Impact of obesity progression or regression on the longitudinal assessment of fibrosing interstitial lung disease

Extract Abnormalities in lung mechanics (restriction) and pulmonary gas exchange (hypoxaemia) may jointly conspire to elicit exertional dyspnoea and decrease exercise tolerance in patients with fibrosing interstitial lung disease (f-ILD) [1]. Obesity (body mass index (BMI) ≥30 kg·m–2), a prevalent comorbidity of f-ILD [2], may negatively impact on "static" (e.g. total lung capacity (TLC)) and dynamic (forced vital capacity (FVC)) lung volumes relevant to dyspnoea genesis [3]. Arterial oxygenation decreases as obesity worsens, particularly on exertion when poorly ventilated areas are perfused with less oxygenated mixed venous blood [4]. Mass loading in the thorax increases the elastic work of breathing [5], and heightened ventilation in response to high metabolic demands [6] contributes to breathlessness and exercise intolerance in a "dose" (weight)-response fashion [7]. It is conceivable, therefore, that the functional and sensory consequences of moderate-to-severe obesity (BMI ≥35 kg·m–2) may confound the assessment of disease severity and stability in these patients.
Source: European Respiratory Journal - Category: Respiratory Medicine Authors: Tags: Research Letters Source Type: research