Y Kishi1, H Kurosawa, S Endo. 1. Department of Psychiatry, Nippon Medical School, Chiba Hokusoh Hospital, Japan.
Abstract
OBJECTIVE: Psychiatric patients presenting with polydipsia are often difficult to treat with standard psychiatric interventions. Pharmacological intervention was attempted in these patients based on the hypothesis that angiotensin II, a potent dipsinogen, may be involved in the drinking behavior of patients with polydipsia. Beta-blockers inhibit renin release (and thus indirectly angiotensin II) by blocking beta receptors in the kidney. METHODS: Three patients were identified as excessive water drinkers during their hospital admissions. All three patients were eunatremic but polydipsic at the time of study. Two of the three had histories of hyponatremia and required emergency medical treatment on more than one occasion. No patients had been controlled by strict fluid restriction. Trials of propranolol were initiated to control their water drinking. RESULTS: After starting propranolol, two patients responded quickly. In one patient, fluid intake decreased from 2650 +/- 647 to 1577 +/- 361, p < .001. In the other, fluid intake decreased from over 7000 ml before starting propranolol to around 3000 ml. The mean noon body weight of the third patient, in whom it was not possible to document fluid intake or urine volume before and after administering beta-blocker, was 72.6 +/- 2.6 Kg and 66.0 +/- 1.0 Kg, respectively (p < .0001). CONCLUSIONS: These results suggest that propranolol may be useful for the treatment of polydipsia in patients with schizophrenia. Its efficacy could be related to inhibition of the renin-angiotensin system. Additional research using the controlled pharmacotherapeutic trials is required to confirm these findings.
OBJECTIVE:Psychiatricpatients presenting with polydipsia are often difficult to treat with standard psychiatric interventions. Pharmacological intervention was attempted in these patients based on the hypothesis that angiotensin II, a potent dipsinogen, may be involved in the drinking behavior of patients with polydipsia. Beta-blockers inhibit renin release (and thus indirectly angiotensin II) by blocking beta receptors in the kidney. METHODS: Three patients were identified as excessive water drinkers during their hospital admissions. All three patients were eunatremic but polydipsic at the time of study. Two of the three had histories of hyponatremia and required emergency medical treatment on more than one occasion. No patients had been controlled by strict fluid restriction. Trials of propranolol were initiated to control their water drinking. RESULTS: After starting propranolol, two patients responded quickly. In one patient, fluid intake decreased from 2650 +/- 647 to 1577 +/- 361, p < .001. In the other, fluid intake decreased from over 7000 ml before starting propranolol to around 3000 ml. The mean noon body weight of the third patient, in whom it was not possible to document fluid intake or urine volume before and after administering beta-blocker, was 72.6 +/- 2.6 Kg and 66.0 +/- 1.0 Kg, respectively (p < .0001). CONCLUSIONS: These results suggest that propranolol may be useful for the treatment of polydipsia in patients with schizophrenia. Its efficacy could be related to inhibition of the renin-angiotensin system. Additional research using the controlled pharmacotherapeutic trials is required to confirm these findings.