Diffuse Lung Disease |

Obstructive Airways Disease in Sarcoidosis: Still Few Answers FREE TO VIEW

Gloria Westney*, MD
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Morehouse School of Medicine, Atlanta, GA

Chest. 2012;142(4_MeetingAbstracts):443A. doi:10.1378/chest.1390708
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PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM

PURPOSE: Sarcoidosis, a systemic granulomatous disease of undetermined etiology, involves the lung 90% or more of the time. Although historically the interstitial granulomatous inflammation has manifested as a restrictive ventilatory defect, an obstructive ventilatory defect from a variety of hypothesized areas of airway involvement has been reported. The factors that contribute to or can predict this development are not clear, however. We performed a retrospective study in a cohort of sarcoidosis patients to determine the prevalence of obstructive airways disease (OAD) and its association with risk factor exposure and CXR severity.

METHODS: The records of patients participating in a study on sarcoidosis disease severity were reviewed for current/former smoking status, pulmonary function values for the presence or absence of OAD, decreased diffusion, and CXRs dichotomized into low (0,1,2) or high (3 & 4) Scadding stages. Data are expressed as the mean ± the standard deviation or as frequencies and proportions where applicable. The Chi Squared test was used to compare categorical variables between groups. Analyses were performed using SPSS statistics version 17. A p-value of < 0.05 was considered significant.

RESULTS: The cohort of 23 African American sarcoidosis subjects (M= 35%; F=65%; age 48 ± 7 yrs) showed normal (26%), obstructive (26%), restrictive (30%), or a mixed (18%) spirometry pattern with 48% having reduced diffusing capacity. Current/former smokers comprised 61%. CXR stages ranged from 0 (30%), I (13%), II (4%), III (39%), and IV (13%). Significant associations were seen between OAD & smoking, and higher CXR severity & smoking. There was no apparent significance between OAD and CXR severity, diffusion, or interestingly the use of inhaled bronchodilators (steroids or B2 agonists).

CONCLUSIONS: The risk of developing obstructive airways disease in sarcoidosis may be increased by smoking, however, how noncaseating granulomatous inflammation may confound the pulmonary pathology in the presence of this risk factor remains unclear. Ongoing studies to clarify the indications and effectiveness of inhaled medications for airway symptoms in sarcoidosis would improve the management of these patients.

CLINICAL IMPLICATIONS: The management approach to airway symptoms in sarcoidosis patients should benefit from accurate symptom assessment, guidance from utilization of diagnostic tools and documentation of response to therapy.

DISCLOSURE: The following authors have nothing to disclose: Gloria Westney

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Morehouse School of Medicine, Atlanta, GA




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