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Abstract Introduction Sarcoidosis is a multi-systemic disorder of unknown origin and most commonly affects the lungs. Diagnosis relies on the presence of non-caseating granulomas on histologic specimens. In high-resolution computed tomography, the most characteristic findings are peribronchovascular thickening, perilymphatic nodular distribution, and bilateral hilar adenopathy. Confluent nodular opacities or large masses are rare manifestations of the disease. It is well recognized that sarcoidosis can mimic infectious, malignant, and granulomatous conditions. Here, we report a case with a high initial index of suspicion for lung malignancy in terms of clinical, lung imaging, and endoscopic findings. Case presentation A 65-year-old Caucasian woman, lifelong non-smoker with an unremarkable medical history, presented with a 10-month history of progressive breathlessness, dry cough, fatigue, arthralgias, and mild weight loss. The only significant clinical finding was bilateral enlargement of auxiliary lymph nodes. High-resolution computed tomography revealed a soft tissue density mass at the right hilum which was surrounding and narrowing airways and vascular components, nodules with vascular distribution, enlarged mediastinal lymph nodes, and pericardial effusion. Our patient underwent a bronchoscopy, which revealed the presence of submucosal infiltration and narrowing of the right upper bronchus. Endobronchial biopsies showed non-caseating granulomas. As local sarcoid reactions with non-caseating granulomas can be observed near tumors, our patient underwent video-assisted thoracoscopy and surgical removal of an auxiliary lymph node, both of which confirmed the presence of non-caseating granulomas and the diagnosis of sarcoidosis. She was treated with steroids with improvement of clinical and imaging findings. However, while on a maintenance dose, she presented with a pleural effusion, which, after the diagnostic work-up, proved to be sarcoidosis-related. Treatment with initially high doses of steroids plus a steroid-sparing agent led to resolution of the effusion. Conclusions We report a case with a high initial index of suspicion for lung malignancy. Clinicians should always be aware that sarcoidosis enters the differential diagnosis of patients presenting with a lung mass that encases and narrows bronchial and vascular structures with associated pericardial effusion. Rarely, pleural effusion can be the presenting symptom of disease relapse despite maintenance treatment.

Background and aim: Toll-like receptors (TLRs), a key component of innate immunity, have recently been implicated in the pathogenesis of interstitial lung diseases (ILDs). As the involvement of TLRs has not yet been fully elucidated, the aim of the current study was to examine the expression of various TLRs in the bronchoalveolar lavage fluid (BALF) of patients with ILDs. Patients and Methods: We studied prospectively three groups of patients: (1) one group of 35 patients with fibrotic disorders, 16 with idiopathic pulmonary fibrosis (IPF) and 19 with fibrotic interstitial pneumonias associated with collagen tissue disorders (CTD-IPs); (2) one group of 14 patients with pulmonary sarcoidosis; and (3) 11 normal subjects. We evaluated TLR expression with flow cytometry and mRNA expression with real-time PCR. Results: An overexpression of TLR-3 mRNA was found in fibrotic disorders (CTD-IPs/IPF) in comparison with sarcoidosis (mean ± SD, 1.104 ± 1.087 versus 0.038 ± 0.03; P = 0.04). Additionally, TLR-3 mRNA was increased in CTD-IPs in comparison with IPF (P = 0.001), sarcoidosis (P = 0.002) and controls (P = 0.05). An upregulation in TLR-7 and -9 mRNA expression was detected in IPF (P = 0.05) and sarcoidosis (P = 0.05), respectively, when compared to controls. A higher percentage of TLR-9-expressing cells was found in BALF of CTD-IPs when compared to IPF (mean ± SD, 36.7 ± 7.06 versus 14.85 ± 3.82; P = 0.025). Conclusion: We observed distinct profiles of TLR expression in fibrotic and granulomatous disorders. It is likely that they could play a key role in the pathogenesis of these diseases and represent future therapeutic targets. [ABSTRACT FROM AUTHOR]