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PubMed2004

A case of gastric cancer initially presenting with polydipsia.

Metastatic brain tumors from gastric cancer are extremely rare. A 61-year-old Korean woman, initially presenting with polydipsia and polyuria, was found to have metastatic lesions in the brain by MRI. We performed several diagnostic procedures to determine the origin of the brain metastases. She was revealed to have a soft tissue mass of the right adrenal gland and fungating ulcers in the stomach. Histologic studies of both the adrenal gland mass and gastric tissues revealed malignant tumors composed of anaplastic cells. Based on the electron microscopy study, the malignant tumor of the right adrenal gland was a metastatic lesion from the anaplastic carcinoma of stomach. Therefore, the malignant tumors of the brain were assumed to have originated from the gastric cancer. This case report is presented to make clinicians aware of the possibility that diabetes insipidus (polydipsia) may present as an initial manifestation of brain metastases.

Adrenal Gland Neoplasms↗
PubMed1998

Effects of d-amphetamine, diazepam and buspirone on schedule-induced polydipsia suppressed by response-dependent and response-independent shock.

Food deprived Wistar rats were exposed to a fixed time 60 s food schedule until they developed schedule-induced polydipsia. Rats were matched in pairs according to their licking rate, being designated experimental or yoked control at random. Every fifth lick by experimental rats was then followed by an electric shock (0.05, 0.1, or 0.2 mA) while the food schedule continued in operation. Yoked-control rats received the same shocks as experimental rats, but independently of their own licking. Drugs were then tested on the suppressed rates of licking. Diazepam (0.5-2.0 mg/kg) increased punished schedule-induced polydipsia, a result not observed in yoked controls. No increases in the licks per minute of experimental or control animals were found after d-amphetamine (0.25-4.0 mg/kg) or buspirone (0.5-8.0 mg/kg). In comparison with previous results it is concluded that the antipunishment effects of drugs on schedule-induced behaviour depend on the type of punishment contingency.

Adrenergic Agents↗
PubMed1999

Congenital renal dysplasia and psychogenic polydipsia in a Bernese mountain dog.

Congenital renal dysplasia was tentatively diagnosed, based on ultrasound and an intravenous urogram, in a 5-month-old female with polyuria and polydipsia. Creatinine clearance measurement revealed that the renal dysplasia was not the cause of the polyuria. A modified water deprivation test eliminated other differential diagnoses and confirmed psychogenic polydipsia.

Animals↗
PubMed2006

[Polyuria and polydipsia due to renal diabetes insipidus during the use of lithium].

Polyuria, thirst and polydipsia due to renal diabetes insipidus (RDI) are common side effects of long-term lithium treatment. In a man aged 56 years, the polyuria could be reduced considerably by diuretics. However, as shown in the case of a 49-year-old man, such treatment carries the risk of acute lithium intoxication due to volume depletion and reduced renal lithium clearance. A reduction in the dose of lithium prior to diuretic treatment is therefore mandatory. Although polyuria and polydipsia are generally mainly a nuisance, the condition may become life-threatening when free access to fluids is impossible. This is demonstrated by the case of a 46-year-old man who was on chronic lithium treatment with probable RDI and who developed fatal severe dehydration and hypernatraemia after traumatic brain injury. Awareness of the possibility of RDI in patients on chronic lithium treatment is therefore important.

Diabetes Insipidus, Nephrogenic↗
PubMed1979

Long-term estrogenization in mammals. I. Histopathology of kidney, bladder, adrenals, and gonads; polydipsia; body weight; and serum levels of corticosterone and testosterone in estrogenized Marsh mice.

Single, sublethal, long-acting doses of estrone or estradiol cypionate produced the following histologic, behavioral, and blood chemistry effects in Marsh mice: (a) Bladder pathology developed following estrogen-induced polydipsia but was not consistently associated with kidney damage. (b) This polydipsia was more intense (a maximum of 250% over control intake) when the housing was in metal cages with floor screens than in plastic cages with bedding. Water intake of control mice was unaffected by housing changes. (c) Comparing litter-mate 2.5-month-old males and females, body weight loss following estrogen administration was transient with the females. With males, initial weight losses as compared with weight gains in the controls were demonstrated over a 20-week period. (d) Estrogenization markedly increased corticosterone and decreased testosterone serum levels with a significant negative correlation for these levels in the estrogenized mice. A significant positive correlation was also observed between testosterone levels and testis weights in the estrogenized mice.

Adrenal Glands↗
PubMed1983

Somatic findings in patients with psychogenic polydipsia.

An epidemiologic investigation found a 17.5% prevalence of psychogenic polydipsia in 241 hospitalized psychiatric patients. A randomly selected sample of 10 polydipsic patients revealed such associated disorders as sporadic convulsive seizures, comatose states, hydronephrosis, enuresis/urinary incontinence, projectile type vomiting, malnutrition and, in one case, cardiomegaly and edema. Psychogenic polydipsia is a frequently overlooked disorder, and the somatic consequences of the excessive fluid intake are usually ascribed to other causes.

Drinking↗
PubMed1981

Vasopressin secretion in primary polydipsia and cranial diabetes insipidus.

Vasopressin secretion was studied in a group of 18 patients with polydipsia (urine volume greater than 21/24 h) in whom nephrogenic diabetes insipidus had been excluded. Osmoregulation of vasopressin release was defined by hypertonic saline infusion, and three independent non-osmotic tests of vasopressin release were also applied. A wide spectrum of abnormalities in vasopressin secretion was observed. Four patients seem to have primary polydipsia, since they showed a normal response to osmotic stimulation, but non-osmotic vasopressin release was subnormal in two. The remaining 14 patients had cranial diabetes insipidus, as judged by subnormal or absent vasoprsssin responses to hypertonic saline infusion. Of these 14, five had undetectable vasopressin during osmotic stimulation, but each mounted a response to the non-osmotic stimuli; three of these had familial polyuria. Three further patients appeared to have isolated osmoreceptor defects, showing normal responses to non-osmotic stimuli but none to osmotic stress. Four patients with partial cranial diabetes insipidus, as judged by subnormal vasopressin response to osmotic stimuli, seemed to have normal osmoreceptor function but deficient vasopressin release. There was no correlation between the degree of vasopressin response to osmotic stimuli and the three non-osmotic tests of vasopressin release, and in particular vasopressin release should not replace osmotic tests to define cranial diabetes insipidus.

Adult↗
PubMed1980

[Partial defect in the secretion of antidiuretic hormone and disproportionate polydipsia (author's transl)].

A 20-year-old patient was evaluated because of polydipsia and polyuria; by means of the dehydration test a partial defect in the secretion of antidiuretic hormone (ADH) was demonstrated, since the urinary osmolality after the administration of exogenous vasopressin was superior by 25 percent to the maximum spontaneous urinary osmolality reached after a period of fluid restriction. Nevertheless, there was also a component of psychogenic polydipsia because the daily basal fluid intake was superior to 15 liters, and in view of the fact that the urinary osmolality could reach 600 mOsm/kg, the endocrine defect cannot totally be responsible for the enormous volume of fluid intake. This is the first case in the world literature in which the association between potomania and deficiency in the secretion of ADH is reported. Since ADH is one of the factors which regulate the behaviour of various animal species it is possible that its deficiency may be directly responsible for the psychic disorder which led to the potomania. It is also possible that an anatomical hypothalamic lesion, too small to be demonstrated, might have a simultaneous effect on the centers regulating thirst and the neurons producing vasopressin.

Adult↗
PubMed1980

Psychogenic polydipsia with hydronephrosis in an infant.

Psychogenic polydipsia can occur in infants and may be associated with urinary tract dilation. It is not known whether this dilation can lead to a decline in renal function, as has been reported in patients with diabetes insipidus and hydronephrosis. The structural changes may be reversed by treatment of polydipsia through fluid restriction and counseling.

Humans↗
PubMed1980

Long-term estrogenization in mammals. II. Environmental influences of housing conditions upon estrogen-induced polydipsia and food intake in Marsh mice.

Estrogen-induced polydipsia was influenced by environmental conditions in which Marsh mice were housed in plastic cages with bedding or in metal cages having grilled floors and no bedding. Increases in this polydipsia with metal-cage housing were reversed upon return to plastic. The increases over controls as ml/kg body weight ranged from 40 to 250%. After an initial fall in food consumption following estrogenization, controls and estrogenized mice consumed nearly the same amount of food/mouse but 10% more for the estrogenized mice on a g/kg body-weight basis. Increased food consumption for controls and estrogenized mice following the change from plastic to metal cages was attributed to compensation for increased loss of body heat. Whether in plastic or metal cages, core temperatures of controls were higher than those of estrogenized mice; both groups had relatively higher temperatures in the metal cages. The older mice in metal cages developed a gnawing pattern wasting food. In five experiments with males, body-weight losses following estrogenization were maintained 43 to 70 days but recovered in 2 of 4 experiments with females under comparable conditions.

Animals↗
PubMed1980

Fatal water intoxication in a case of psychogenic polydipsia.

The term "water intoxication" is used to describe a condition of agitation, delirium, convulsion, and coma brought on by excessive intake of water, resulting in severe hyponatremia. Psychogenic polydipsia (compulsive water drinking) has until recently been considered a relatively benign process. Since 1974, however, three fatal cases of water intoxication, resulting from psychogenic polydipsia, have been reported. All three individuals died while hospitalized, thereby permitting performance of blood electrolyte determinations and documentation of the associated electrolyte imbalance. In the authors' case, there was a well-documented prior episode of water intoxication in which serum electrolytes showed a pattern typical of this entity. Death, however, occurred at home, thus preventing valid serum electrolyte determinations to be performed. Analysis of the vitreous humor revealed a severe hyponatremia, thus substantiating the diagnosis of fatal water intoxication. This case, once again, points out the usefulness of electrolyte analyses on the vitreous humor as an aid to establishing a cause of death.

Chlorides↗
PubMed1980

Hyponatremia in psychogenic polydipsia.

Twenty psychotic patients with psychogenic polydipsia had hyponatremia (98 to 124 mEq/L) lasting up to 28 months, with headache, hypertension, dementia, seizures, lethargy, and coma. Two deaths also may be attributed to this syndrome. Patients drank 7 to 43 L of water daily. Urine was dilute during this water load (37 to 95 mOsm/kg), and free water clearance ranged from 12 to 36 L/day, while plasma osmolality was 236 to 244 mOsm/kg. During fluid deprivation in seven such patients, urinary osmolality exceeded plasma osmolality when plasma concentration had risen to between 242 and 272 mOsm/kg, thus suggesting a "reset osmostat" or antidiuretic hormone response to nonosmotic stimuli. This tended to sustain hyponatremia. Polydipsia should be recognized as a cause of hyponatremia, perhaps with reset osmostat. This ultimately may cause dementia or death, possibly secondary to recurrent cerebral edema. This sequence of events is potentially preventable or correctable.

Adult↗
PubMed1994

Differential effects of neuroleptic and clozapine on polydipsia and intermittent hyponatremia.

Recent reports indicate that clozapine may dramatically decrease both polydipsia and intermittent hyponatremia associated with chronic psychosis. In contrast, there are conflicting reports regarding the impact of standard neuroleptic treatment in this syndrome. We review the relevant literature examining the effects of antipsychotics on the excessive thirst drive and inordinate arginine vasopressin activity observed in patients with water intoxication. Confounding interpretation of the current literature are inconsistent use of diagnostic criteria and treatment outcome measures. If results of preliminary trials is substantiated, clozapine treatment may provide an opportunity to correct methodological problems and provide greater insight into the syndrome of polydipsia and intermittent hyponatremia.

Antipsychotic Agents↗
PubMed1994

Treatment strategies in the polydipsia-hyponatremia syndrome.

The clinician must first identify the patient at risk of developing water intoxication and its complications including seizures, coma, and death. In the polydipsic patient, behavioral approaches correcting or limiting polydipsia may prevent progression to dilutional hyponatremia. Drugs that oppose the central release or renal action of antidiuretic hormone will usually normalize morning serum sodium concentration in patients with the polydipsia-hyponatremia syndrome. The clinician can monitor such patients by observing diurnal changes in body weight. Specific interventions derive from specific weight changes. For the symptomatic patient suffering from water intoxication, intravenous administration of saline raising the serum sodium concentration to the 120-mmol/L range, followed by fluid restriction to further correct hyponatremia, will almost always successfully correct hyponatremia and protect against central pontine myelinolysis.

Behavior Therapy↗
PubMed1996

Besipirdine (HP 749) reduces schedule-induced polydipsia in rats.

The aim of the present paper is to report on the adrenergic and serotonergic effects of besipirdine (HP 749) in vivo and to discuss its potential use in the treatment of obsessive compulsive disorder. Besipirdine inhibited biogenic amine uptake in vitro. It prevented tetrabenazine-induced ptosis in mice and potentiated the 5-hydroxytryptophan-induced serotonin syndrome in rats. Furthermore, it decreased schedule-induced polydipsic behavior in rats. Schedule-induced polydipsia may be a model for obsessive compulsive disorder. Previous results from our group have shown that certain selective serotonin reuptake inhibitors decrease schedule-induced polydipsia after 14-21 days of treatment. Besipirdine reduced schedule-induced polydipsic behavior immediately and this reduction lasted throughout the duration of the experiment (29 days).

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1961

Production of polydipsia in normal rats by an intermittent food schedule.

Marked polydipsia was produced in all animals trained to press a bar for food pellets on a 1-minute variableinterval schedule. It is suggested that since this feeding arrangement produces a sustained, high fluid intake in the normal, unrestrained animal, it might serve as a useful tool in the study of renal function.

Animals↗
PubMed1963

Compulsive polydipsia with defective renal concentrating capacity.

Observations are presented on two patients with chronic compulsive polydipsia who showed a relative defect in renal concentrating capacity. After excluding all possible metabolic and renal causes of hyposthenuria and after obtaining normal kidney biopsies, both patients were studied in metabolic balance on a constant diet under the following conditions: (a) dehydration (loss of 3-5% body weight), (b) water loading and response to hypertonic saline, and (c) water loading and response to intravenous vasopressin (Pitressin). Throughout these studies the following parameters were observed: plasma and urine osmolality, glomerular filtration rate (inulin), renal plasma flow (P.A.H.), osmolar clearance and clearance of free water. In both patients the concentration defect was not related to variations in glomerular filtration rate or osmotic load. There was no correlation between the degree of hypoosmolality and the renal concentrating defect. Contrary to reports from other laboratories, restriction of water intake and chronic administration of intramuscular vasopressin did not correct the concentration defect.

Arginine Vasopressin↗