To the Editors:
We read with great interest the article by Alagha et al. [1] in the June issue of the European Respiratory Review. Since, in our opinion, eosinophilic pleural effusion (EPE), and drug-induced EPE in particular, is an interesting issue, we would like to add some comments to this article.
It should be realised that our knowledge on drug-induced EPE comes almost exclusively from case reports. Although none of the larger series presenting the aetiology of EPE reported the true incidence of drug-induced EPE, the percentage of patients with drug-induced EPE seems to be low. Nevertheless, as in the majority of these patients drug discontinuation is sufficient for resolution of pleural effusion, pharmacological agents should always be considered as a potential cause of pleural effusion, particularly in EPE.
Although numerous drugs can induce pleuritis and pleural effusion, the list of agents associated with eosinophilic pleuritis is not extensive [2–4]. Some drugs used in psychiatry and neurology are some of the most important, including valproic acid (and its derivatives) and dantrolene [5–8]. EPE was also reported as a complication of treatment with tazinidine, trimipramine and fluoxetine [9–11]. It is interesting that, in a substantial number of reports on …