Cardiopulmonary exercise testing following hay exposure challenge in farmer's lung

Abstract

In patients experiencing an acute episode of hypersensitivity pneumonitis (HP), the alveoli and interstitium show a marked inflammation. The effects of this infiltration with effector cells on gas exchange and the cardiopulmonary system are not well characterized, and there are no data regarding cardiopulmonary exercise testing during hypersensitivity pneumonitis. The aim of this study was to gain new insights into the pathophysiology of acute farmer's lung using cardiopulmonary exercise testing. Cardiopulmonary exercise testing was performed in patients who had farmer's lung (n=21) before and 4 h after a standardized exposure with mouldy hay. Farmers who were asymptomatic for this condition (n=15) served as controls.At baseline, patients who had farmer's lung had a decreased breathing reserve and a greater alveolar to arterial oxygen difference. Following exposure, all of these patients developed hypersensitivity pneumonitis. Compared to the asymptomatic farmers, they showed an increase of alveolar to arterial oxygen difference and functional dead space ventilation during exercise and a reduction of the breathing reserve. In addition, 40% of the asymptomatic farmers demonstrated a pathological increase of the alveolar to arterial oxygen difference during exercise following exposure.In conclusion, our data signify that acute hypersensitivity pneumonitis induces significant changes in pulmonary gas exchange during exercise. Cardiopulmonary exercise testing may help to identify individuals with possible subclinical farmer's lung disease.

The Hypersensitivity Pneumonitis Diagnostic Index: Use of non‐invasive testing to diagnose hypersensitivity pneumonitis in metalworkers

“…A combination of a high A-a gradient (which appears to be the most consistent change, even with mild forms of HP) and/or a low DL CO ; plus an elevated ESR and dry crackles on lung exam in a patient with appropriate work-related symptoms may establish the diagnosis. This should not be surprising, because elevated A-a gradients, decreased DL CO , and crackles in the lungs are all recognized as occurring with HP [Krasnick et al, 1996;Schwaiblmair et al, 1997]. In some cases, spirometry, HRCT, and gallium scans may be helpful for making the diagnosis with confidence.…”

Every breath you take: Impacts of environmental dust exposure on intestinal barrier function–from the gut-lung axis to COVID-19

“…This severe respiratory condition is triggered by the inhalation of mold spores (e.g., Micropolyspora faeni and Aspergillus fumigatus; $2-10 mm) that grow in hay and grain (129,130). Mold spores have the capability of attaching to airborne dust particles (129,130) and preventing normal lung function ( 131) such as gas exchange (132). Comparably, swine farm workers also increase their risk of lung function decline and chronic bronchitis from long-term exposure to swine farm dust (133,134).…”

Mechanisms of exercise limitation in patients with chronic hypersensitivity pneumonitis

“…Few studies have assessed exercise capacity in cHP patients [ 10 , 11 ]; however, the mechanisms underlying these exercise limitations were not properly evaluated. One study evaluating patients with farmer's lung acutely exposed to mould showed an increased alveolar–arterial gradient, increased dead space and decreased ventilatory reserve at the end of cardiopulmonary exercise testing (CPET) [ 11 ]. Another investigation evaluated the prevalence of pulmonary hypertension in cHP patients using haemodynamic evaluation, and CPET was performed as a complimentary test [ 10 ].…”