Chest
Clinical Investigations: Idiopathic DiseaseColchicine, D-Penicillamine, and Prednisone in the Treatment of Idiopathic Pulmonary Fibrosis: A Controlled Clinical Trial
Section snippets
Study Population
Fifty-six adult patients with clinical, radiologic, and functional features of interstitial lung disease and histologically proven diagnosis of IPF were enrolled in this prospective study. The patients were seen at the National Institute of Respiratory Diseases in Mexico City between 1983 and 1990, and the protocol was approved by the corresponding Scientific and Ethical Committees. Diagnosis of IPF was suspected in patients with progressive dyspnea, diffuse reticulonodular infiltrates on chest
Results
Baseline characteristics of the four groups are summarized in Table 1. Dyspnea score and pulmonary function test results were comparable among the groups. Younger patients were located in group 4 who received prednisone, colchicine, and D-penicillamine when compared with the prednisone and prednisone plus colchicine groups (p<0.05). Five patients were unavailable during the 5-year follow-up. The end points examined for therapeutic outcome were measurable change in dyspnea score, lung function
Discussion
IPF represents a prototype of an aggressive and usually progressive interstitial lung disease that continues being a therapeutic problem for the clinician.
Corticosteroids are currently the recommended pharmacologic therapy, mainly with the rationale of stabilizing or preventing disease progression by suppression of the chronic inflammation. However, their long-term benefits are questionable. Thus, although a number of patients treated with corticosteroids feel better, results of objective
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2012, Immunology and Allergy Clinics of North AmericaCitation Excerpt :Supporting that concept, studies of gene expression profile patterns have demonstrated that, when compared with lungs with chronic hypersensitivity pneumonitis, which is characterized by a significant inflammatory component, IPF lungs have a shift toward extracellular matrix turnover and epithelium development, growth, and differentiation.7 Moreover, older reports exploring antiinflammatory agents have largely failed to demonstrate a treatment benefit in IPF.8–10 Alveolar epithelial cells and the myofibroblast are thought to be the key target cells in the pathogenesis of IPF; there is growing evidence that genetic susceptibility, cellular senescence, endoplasmic reticulum stress and oxidative stress, as well as epigenetic factors associated with micro-RNAs are critical factors for the injury continuum that ultimately leads to the extensive fibrotic changes and loss of lung function seen in IPF.
Dyspnea in idiopathic pulmonary fibrosis: A systematic review
2012, Journal of Pain and Symptom ManagementCitation Excerpt :Based on available evidence, recommendations for the treatment of dyspnea in IPF are provided in Fig. 2. No potential disease-modifying treatment (i.e., treatment aimed at modifying the underlying pathogenesis of IPF) has been shown to reliably improve dyspnea.6,13–19 The combination of prednisone and colchicine was studied in two unblinded trials.14,19