Interventions in Alzheimer's disease

✍ Scribed by Romola S. Bucks; Lucie Byrne; Judy Haworth; Gordon Wilcock; Julia Hyde; Catherine Emmerson; Deborah Spaull

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 31 KB
• Volume: 17
• Category: Article
• ISSN: 0885-6230
• DOI: 10.1002/gps.637

✦ Synopsis

Discussion

To date, the mechanism underlying drug-induced hyponatremia remains poorly understood. While some authors have suggested that the phenomenon may be a class effect of the SSRIs (Ball and Herzberg, 1994), others have cautioned that hyponatremia may develop with virtually any antidepressant (Committee on Safety of Medicines, 1994). To judge by the present findings, the electrolyte abnormality does not appear to relate specifically to the reuptake of serotonin. Several reports on hyponatremia following administration of venlafaxine, a norepinephrine reuptake inhibitor at higher doses, are in line with this view (Gupta and Saravay, 1997;Ranieri et al., 1997;Masood et al., 1998).

Symptom overlap can, at times, render difficult the differentiation of hyponatremia's clinical features from the symptomatology of depressive illness. The former may lead to mild cognitive impairment, slowing of thought and lethargy, thereby suggesting possible correlates of depressed mood. This may prompt augmentation of SNRI rather than discontinuation of treatment unless changes in sodium concentrations are taken into account. In the present case, hyponatremia was not severe and reversed by withdrawal of the antidepressant as in 96% of SSRI-related cases reviewed by Liu et al. (1996). Still, as SIADH following SSRI treatment has progressed to serious manifestations (Odeh et al., 2001), we considered a rechallenge to be unethical. On the grounds of our findings and a large body of evidence for SSRIinduced SIADH, we advocate regular monitoring for electrolyte changes in patients receiving reboxetine or another SNRI.