OBJECTIVE: To investigate the circadian variation of plasma antidiuretic hormone (ADH) and urine output in patients with severe nocturia (> three times per night) and to assess the effect of oral desmopressin on nocturnal urine output in these patients. PATIENTS AND METHODS: Twelve patients with severe nocturia and five age-matched controls without were assessed over 24 h (circadian sampling) during a 72-h hospital admission. Blood levels of ADH and changes of urine output were measured in the patients before and after the oral administration of desmopressin (0.2 mg, at 22.00 hours in the second day), and in the controls not treated with desmopressin. RESULTS: Compared with the normal control, the patients had no diurnal variation in urine output and greater nocturnal urine production, associated with a lack of nocturnal increase in ADH level. Compared with the baseline urine output, desmopressin significantly decreased night-time (23.00-08.00 hour) urine output in the patients (P < 0.05). Desmopressin significantly increased the osmolality of night-time urine (P < 0.05), and there was no systemic adverse reaction. CONCLUSIONS: Severe nocturia in a large proportion of elderly men with lower urinary tract symptoms is caused by nocturnal polyuria and natriuresis, because they have no nocturnal increase in ADH. These results suggest that desmopressin may be effective in decreasing nocturnal urine production in patients with severe nocturia who do not respond to conventional treatment.
OBJECTIVE: To investigate the circadian variation of plasma antidiuretic hormone (ADH) and urine output in patients with severe nocturia (> three times per night) and to assess the effect of oral desmopressin on nocturnal urine output in these patients. PATIENTS AND METHODS: Twelve patients with severe nocturia and five age-matched controls without were assessed over 24 h (circadian sampling) during a 72-h hospital admission. Blood levels of ADH and changes of urine output were measured in the patients before and after the oral administration of desmopressin (0.2 mg, at 22.00 hours in the second day), and in the controls not treated with desmopressin. RESULTS: Compared with the normal control, the patients had no diurnal variation in urine output and greater nocturnal urine production, associated with a lack of nocturnal increase in ADH level. Compared with the baseline urine output, desmopressin significantly decreased night-time (23.00-08.00 hour) urine output in the patients (P < 0.05). Desmopressin significantly increased the osmolality of night-time urine (P < 0.05), and there was no systemic adverse reaction. CONCLUSIONS: Severe nocturia in a large proportion of elderly men with lower urinary tract symptoms is caused by nocturnal polyuria and natriuresis, because they have no nocturnal increase in ADH. These results suggest that desmopressin may be effective in decreasing nocturnal urine production in patients with severe nocturia who do not respond to conventional treatment.