Carbimazole-induced eosinophilic pleural effusion

Abstract

We report the case of a 41-year-old woman who presented with a unilateral exudative effusion with prominent eosinophils on pleural cytology. Carbimazole had been started 4 weeks prior to presentation. No immediate cause was identified on imaging or laboratory testing. The effusion persisted at 2-month follow-up. Further investigation at this time, including autoimmune serology was negative. At 2-month follow-up, the effusion was loculated on ultrasound imaging and had a low fluid pH on diagnostic aspiration, in keeping with an empyema. The patient received treatment for pleural empyema, including antibiotics, intercostal drain insertion and video-assisted thoracoscopic pleural biopsy. Carbimazole was stopped, and following treatment for the empyema, the effusion did not reaccumulate.This case illustrates the diagnostic difficulties that pleural effusions may present. It demonstrates that drug reactions should be considered in the differential diagnosis following thorough investigation for other potential causes and also describes the complications that may occur.

Incidence, Aetiology and Clinical Features of Eosinophilic Pleural Effusion: A Retrospective Study

“…The differences in results may be explained by the different prevalences of the aetiology of PE at some institutions [10]. Although there was no drug-induced EPE in our study, the list of possible aetiologies has been increasing in recent years, including methimazole, carbimazole, valproic acid, mesalamine, olanzapine and others [11][12][13][14][15][16]. Adverse drug reactions should be considered in the differential diagnosis following thorough investigation for other potential causes of EPE.…”

Pleuropericardial Compromise Associated With Graves’ Disease: A Systematic Review

“…Eight cases were considered as the consequence of heart failure [15][16][17][18][19][20]. Four cases consisted of pleural effusions as a rare adverse reaction due to ATD intake [21][22][23][24]. Two cases were associated with polyglandular autoimmune syndromes [25,26].…”