H ypersensitivity pneumonitis (HP) is an interstitial lung disease (ILD) characterized pathologically by varying degrees of inflammation and/or fi brosis that result from the inhalation of an antigen to which a person has been previously sensitized. The clinical expression of HP can vary and includes acute, sub acute, and chronic forms. Symptom onset that coincides with antigen exposure provides the fi rst diagnostic clue; however, despite an exhaustive search, a recognizable, temporal relationship (between exposure and symptoms) is frequently absent, particularly in patients who present with the chronic form of HP.Chronic HP, characterized clinically by ventilatory restriction and, most commonly, upper-zonepredominant fi brosis on high-resolution CT (HRCT) scan, is irreversible and often progressive. It is believed that continued exposure to an inciting antigen (IA) perpetuates progression and the development of fi brosis in HP, but this belief hinges more on scientific rationale than systematic research. In this study, we hypothesized that among patients with histologic and Background: The cornerstone of hypersensitivity pneumonitis (HP) management is having patients avoid the inciting antigen (IA). Often, despite an exhaustive search, an IA cannot be found. The objective of this study was to examine whether identifying the IA impacts survival in patients with chronic HP. Methods: We used the Kaplan-Meier method to display, and the log-rank test to compare, survival curves of patients with well-characterized chronic HP stratifi ed on identifi cation of an IA exposure. A Cox proportional hazards (PH) model was used to identify independent predictors in time-todeath analysis. Results: Of 142 patients, 67 (47%) had an identifi ed IA, and 75 (53%) had an unidentifi ed IA. Compared with survivors, patients who died (n 5 80, 56%) were older, more likely to have smoked, had lower total lung capacity % predicted and FVC % predicted, had higher severity of dyspnea, were more likely to have pulmonary fi brosis, and were less likely to have an identifi able IA. In a Cox PH model, the inability to identify an IA (hazard ratio [HR], 1.76; 95% CI, 1.01-3.07), older age (HR, 1.04; 95% CI, 1.01-1.07), the presences of pulmonary fi brosis (HR, 2.43; 95% CI, 1.36-4.35), a lower FVC% (HR, 1.36; 95% CI, 1.10-1.68), and a history of smoking (HR, 2.01; 95% C1, 1.15-3.50) were independent predictors of shorter survival. After adjusting for mean age, presence of fi brosis, mean FVC%, mean diffusing capacity of the lung for carbon monoxide (%), and history of smoking, survival was longer for patients with an identifi ed IA exposure than those with an unidentifi ed IA exposure (median, 8.75 years vs 4.88 years; P 5 .047). Conclusions: Among patients with chronic HP, when adjusting for a number of potentially infl uential predictors, including the presence of fi brosis, the inability to identify an IA was independently associated with shortened survival. CHEST 2013; 144(5):1644-1651Abbreviations: D lco 5 diffusing capacity of the lung f...
Purposes:To provide a new detailed visual assessment scheme of computed tomography (CT) for chronic obstructive pulmonary disease (COPD) by using standard reference images and to compare this visual assessment method with quantitative CT and several physiologic parameters. Materials and Methods:This research was approved by the institutional review board of each institution. CT images of 200 participants in the COPDGene study were evaluated. Four thoracic radiologists performed independent, lobar analysis of volumetric CT images for type (centrilobular, panlobular, and mixed) and extent (on a six-point scale) of emphysema, the presence of bronchiectasis, airway wall thickening, and tracheal abnormalities. Standard images for each finding, generated by two radiologists, were used for reference. The extent of emphysema, airway wall thickening, and luminal area were quantified at the lobar level by using commercial software. Spearman rank test and simple and multiple regression analyses were performed to compare the results of visual assessment with physiologic and quantitative parameters. Results:The type of emphysema, determined by four readers, showed good agreement (k = 0.63). The extent of the emphysema in each lobe showed good agreement (mean weighted k = 0.70) and correlated with findings at quantitative CT (r = 0.75), forced expiratory volume in 1 second (FEV 1 ) (r = 20.68), FEV 1 /forced vital capacity (FVC) ratio (r = 20.74) (P , .001). Agreement for airway wall thickening was fair (mean k = 0.41), and the number of lobes with thickened bronchial walls correlated with FEV 1 (r = 20.60) and FEV 1 /FVC ratio (r = 20.60) (P , .001). Conclusion:Visual assessment of emphysema and airways disease in individuals with COPD can provide reproducible, physiologically substantial information that may complement that provided by quantitative CT assessment.q RSNA, 2012 Supplemental material: http://radiology.rsna.org/lookup /suppl
Oral azithromycin may antagonize the therapeutic benefits of inhaled tobramycin in subjects with CF with P. aeruginosa airway infection.
Background Immunosuppressive (IS) therapy is indicated to treat progressive sarcoidosis, but randomized controlled trials to guide physicians in the use of steroid sparing agents are lacking. The aim of this retrospective study was to examine the role of Mycophenolate Mofetil (MMF) as an alternative therapy in the treatment of sarcoidosis. Methods A retrospective chart review of all patients who had been prescribed MMF between January 2008 and October 2011 was conducted. Patients with insufficient data or who had another IS therapyinitiated concomitantly with MMF, including prednisone, were excluded. Physiological data obtained at the time MMF therapy was initiated as well as six and twelve months before and after therapy was extracted. Longitudinal analyses of the effect of MMF on changes in pulmonary function at MMF start, 6 months, 12 months pre and post MMF therapy were conducted. Results 37/76 patients met our inclusion/exclusion criteria. There were no statistically significant changes in PFT measurements pre and post MMF therapy. We did find a trend (p=0.07) towards improvement in DLCO 12 months pre and post MMF in patients who were started on MMF due to intolerance to previous IS therapy compared to those who were unresponsive to their previous IS therapy. We also noted a reduction in prednisone dose in those treated with MMF. Conclusion MMF appears to offer no extra benefit to sarcoidosis patients unresponsive to previous steroid-sparing agents, but may be beneficial in patients intolerant to their previous steroid-sparing agent. Additional studies investigating the efficacy of MMF as the initial steroid-sparing agent are needed to further clarify the role of MMF in sarcoidosis.
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