Clinico-morphological and molecular-biological characteristics of idiopathic fibrous alveolitis and lung sarcoidosis
Kogan, E.A.; Den'gin, V.V.; Jack, G.; Kornev, B.M.
Arkhiv Patologii 62(6): 32-37
2000
ISSN/ISBN: 0004-1955 PMID: 11198120 Document Number: 512690
Lung biopsies of 16 patients with classic idiopathic fibrosing alveolitis (IFA) and 6 patients with sarcoidosis were studied immunohistochemically. It was found that adenomatous hyperplasia (AH) and fibrosing in IFA are potentiated by high expression of thrombocytic growth factor (TGF) and insulin-like growth factor type 1 (IGF-1). Tumor necrosis factor alpha (TNFa) in IFA is actively produced at early stages of the disease. TNFa is drastically reduced in IFA with atypical AH. High level of TNFa produced by alveolar macrophage, pneumocytes type 2 and by other cells is observed in the lungs in sarcoidosis. The level of transforming growth factor (B1-TGF) is rather low in sarcoidosis this being combined with weak interstitial fibrosis (3.75 against 5.06 in IFA). Sarcoidosis granuloma contains proliferating epithelioid cells (as judged by Ki-67), produces a high amount of FTN (4.66), moderate amount of cell fibronectin (2.7), fibroblast growth factor, beta-TGF and IGF-system (1.7; 1.1; 0.8, respectively). Thus, IFA and sarcoidosis are distinguished not only morphologically but by the cytokine profile as well. This implies different approaches to their diagnosis and treatment.