Hostname: page-component-586b7cd67f-t7czq Total loading time: 0 Render date: 2024-12-01T07:40:19.238Z Has data issue: false hasContentIssue false

P-1117 - Paroxetine and Herpes Zoster

Published online by Cambridge University Press:  15 April 2020

E. Tzavellas
Affiliation:
Psychiatry, Eginition Hospital, University of Athens, Athens, Greece
D. Karaiskos
Affiliation:
Psychiatry, Eginition Hospital, University of Athens, Athens, Greece
J. Liappas
Affiliation:
Psychiatry, Eginition Hospital, University of Athens, Athens, Greece
S. Kanelli
Affiliation:
Psychiatry, Eginition Hospital, University of Athens, Athens, Greece
I. Theotoka
Affiliation:
Psychiatry, Eginition Hospital, University of Athens, Athens, Greece
T. Paparrigopoulos
Affiliation:
Psychiatry, Eginition Hospital, University of Athens, Athens, Greece

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Purpose of the study

Paroxetine is a selective serotonin reuptake inhibitor antidepressant. We present a case of a patient who developed herpes zoster 4 weeks after initiating paroxetine.

Methods

A 35 year old female was referred to our hospital due to obsessive compulsive disorder. She complained of intrusive thoughts of being contaminated and repetitive behaviors.

After a thorough laboratory and imaging tests she was prescribed paroxetine 40 miligrams daily.

Four weeks later she complained of pain followed by rash along the same dermatomal distribution in the lower abdominal area. The involved area was tender to palpation.

A detailed dermatologic evaluation was performed and the rash was attributed to herpes zoster. Despite the potential association of paroxetine with herpetic rash the patient continued treatment and was prescribed acyclovir and pain killers. One month later herpetic rash had fully remitted.

Conclusions

This is the first report of herpes zoster attributed to paroxetine therapy. The pathophysiological mechanism governing the effects of SSRIs in immune function is controversial. In vitro studies have shown that SSRIs decreased splenic lymphocyte proliferation while other studies have shown that chronic SSRI treatment is associated with a reduction of the number of leucocytes and neutrophils. It has been suggested that the immune effects of SSRIs are mediated by endogenously released serotonine, while T leymphocytes express 5HT receptors. Although a casual association of herpes zoster and paroxetine therapy cannot be attributed with the described case, further studies are needed to clarify under which circumstances, paroxetine could trigger herpetic rash.

Type
Abstract
Copyright
Copyright © European Psychiatric Association 2012
Submit a response

Comments

No Comments have been published for this article.