomatic hyponatremia, she excreted a concentrated urine, inappropriate to her hypoosmolar state. She had normal renal, hepatic, thyroid and adrenal functions and their was no evidence of cardiac decompensation. Patient had not taken any drugs in the preceding months. Intracranial disorders known to be associated with SIADH include subarachnoid hemorrhage, cerebrovascular accidents, head injury and various CNS infections.[2] Her investigations and clinical coarse were against any such possibility. Thus, most of the conditions that have been reported to cause SIADH were ruled out.
Idiopathic episodic inappropriate secretion of ADH has been reported once before.[3] In that case recurrent episodes of SIADH occurred over a period of several years in the apparent absence of a predisposing disease. It is important to know that this syndrome could occur spontaneously and is compatible with good prognosis.

  ::   Acknowledgement Top

We are thankful to Dr. C. K. Deshpande, Dean, K.E.M. Hospital for permission to publish the paper.

  ::   References Top

1.Bartter, F. C. and Schwartz, W. B.: The syndrome of inappropriate secretion of antidiuretic hormone. Amer. J. Med., 42: 790-806, 1967.  Back to cited text no. 1    
2.Goldberg, M. and Handler, J. S.: Hyponatraemia and renal wasting of sodium in patients with malfunction of central nervous system. New Eng. J. Med., 263: 1037-1043, 1960.  Back to cited text no. 2    
3.Grumer, H. A., Derryberry, W., Dubin, A. and Waldstein, S. S.: Idiopathic episodic inappropriate secretion of antidiuretic hormone. Amer. J. Med., 32: 954963, 1962.  Back to cited text no. 3    

Print this article  Email this article
Previous article Next article
Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
Published by Wolters Kluwer - Medknow