Compulsive Water Research Articles

Compulsive water drinking and water intoxication

Compulsive water drinking and water intoxication

Histiocytosis X and compulsive water drinking: report of a case

Histiocytosis X and compulsive water drinking: report of a case

Histiocytosis X and Compulsive Water Drinking

We describe a patient with histiocytosis X and compulsive water drinking. The association of diabetes insipidus with histiocytosis X is well recognized, and this patient was initially considered to have diabetes insipidus. It was only after further testing that the proper diagnosis was made.

Mechanism of carbamazepine (Tegretol)-induced antidiuresis: evidence for release of antidiuretic hormone and impaired excretion of a water load.

Four patients with central diabetes insipidus were studied to clarify the mechanism of antidiuretic action of carbamazepine (Tegretol). Oral administration of Tegretol to these patients resulted in a significant decrease in urine volume and in an elevation of U/P osmolar ratio to greater than 1. Antidiuretic hormone (ADH) concentrations in plasma also increased to normal range after the treatment. These studies indicated that the drug was acting through the release of endogenous ADH and thereby induced antidiuresis. During the course of therapy, an acute water load did not suppress ADH release, free water clearance remaining negative. Accordingly, it was concluded that the release of ADH during Tegretol therapy was controlled by the drug itself, not by physiological osmo- and volume-regulations. Tegretol was also effective in reducing polyuria in a patient with compulsive water drinking, but danger of water intoxication was great in this patient. Thus, Tegretol should not be given to this type of polyuria and caution should be exercised against water intoxication.

Psychosis, polydipsia, and water intoxication. Report of a fatal case.

In the absence of complicating medical illness, psychogenic polydipsia has been regarded as a fairly benign process. This paper reports on a case of rapidly fatal water intoxication secondary to psychogenic polydipsia in a psychotic woman. A review of the literature revealed a strong association between psychosis and water intoxication in compulsive water drinkers. The possible role of neuroendocrine changes in psychosis is discussed and the danger of thiazide diuretics in psychogenic polydipsia is emphasized.

Effect of ADH on Rat Renal Papilla, an Ultrastructural and Cytochemical Study

Diabetes insipidus and compulsive water drinking are representative of two categories of antidiuretic hormone (ADH) lack. We studied a strain of rats with congenital diabetes insipidus homozygote (DI) and normal rats on an isocaloric fortified dilute milk diet. In both cases, the collecting tubules could not concentrate urine. Special staining techniques, Alcian Blue-PAS for light microscopy and lanthanum nitrate for electron microscopy were used to demonstrate the changes in interstitial mucopolysaccharides (MPS). The lanthanum staining was done according to the method of Khan and Overton.Electron microscopy shows cytoplasmic lesions, vacules, swelling and degenerating mitochondria and intercellular spaces (IS) in the collecting tubule cells in DI and rats on milk diet.

Compulsive water drinking.

Back to table of contents Previous article Next article ArticleNo AccessCompulsive Water DrinkingWIEBKE K. THOMSEN, BRUCE PRINCE, and TERRY KILGOREWIEBKE K. THOMSENSearch for more papers by this author, BRUCE PRINCESearch for more papers by this author, and TERRY KILGORESearch for more papers by this authorPublished Online:1 Apr 2006https://doi.org/10.1176/ajp.130.5.610-aAboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail "Compulsive Water Drinking." American Journal of Psychiatry, 130(5), pp. 610-a–610 Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - American Journal of Psychiatry $35.00 Add to cart PPV Articles - American Journal of Psychiatry Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byJournal of Psychosomatic Research, Vol. 42, No. 5A Survey of Patient Attitudes toward Self-Induced Water Intoxication1 February 1992 | The Canadian Journal of Psychiatry, Vol. 37, No. 1Polydipsia and hyponatremia in psychiatric patients1 April 2006 | American Journal of Psychiatry, Vol. 145, No. 6Archiv f�r Psychiatrie und Nervenkrankheiten, Vol. 226, No. 4Comprehensive Psychiatry, Vol. 18, No. 2 Volume 130Issue 5 May 1973Pages 610-a-610 Metrics PDF download History Published online 1 April 2006 Published in print 1 May 1973

Psychogenic water intoxication: a case report.

The authors describe a case of a 41-year-old schizophrenic woman who was treated for water intoxication due to compulsive water drinking. The patient presented in a coma, with convulsions and evide...

Polydipsia, Hydrochlorothiazide, and Water Intoxication

On receiving therapeutic doses of hydrochlorothiazide, two long-term compulsive water drinkers developed acute hyponatremic encephalopathy. Although pure water intoxication is a possible explanation for their symptoms, the circumstances suggest that hydrochlorothiazide had an important role. The most likely mechanism was that the urinary sodium loss evoked by the drug compounded the effects of oral water loading and produced an acute hyponatremic state. Among other possible mechanisms considered was that hydrochlorothiazide depressed free water clearance.

Drugs for diabetes insipidus

Diabetes insipidus results from lesions of the supraoptic nuclei or the hypothalamo-hypophysial tract which limit secretion of vasopressin. Less commonly there is a renal defect, inherited predominantly by males, in which the tubules are unresponsive to vasopressin. Symptoms are thirst, polydipsia and excretion of large volumes of dilute but otherwise normal urine. These complaints are often temporary after hypophysectomy or head injury because damaged supraoptic fibres recover to secrete vasopressin. Tests described by de Wardener1 must be applied to establish the diagnosis and distinguish between diabetes insipidus and compulsive water drinking.

Coma and convulsions due to compulsive water drinking.

Coma and convulsions due to compulsive water drinking.

Primary polydipsia—compulsive water drinking: Report of two cases

Two children with primary polydipsia (compulsive water drinking) are reported. Each child had an organic central nervous system disease known to cause diabetes insipidus. However, each child concentrated urine normally and had a normal blood level of antidiuretic hormone. A background of common emotionality, similar to that observed in the compulsive eater, was noted clinically in both children and was substantiated by psychologic examination, thus suggesting the diagnosis of psychogenic polydipsia. However, as lesions of the central nervous system are known to effect the sensation of thirst, the primary polydipsia exhibited by both children could be attributed equally well to organic hypothalamic disease. The precise cause of the polydipsia exhibited by these children must, therefore, remain in doubt.

Differentiation of polyuric states by measurement of responses to changes in plasma osmolality induced by hypertonic saline infusions

Attention has been drawn to two important causes of potential misdiagnosis of diabetes insipidus when standard hypertonic saline infusion tests [1,2] are employed. The first of these results from the fact that the amount of saline solution infused may be inadequate to raise the plasma osmolality sufficiently to stimulate vasopressin release in persons who are excessively hydrated because of compulsive water drinking. The second source of potential misinterpretation results from the occurrence of abnormal natriuresis and osmotic diuresis during the saline infusion in some patients with anterior hypopituitarism. The osmotic diuresis prevents a decrease in urinary volume despite the occurrence of a demonstrably normal decrease in free water clearance in these subjects. These sources of potential error may be eliminated by measuring the urine and plasma osmolality during and after the hypertonic saline infusion, to ensure that plasma osmolality has been elevated at least to 296 mOsm. per kg. and to determine whether the free water clearance has fallen. Studies in thirty-eight hydrated normal subjects have shown that 5 per cent saline infusion at 0.05 ml. per kg. per minute causes a significant fall in free water clearance at a mean plasma osmolality of 288.5 mOsm. per kg., called the osmotic threshold for vasopressin release. The osmotic threshold was elevated significantly by cortisol to 293.2 mOsm. per kg. in normal subjects, and was similar in four patients with anterior hypopituitarism treated with cortisol (mean 294.8 mOsm. per kg.). No osmotic threshold could be found in any of ten patients with diabetes insipidus, despite elevation of the plasma osmolality by saline infusion to between 298 and 332 mOsm. per kg.

Multiple factors in thirst.

Multiple factors in thirst.