A large number of drugs are associated with the development of pleural inflammation.<sup>56 Miller K.S. Drug-induced pleural disease Seminars in Respiratory Medicine 1987 ;  9 : 86-97  [cross-ref]

Cliccare qui per andare alla sezione Riferimenti, 67 Sahn S.A. State of the art, the pleura American Review of Respiratory Disease 1988 ;  138 : 184-234

Cliccare qui per andare alla sezione Riferimenti</sup> Patients may be symptomatic, with evidence of pleural involvement, or remain asymptomatic, with the pleural effects of the drug noted as a corollary to the underlying lung disease. The effect of drugs on the pleura may be reflected in the development of pleural thickening, pleural fibrosis, or a pleural effusion. Although the onset of pleural disease has a temporal relationship to initiation of drug usage, the signs and symptoms may present much later in some cases, particularly if the drug effect is dose related.

Patients with drug-induced pleural disease often have dyspnea as the presenting symptom. The dyspnea may be secondary to the underlying lung parenchymal disease that is commonly associated with pleural disease or may be secondary to the presence of a rapidly increasing pleural effusion or fibrosis. Pulmonary parenchymal toxicity and its related symptoms often bring the patient to the attention of a physician. On radiologic examination, the patient may have parenchymal and pleural involvement secondary to drug-induced disease or, in some cases, the pleura may be involved exclusively.

A detailed history of drug intake is critical to making the diagnosis of drug-induced pleural pulmonary disease. As has been described with nitrofurantoin usage,<sup>36 Haily F.J., Glascock H.W., Hewitt W.F. Pleuropulmonic reactions to nitrofurantoin N Engl J Med 1969 ;  281 : 1087-1090

Cliccare qui per andare alla sezione Riferimenti</sup> a patient may not reveal the use of the drug for occasional urinary tract infections unless asked specifically. When chemotherapy for malignant disease is part of the history, the cause and effect is often readily obvious.<sup>78 Weiss R.B., Muccia F.M. Cytotoxic drug-induced pulmonary disease. Update 1980 Am J Med 1980 ;  68 : 259-266  [cross-ref]

Cliccare qui per andare alla sezione Riferimenti</sup>

The primary method of treatment involves discontinuation of the offending drug.<sup>12 Cooper J.A., White D.A., Matthay R.A. Drug-induced pulmonary disease. Part I: Cytotoxic drugs American Review of Respiratory Disease 1986 ;  133 : 321-340

Cliccare qui per andare alla sezione Riferimenti</sup> The withdrawal of the drug is usually associated with partial or complete resolution of the underlying pleural inflammation.<sup>13 Cooper J.A., White D.A., Matthay R.A. Drug-induced pulmonary disease. Part II: Non-cytotoxic drugs American Review of Respiratory Disease 1986 ;  133 : 488-505

Cliccare qui per andare alla sezione Riferimenti</sup> That may be more difficult to implement than it seems because drugs such as amiodarone, which may be critically important for the treatment of arrhythmia, may not be easily withdrawn without the development of other problems. The use of steroids to suppress inflammation may help in resolving the underlying disease. In some critically ill patients, several drugs that may cause pleural disease may be used, making it difficult to define the inducing agent. Considering the specific characteristics of different drugs and their toxicity may be helpful in reaching a logical conclusion. A significant number of data have now accumulated about the mechanisms of toxicity of different drugs. They may range from oxidant-induced mesothelial cell injury to the development of an acute hypersensitivity-type reaction. A direct dose-related toxic effect or a chemical-induced inflammation may also cause pleural inflammation. Although a general knowledge of the mechanisms of drug-induced toxicity exists, the details of cytokines, secondary messengers, and other factors that play a role in producing pleural changes remain unclear.