Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antifibrotic potential of pirfenidone (5-methyl-1-phenyl-2-[1H]-pyridone) was examined in a single intratracheal bleomycin dose hamster model of pulmonary fibrosis. Bleomycin-induced fibrosis and the effectiveness of pirfenidone treatment were assessed by measuring pulmonary functions (Cqst, TLC, VC, IC, FRC, RV) and the level of hydroxyproline in whole lung homogenates. Thirty-five male golden Syrian hamsters were randomized into four experimental groups: saline instilled and fed a control diet of rat chow (SCD, n = 8); saline instilled and fed the control diet containing 0.5% (w/w) pirfenidone (SPD, n = 8); bleomycin instilled and fed the control diet (BCD, n = 7); and bleomycin instilled and fed the control diet containing 0.5% pirfenidone (BPD, n = 10). Twenty-one days following bleomycin instillation Cqst/TLC, TLC, VC, and IC were significantly reduced and total lung hydroxyproline levels were significantly increased in the BCD and BPD groups as compared with the SCD and SPD groups, respectively. Pirfenidone ingestion significantly attenuated these bleomycin-induced pertubations in pulmonary functions and lung hydroxyproline levels (BCD versus BPD). The data obtained in this study provide evidence of the benefical effects of pirfenidone in the hamster model of bleomycin-induced pulmonary fibrosis both at the functional and biochemical level.
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PMID:Pirfenidone attenuates bleomycin-induced changes in pulmonary functions in hamsters. 940 44

We measured serum levels of SP-D in collagen diseases (110 cases) such as systemic scleroderma (SSc), scleroderma spectrum disorders (SSD), systemic lupus erythematodes (SLE), Sjogren syndrome (Sjs), dermatomyositis (DM), rheumatoid arthritis (RA), and dermatitis (DE) (109 cases) as a control. Additionally, we performad a correlation analysis to determine how these levels were related to pulmonary fibrosis and function test (vital capacity, %DLco). The serum levels of SP-D increased in SSc patients with Barnett type III more than in SSc patients with Barnett type I or II, while they increased slightly in SSD (incomplete type of SSc) patients. The differences in these figures were statistically significant between the SSc (SSc & SSD) and non-SSc (SLE, DM, Sjs & RA) groups (p<0.005). The serum levels of SP-D in SSc patients with anti-topoisomerase I antibodies were statistically higher than those in SSc patients with other types of anti-nuclear antibodies. There was a statistically significant correlation between the severity of pulmonary fibrosis and the serum levels of SP-D, and a statistically negative correlation between SP-D levels and vital capacity or %DLco, but there was no proportional correlation with the forced expiatory volume (FEV1.0%). There was no statistical relationship between pre- and post-therapy with photopheresis; however, there was a statistical correlation between the serum levels of SPD and KL-6. In the group of collagen diseases, plasma levels of SP-D were higher than serum levels of SP-D. Patients with SSc possess higher levels of SP-D than do those with other collagen diseases and dermatitis, which may correspond to the severity of pulmonary fibrosis.
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PMID:Surfactant protein D (SP-D) and systemic scleroderma (SSc). 1160 86