A 24-year-old man consulted his primary care physician with general fatigue and chest and back pain. Chest radiography demonstrated a left-sided pleural effusion that was diagnosed as a parapneumonic effusion, and he was treated with oral levofloxacin 500 mg per day. However, neither the pain nor effusion improved; therefore, his primary care physician referred him to our institution.
He had low-grade fever without any symptoms of either respiratory disease or heart failure, but he had a history of interventional RFA for paroxysmal atrial fibrillation three month prior to the onset of symptoms. On physical examination on admission, his temperature was 37.4  C, heart rate 93 beats per min, blood pressure 110/50 mmHg, respiratory rate 16 breaths per min, and pulse oximetry 97% oxygen saturation in room air. Radiography and computed tomography (CT) of the chest demonstrated a left-sided intermediate pleural effusion and slightly thickened parietal pleura. A transthoracic echocardiogram revealed 75% of left ventricular ejection fraction without regional wall motion abnormalities and normal level of pericardial effusion. The result of laboratory examinations were unremarkable except for a trivial increase of C-reactive protein (CRP) level of 0.46 mg/dL. QuantiFERON-TB Gold In-Tube assay was negative. Thoracentesis revealed a nonbloody exudative effusion with lymphocytosis. There was no evidence of infection or neoplasia in either the culture or the cytology results.
He was diagnosed with pleuritis and was prescribed oral loxoprofen in addition to original therapy. Both his symptoms and pleural effusion gradually improved over the following month. However, seven months after his initial treatment, he complained of intense chest pain. Chest radiography and CT showed the reccurence of the left-sided pleural effusion accompanied by a thickening of the parietal pleura (Fig. 1). He had a slightly elevated CRP level at 1.72 mg/dL and a normal peripheral white blood cell count of 7350 cells/muL.
Given his previous RFA for paroxysmal atrial fibrillation three months prior to the onset of his symptoms, we believed that the series of events were highly indicative of PCIS. However, further examination was required to exclude pleural tuberculosis and malignancy. Pleural biopsy by video-assisted thoracoscopic surgery (VATS) under general anesthesia was performed, and the histological specimens from the left parietal pleura demonstrated chronic pleuritis with a non-necrotizing granulomatous reaction (Fig. 2). Furthermore, cultures and polymerase chain reaction analysis of the parietal pleura were negative for mycobacterium. He was clinically diagnosed with PCIS and was successfully treated with colchicine 1 mg and Celecoxib 200 mg daily. The dose of colchicine was reduced to 0.5 mg per day after three weeks and discontinued after one month because of the development of diarrhea.
Chest computed tomography showed a relapse of the left-sided pleural effusion associated with a thickening of the parietal pleura seven months after the first event.