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Friday, August 24, 2007

Paroxetine-Induced Hyponatremia in Older Adults

Ever heard of the file drawer effect?

Did GlaxoSmithKline keep this hidden from us all during the Paroxetine clinical trials?

For those of you who don't know hyponatremia is explained here:

Severe hyponatremia may cause osmotic shift of water from the plasma into the brain cells. Typical symptoms include nausea, vomiting, headache and malaise. As the hyponatremia worsens, confusion, diminished reflexes, convulsions, stupor or coma may occur. Since nausea is, itself, a stimulus for the release of ADH, which promotes the retention of water, a positive feedback loop may be created and the potential for a vicious circle of hyponatremia and its symptoms exists.

Basically ladies and gentlemen hyponatremia is the zaps. We all know what the zaps are don't we? It seems GlaxoSmithKline must have known to. Such a valuable tool is the file drawer effect. I'm sure GlaxoSmithKline lawyers know what it is too.

Now I'd like to ask GlaxoSmithKline, the FDA or the MHRA what constitutes an 'older adult'?

Are we to assume that it is someone over the age of 30,40,50,60?

Surprising that the young and the old seem to be being safeguarded by the various studies out there - what about those that don't fall into these catagories? To be honest I'm unsure as to what catagory I would fall into - I'm 43 now, was 33 (I think) when I first took Seroxat.

Now did GlaxoSmithKline throw hyponatremia into the file drawer effect vault as they did with study 329?

You tell me.

Fid

A 12-Week Prospective Study

Tanya J. Fabian, PharmD; Janet A. Amico, MD; Patricia D. Kroboth, PhD; Benoit H. Mulsant, MD; Sharon E. Corey, PhD; Amy E. Begley, MA; Salem G. Bensasi, BS; Elizabeth Weber, RN, CNP; Mary Amanda Dew, PhD; Charles F. Reynolds III, MD; Bruce G. Pollock, MD, PhD

Arch Intern Med. 2004;164:327-332.

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 underrecognized 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.
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