Answer: Reactive Eosinophilic Pleuritis

Histology: The lesion consists of a cellular infiltrate of histiocytes, mesothelial cells, and eosinophils in association with the visceral pleura of the lungs. In this case, the lesion is associated with a bulla, whose thick wall is comprised of smooth muscle. In other cases, especially in younger patients, the smooth muscle component may be absent.

Discussion: Reactive eosinophilic pleuritis (Arch Pathol Lab Med 101:187-191, 1977) is a nonspecific reaction of the serosal surfaces in the thoracic cavity, seen most commonly in association with pneumothorax. This pneumothorax may be spontaneous, when it usually occurs in young people as a complication of paraseptal emphysema and bleb formation with ultimate rupture. In other patients, common causes of pneumothorax may be traumatic, related to metastatic sarcoma, or associated with bullous disease in the lung. The characteristic finding is the cellular coating of the pleural surface by an infiltrate of normal cells and eosinophils. By immunocytochemistry, the constituent cells can be found to be histiocytes with an admixture of mesothelial cells and chronic inflammatory cells. Eosinophils are focally and variably prominent in the lesion. The histologic features of the underlying lung reflect the etiology of the pneumothorax, and as described by Luna, Tomaschefski, et al. (Am J Surg Pathol 18:195-199, 1994), there may be an associated pulmonary vascular infiltrate by eosinophils in some cases. This infiltrate simply represents eosinophils in passage and is not an active vasculitis. The lesion seen in reactive eosinophilic pleuritis is part of a spectrum of reactions that can be seen in other organs (including as a complication of pneumo-mediastinum: Hum Pathol 15:1137-1144, 1984), in hernia sacs and even in the lesion known as “cardiac MICE”.

Reactive eosinophilic pleuritis was originally described in the context of separating spontaneous pneumothorax from pneumothorax in pulmonary eosinophilic granuloma (Langerhans Cell Histiocytosis in the lung). Since pneumothorax occurs in approximately 25% of patients with pulmonary eosinophilic granuloma (LCG), the importance of avoiding the trap of an unwarranted diagnosis of eosinophilic granuloma was felt to be important. As a matter of fact, since patients with pulmonary eosinophilic granuloma can have pneumothorax, it should not be unexpected that they might also have reactive eosinophilic pleuritis. Patients with pulmonary eosinophilic granuloma, however, have a very different chest radiographic appearance than do patients with spontaneous pneumothorax. Separation of reactive pleuritis from mesothelioma should be easily accomplished by knowledge of the clinical situation, radiographic appearance and the mixed nature of the infiltrate in REP. Further, the infiltrate does not invade the underlying tissues or the soft tissues of the chest wall. The diagnosis of eosinophilic granuloma (LCH) would also involve knowledge of the presence or absence of a peribronchial and a stellate interstitial infiltrate by characteristic Langerhans cells with grooved nuclei and S-100 and CD-1A positive cytoplasm in LCH.