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Chlorpromazine-induced lupus with circulating anticoagulant. A case report

Published online by Cambridge University Press:  23 March 2020

W. Abbes
Affiliation:
Hédi Chaker University Hospital, Psychiatry “A”, Sfax, Tunisia
B. Imen
Affiliation:
Hédi Chaker University Hospital, Psychiatry “A”, Sfax, Tunisia
A. Hanene
Affiliation:
Faculty of Medicine of Sfax, Regional Pharmacovigilance Centre, Sfax, Tunisia
S. Mouna
Affiliation:
Hedi Chaker University Hospital, Department of Internal Medicine, Sfax, Tunisia
K. Kamilia
Affiliation:
Faculty of Medicine of Sfax, Regional Pharmacovigilance Centre, Sfax, Tunisia
B. Zouheir
Affiliation:
Faculty of Medicine of Sfax, Regional Pharmacovigilance Centre, Sfax, Tunisia
M. Jawaher
Affiliation:
Hédi Chaker University Hospital, Psychiatry “A”, Sfax, Tunisia

Abstract

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The drug-induced lupus erythematosus (DILE) is an autoimmune disorder caused by chronic use of certain drugs, including chlorpromazine. Chlorpromazine-induced lupus associated to circulating anticoagulant antibodies (CAC) would be even less frequent. Our observation is an illustration of this association.

We report the case of Mrs. H., 33-year-old, without medical or surgical history, who has been followed in psychiatry since the age of 20 for bipolar disorder type 1. This patient was initially stabilized by an association of fluphenazine, sodium valproate and levomepromazine. The introduction of chlorpromazine in June 2015 induced a leuconeutropenia, which was corrected after stopping this drug. During subsequent decompensations, rechallenge with chlorpromazine and administration of other phenothiazines (levomepromazine, fluphenazine) or atypical anti-psychotics (olanzapine, risperidone, aripiprazole) induced a leuconeutropenia reversible after drug withdrawal. Within the etiological investigation of this leuconeutropenia, physical examination was normal; inflammatory tests (erythrocyte sedimentation rate, serum protein electrophoresis) and serology for hepatitis B and C and HIV were negative; antinuclear antibodies (ANA) titre was positive (1: 160) with a negative antibodies screen; rheumatoid factor and complement levels were normal. Activated partial thromboplastin time (APTT) was prolonged (47/29 s) and not corrected by addition of normal plasma. Lupus anticoagulant antibodies were positive. ANA became negative six months after cessation of implicated drugs. Thus, the diagnosis of “chlorpromazine-induced lupus with CAC” was retained. The pathophysiological mechanism of this association remains a subject of discussion. This induced autoimmunity, involving several anti-psychotics, is a real therapeutic challenge in our patient's case.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
e-Poster Viewing: Psychopharmacology and pharmacoeconomics
Copyright
Copyright © European Psychiatric Association 2017
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