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At least 145 records · Page 8Linked to original sources
PubMed2002

Risperidone failed to improve polydipsia-hyponatremia of the schizophrenic patients.

The effect of risperidone on polydipsia-hyponatremia was evaluated in six hospitalized schizophrenic patients. The normalized diurnal weight gain (NDWG), urine-specific gravity (USG), urine and plasma osmolarity, and serum sodium were monitored during 9 months of risperidone treatment. The dose of risperidone (mean +/- SD=8.0 +/- 1.0, range=6-9 mg/day) was determined as approximately half of the haloperidol-equivalent dose of previous neuroleptics. Before risperidone treatment, the mean (+/- SD) BPRS score was 23.5 +/- 7.1; no significant improvement was observed after risperidone (22.0 +/- 7.5). The subjects showed relatively high serum prolactin before risperidone treatment (mean +/- SD=16.5 +/- 9.7 ng/mL), that was not significantly decreased by risperidone (14.2 +/- 7.9 ng/mL). The monthly means (+/- SD) of NDWG and USG before risperidone were 5.5 +/- 1.5 (%) and 1.002 +/- 0.001, respectively. These and other indices did not significantly improve throughout the study period. Although the sample size is relatively small, our preliminary data showed that risperidone might not be effective on polydipsia-hyponatremia of schizophrenic patients.

Adult↗
PubMed1998

Factitious illness by proxy presenting as anorexia and polydipsia by proxy.

Factitious illness by proxy is a highly pathological form of parent-child relationship. To our knowledge no former case of polydipsia by proxy has been published. The case of a 2-y-old boy suffering from malnutrition due to displacement of maternal anorexia and polydipsia is presented. Child psychiatric evaluation found cognitive delay and psycho-social impairment in the child, as well as a severe mother-child relationship disturbance. Psychological assessment showed a personality disorder with depressive and paranoid features in the mother. The father was described as a schizoid personality. The possible mechanisms of displacement are hypothesized.

Anorexia↗
PubMed1990

Depression, episodic behavioral dyscontrol, and polydipsia following right temporal lobe damage.

A patient referred to the authors for evaluation and treatment of depression, behavioral dyscontrol syndrome, and polydipsia is described. The authors reviewed his medical status and, finding damage to his right temporal lobe, conceptualized his symptom constellation as representing interictal syndrome and treated him with carbamazepine. His affective symptoms, but not the polydipsia, improved following treatment with carbamazepine.

Adult↗
PubMedDate not supplied

Behavioral and medical treatment of chronic polydipsia in a patient with schizophrenia and diabetes insipidus.

OBJECTIVE: This case report describes a novel outpatient behavioral treatment intervention for chronic polydipsia. The program was used in an effort to reduce excessive fluid intake in a woman with chronic paranoid-type schizophrenia who also had a diagnosis of diabetes insipidus. METHODS: The 12-session individual behavioral intervention incorporated self-monitoring, stimulus control, coping skills training, and reinforcement components. RESULTS: The patient engaged fully in the treatment program, and she successfully restricted her fluid intake. Her diabetes insipidus could therefore be treated with desmopressin, a medication that requires fluid restriction, and she experienced a concomitant reduction in polyuria and urinary incontinence. CONCLUSIONS: The outpatient behavioral intervention demonstrated promising outcomes in a chronically mentally ill patient whose polydipsia had underlying psychogenic and physiological components. This case highlights the efficacy of combining behavioral and medical interventions.

Ambulatory Care↗
PubMed1984

Ingestive behavior evoked by hypothalamic stimulation and schedule-induced polydipsia are related.

Some, but not all, rats eat or drink in response to electrical stimulation of the lateral hypothalamus. Similarly, some, but not all, rats given food intermittently display schedule-induced polydipsia. In this experiment, animals that ate or drank during electrical stimulation tended also to be those displaying polydipsia. Thus, individual differences in predisposition to engage in ingestive behavior are consistent under two very different conditions.

Animals↗
PubMed1977

On the mechanism of polyuria in potassium depletion. The role of polydipsia.

The association of potassium (K) depletion with polyuria and a concentrating defect is established, but the extent to which these defects could be secondary to an effect of low K on water intake has not been systematically investigated. To determine whether hypokalemia has a primary effect to increase thirst and whether any resultant polyuria and polydipsia contribute to the concentrating defect, we studied three groups of rats kept in metabolic cages for 15 days. The groups were set up as follows: group 1, normal diets and ad lib. fluids (n = 12); group 2, K-deficient diet on ad lib. fluids (n = 12); and group 3, K-deficient diet and fluid intake matched to group 1 (n = 14). Daily urine flow and urinary osmolality of groups 1 and 3 were not significantly different throughout the study. In contrast, as of day 6, group 2 rats consistently had a higher fluid intake (P < 0.0025), higher urine flow (P < 0.001), and lower urinary osmolality (P < 0.001) than the other two groups. These alterations in fluid intake and urine flow preceded a defect in maximal concentrating ability. On day 7, maximal urinary osmolality was 2,599+/-138 msmol/kg in rats on K-deficient intake and 2,567+/-142 msmol/kg in controls. To determine whether this primary polydipsia is itself responsible for the development of the concentrating defect, the three groups of rats were dehydrated on day 15. Despite different levels of fluid intake, maximal urinary osmolality was impaired equally in groups 2 and 3 (1,703 and 1,511 msmol/kg, respectively), as compared to rats in group 1 (2,414 msmol/kg), P < 0.001. We therefore conclude that K depletion stimulates thirst, and the resultant increase in water intake is largely responsible for the observed polyuria. After 15 days of a K-deficient diet, the impaired maximal urinary concentration in hypokalemia, however, was not related to increased water intake, since fluid restriction did not abolish the renal concentrating defect.

Animals↗
PubMedDate not supplied

Successful treatment with captopril of an elderly man with polydipsia and hyponatremia.

A case of severe hyponatremia in a polydipsic 64-year-old man is described. He was unsuccessfully treated with both demeclocycline and lithium carbonate. However, low-dose captopril reversed the polydipsia and resulted in sustained normal serum sodium levels. We believe the antidipsogenic effect of captopril may benefit some patients with polydipsia and hyponatremia.

Brain Damage, Chronic↗
PubMed1988

Polydipsia in chronic psychiatric patients. Body weight and plasma sodium.

Eight chronic psychiatric in-patients with polydipsia, and polyuria, up to 22 litres per 24 hours, were studied by frequent timed body weight and urine volume measurements, and episodic plasma electrolyte estimations. During the day they all showed irregular water retention, with hyponatremia in proportion to the weight gain. During the night they always lost water and weight, returning to their individual lowest weights and to normal plasma sodium. Measurement of weight in chronic psychiatric patients can be used to identify patients with significant polydipsia, to monitor those with the disorder and permit targeted fluid restriction, and to assess the efficacy of treatment procedures such as medication.

Adult↗
PubMed1990

Vasopressin in chronic psychiatric patients with primary polydipsia.

Twelve chronic in-patients with primary polydipsia were studied, during free drinking and after fasting, by concurrent measurements of plasma AVP, serum sodium and osmolality, and urine volume, AVP, osmolality, and creatinine. A majority of the patients showed inappropriately high levels of AVP: plasma AVP estimations demonstrated that seven had Type I SIADH and two had Type II SIADH. Urinary AVP estimations confirmed inappropriately raised AVP in seven of the subjects tested, and there was a significant agreement between the plasma and urine diagnoses. Although able to concentrate their urine in response to fluid deprivation, the patients showed a decreased renal sensitivity to AVP. Despite the mitigating effect of decreased renal sensitivity to AVP, the SIADH seen in these patients appears to contribute to the development of water intoxication caused by polydipsia.

Adult↗
PubMed1996

The influence of polydipsia on water excretion in hyponatremic, polydipsic, schizophrenic patients.

To determine whether polydipsia is responsible for the altered water excretion in the subset of polydipsic schizophrenic patients who develop hyponatremia, the regulation of antidiuretic function was assessed in polydipsic schizophrenic patients with hyponatremia (n = 5), polydipsic schizophrenic patients without hyponatremia (n = 5), nonpolydipsic schizophrenic patients (n = 6), and normal controls (n = 8). The severity and duration of polyuria were similar in the two polydipsic groups. After oral water loading, maximal free water clearance was similar across all four groups. Free water clearance diminished, however, at lower plasma osmolalities in the hyponatremic polydipsics (P < 0.02) and at higher plasma osmolalities in the normonatremic polydipsics (P < 0.05) relative to that in the nonpolydipsic schizophrenics and normal subjects. The increase in plasma vasopressin after osmotic stimulation with hypertonic saline was slightly, but significantly (P < 0.02), blunted in both polydipsic groups. Hyponatremia occurs in some polydipsic schizophrenics because the relationship between free water clearance to plasma osmolality/sodium is shifted to the left. Polydipsia per se is not responsible for this still unexplained shift.

Adult↗
PubMedDate not supplied

Constipation, polyuria, polydipsia, and edema associated with orlistat.

OBJECTIVE: To report the occurrence of a novel group of adverse effects associated with initiation and rechallenge of orlistat. CASE SUMMARY: A 42-year-old white woman developed symptoms of constipation, polyuria, polydipsia, and increased lower-leg edema after 2 weeks of treatment with orlistat 120 mg 3 times daily. The drug was discontinued for 4 days and the symptoms resolved. On reinstitution of the orlistat treatment, the symptoms reappeared within 2 days. Thereafter, the medication was permanently discontinued. DISCUSSION: Common gastrointestinal adverse reactions associated with orlistat use include fecal urgency and abdominal pain and discomfort. Pedal edema has also been reported to occur, although less frequently. No reports were discovered documenting the occurrence of constipation, polydipsia, and polyuria associated with the use of orlistat. Despite careful consideration of other possible causes of these symptoms, the temporal association between initiation, discontinuation, and rechallenge of orlistat and the patient's symptoms suggest a medication-related adverse event. Based on the Naranjo probability scale, the likelihood that orlistat was the cause of this cluster of adverse effects is possible. CONCLUSIONS: It is important for the healthcare provider to be aware of these adverse effects to promptly evaluate and differentiate between possible causes of similar reactions.

Adult↗
PubMed2005

Rhabdomyolysis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone.

OBJECTIVE: To report a case of rhabdomyolysis related to correction of hyponatremia secondary to psychogenic polydipsia, possibly complicated by the use of ziprasidone. CASE SUMMARY: A 50-year-old white man treated for 3 weeks with ziprasidone 40 mg twice daily for chronic paranoid schizophrenia was admitted to the intensive care unit after a witnessed generalized seizure. Marked hypotonic hyponatremia was present secondary to psychogenic polydipsia. After correction of hyponatremia with intravenous NaCl 0.9%, he developed a substantial elevation in the creatine kinase level without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome. Renal failure or compartment syndrome did not complicate the clinical picture. DISCUSSION: It is well known that severe hyponatremia can cause neurologic complications such as stupor, seizures, and even coma. Hyponatremia from water intoxication (n = 28) and its correction with intravenous fluids (n = 2) may cause non-neurologic complications such as rhabdomyolysis. An explanation may lie within the calcium-sodium exchange mechanism across the skeletal myocyte or the failure of cell volume regulation secondary to extracellular hypo-osmolality. Neuroleptic medications have been linked to the development of rhabdomyolysis, with antipsychotics being the primary offenders. As of August 2005, there has been only one reported case of rhabdomyolysis related to correction of hyponatremia complicated by an atypical antipsychotic (clozapine). It is possible that ziprasidone, like clozapine, may enhance muscle cell permeability leading to rhabdomyolysis under similar conditions. CONCLUSIONS: Psychiatric patients treated with atypical antipsychotic medications should be closely monitored for rhabdomyolysis during correction of hyponatremia, thus permitting prompt therapy to limit its complications.

Antipsychotic Agents↗
PubMed1986

Neural lobe function in aged Wistar/Tw strain rats showing polydipsia and polyuria.

Neural lobe function in male rats of the Wistar/Tw strain was studied at 3, 7 and 16-18 months of age. A significant rise in the serum arginine vasopressin (AVP) level was noted in 16-18-month-old rats showing polydipsia and polyuria. The content and concentration of AVP in the neural lobe of aged rats were significantly less than those of younger animals (3 and 7 months). These results point out an enhancement of AVP release from the neural lobe of aged rats. The reduction in urinary volume in aged rats subjected to 24 hours of water deprivation was less than those in younger animals. No increase in urinary sodium, potassium and chloride concentrations was observed in aged rats, and the decrease in electrolyte excretion from urine during the dehydration period was less in aged rats than younger ones. These results suggest that the antidiuretic response to osmotic stimuli was reduced in aged rats. The administration of AVP to aged rats resulted in a significant decrease in water intake and urinary volume, but AVP administration did not induce any change in the electrolyte balance. Therefore, it is concluded that the main cause of the development of polydipsia and polyuria is the decline in renal function but not in neurosecretory activity, although exogenous AVP can effectively reduce water intake and urinary output in aged rats.

Aging↗
PubMed1966

Analysis of water and NaCl solution acceptance by schedule-induced polydipsia.

Animals were trained on a VI 1-min schedule for food pellets, and concurrent water intake was measured. The polydipsia induced was analyzed in terms of the frequency distribution of post-pellet licking burst sizes and the trend of polydipsia throughout the session. An ascending series of NaCl solutions was presented consecutively over daily sessions and a typical NaCl acceptance-rejection intake function was generated. Beginning in the 0.9-1.2% NaCl range, the animals drank less often during the session but took larger drinks when they did drink. Neither the frequency of drinks nor the mean licking burst size were simply related to the volumes of NaCl solution consumed. The NaCl acceptance-rejection function cannot be explained in terms of water repletion factors alone.

Animals↗
PubMed1977

Spaced food but not electrical brain stimulation induces polydipsia and air licking.

An attempt was made to induce polydipsia in rats whose lever pressing was reinforced with food pellets or electrical brain stimulation. Nine food-deprived, water-sated rats drank water excessively during sessions in which food pellets were delivered. When brain stimulation was substituted for food, drinking immediately ceased. Delivering brain stimulation according to a variety of schedules, pairing brain stimulation with food reinforcement, and substituting an air stream for water, each failed to produce polydipsic licking. These results show that polydipsia is not induced by all reinforcers.

Animals↗
PubMed1981

Stimulus generalization of schedule-induced polydipsia.

Five rats were exposed to an intradimensional discrimination by associating two tones of different frequency with the components of a multiple random-time 30-sec, extinction schedule of food presentation. After schedule-induced polydipsia developed and the intermittent schedule of food presentation established stable differential licking rates during the stimuli associated with the multiple schedule, a stimulus generalization test was conducted. When generalization testing was conducted by presenting stimuli that varied on the frequency dimension during the random-time 30-sec component of the multiple schedule, all five rats demonstrated moderately sloping symmetrical gradients. Thus, schedule-induced polydipsia can be brought under the control of stimuli other than the food pellet.

Journal Article↗
PubMed1994

Clozapine treatment of polydipsia.

A patient with refractory chronic schizophrenia having severe polydipsia and hyponatremia was treated with clozapine. There followed a dramatic improvement in the polydipsia and correction of the hyponatremia. This improvement has been sustained throughout a 6-month follow-up.

Adult↗