Paroxetine-induced hyponatremia in older adults: a 12-week prospective study.

BACKGROUND: Older depressed patients are at high risk for development of hyponatremia after initiation of the selective serotonin reuptake inhibitor paroxetine, despite clinical monitoring and preventive management. The purposes of this study were to determine the incidence and etiology of paroxetine-induced hyponatremia in older patients and to identify patient characteristics that may account for variability in susceptibility to this adverse event. METHODS: This prospective, longitudinal study was conducted in a university-based ambulatory psychiatric research clinic from August 1999 through September 2001. Patients included 75 men and women aged 63 through 90 years (mean +/- SD age, 75.3 +/- 6.0 years) who received a diagnosis of a current Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, major depressive episode and were prescribed paroxetine. We monitored plasma sodium levels before initiating paroxetine therapy and after 1, 2, 4, 6, and 12 weeks of treatment. In a subset of individuals, we measured levels of antidiuretic hormone, glucose, serum urea nitrogen, and creatinine. Hyponatremia was defined as a plasma sodium level of less than 135 mEq/L after initiation of paroxetine therapy. RESULTS: Hyponatremia developed in 9 (12%) of the 75 patients after initiation of paroxetine treatment. Mean +/- SD time to development of hyponatremia was 9.3 +/- 4.7 days (median, 9 days; range, 1-14 days; n = 8). In the multivariate regression, lower body mass index and lower baseline plasma sodium level (<138 mEq/L) were significant risk factors for the development of hyponatremia in these patients. CONCLUSIONS: Hyponatremia is an under recognized and potentially serious complication of paroxetine treatment in older patients. Our results provide a foundation for understanding the etiology and risk factors associated with paroxetine-induced hyponatremia.

Decreasing pain and anxiety associated with patient-activated atrial shock: a placebo-controlled study of adjunctive sedation with oral triazolam.

INTRODUCTION: Implantable atrial defibrillators (IADs) have proved to be safe and effective in the management of atrial fibrillation. A potential limitation of self-activated IAD therapy is patient-reported pain and anxiety. The main objective of the present study was to determine whether triazolam improved patient perception of the shock experience or altered patient memory of shock discomfort relative to placebo. METHODS AND RESULTS: A total of 15 men and women (mean age: 59 +/- 6 years) were enrolled in this double-blind, placebo-controlled, crossover study of triazolam. Randomized study medication was administered orally 75 minutes prior to scheduled atrial shock delivery. Patient perception of the shock experience was assessed along with sedation, memory, anxiety, and mood. Triazolam reduced mean pre-shock anxiety (t= 2.98, df = 14, P = 0.01) and shock-related pain (t= 2.74, df = 13, P = 0.01) and intensity (t= 2.64, df = 13, P = 0.018) relative to placebo. Similarly, participants recalled less discomfort the morning after shock with triazolam than with placebo (t= 2.82, df = 11, P = 0.017). CONCLUSIONS: This study was the first to investigate the use of an oral benzodiazepine administered prior to patient-activated shock delivery with an IAD. Our data indicate that oral triazolam is beneficial in decreasing pain and anxiety associated with self-activated atrial defibrillation. If triazolam provides a similar benefit in the community to that which has been reported here, this medication could be offered to patients as an adjunct to intermittent IAD therapy.