Reduction of exercise capacity in sarcoidosis in relation to disease severity

INTRODUCTION Pulmonary function tests (PFTs) do not always predict functional limitations during exercise in sarcoidosis. Cardiopulmonary exercise testing (CPET) may facilitate the recognition of exercise intolerance in these patients. AIM As relevant data in sarcoid patients are limited, the aim of the study reported here was to assess exercise capacity impairment during a maximal CPET and to evaluate potential correlations with PFT measurements and radiological stages of the disease. METHOD A total of 83 sarcoid patients consecutively referred for evaluation of exertional dyspnea over a 3-year period were studied retrospectively with PFTs, including spirometry, diffusing capacity of the lung for carbon monoxide (DLCO) and lung volumes, and CPET using standard protocol. Patients were grouped according to their radiological stages: Stage I (n=43), Stages II-III (n=31), and Stage IV (n=9). RESULTS Forced expiratory volume in 1 second, forced vital capacity, and total lung capacity were mildly impaired only in Stage IV (means ± standard deviation: 72.44±28.00, 71.33±26.70, and 59.78±21.72, respectively), while DLCO was mildly and moderately reduced in Stages II-III and IV (72.68±14.13 and 51.22±18.50, respectively) and differed significantly between all stages (I vs II-III: P=0.003, I vs IV: P=0.003, and II-III vs IV: P=0.009). Exercise capacity (as expressed by peak oxygen consumption <84% predicted) was decreased in 53% of patients (Stage I: 48%, Stages II-III: 52%, Stage IV: 78%); however, significant differences were noticed only between Stages I and IV (P=0.0025). Of note, significant correlations were found between peak oxygen consumption and DLCO (P=0.0083), minute ventilation (P<0.0001), oxygen pulse (P<0.0001), lactate threshold (P<0.0001), and peak ventilatory threshold (P<0.0001). CONCLUSION CPET could be considered a useful tool in exercise intolerance evaluation in sarcoid patients with mild PFT abnormalities. Exercise limitation in sarcoidosis may be attributed to both ventilatory and cardiocirculatory impairment.