Pulmonary function testing and chest tomography in patients with acromegaly

Background Despite the gradual improvement in treatment procedures and cure rates of acromegaly, a steady increase in the mortality rate due to respiratory disease has been documented in recent decades. In this study, our objectives were to describe the abnormalities in lung structure and function that occur in acromegalic patients and to correlate these changes with hormonal levels. Methods This cross-sectional study included 20 acromegalic patients and 20 age-and height-matched control subjects, all non-smokers. All subjects underwent spirometry, whole body plethysmography, carbon monoxide diffusing capacity, and respiratory muscle strength. Acromegalic patients also performed high-resolution computed tomography (HRCT). Results Most patients were female (65%), with a mean age of 52.5 ± 13 years. Acromegalic patients showed lower values of maximum expiratory pressure (55.9 ± 17.1 vs. 103.7 ± 19.2%; p < 0.001) and maximum inspiratory pressure (71.4 ± 27.8 vs. 85.3 ± 24.1%; p = 0.005) compared to control subjects. The values of forced vital capacity (107.1 ± 15.9 vs. 98.9 ± 21.4%; p = 0.028), total lung capacity – TLC (107.3 ± 12.9 vs. 93.7 ± 7.60%; p = 0.002), residual volume (114.1 ± 22.7 vs. 90.0 ± 14.6%; p < 0.001), and airways’ resistance (3.82 vs. 2.31 cmH 2 O/L/s; p = 0.039) were greater in acromegalic patients than in control subjects. The difference between the TLC measured by plethysmography and the V A (alveolar volume) measured during the DL CO maneuver was higher in acromegalic patients than in control subjects (0.69 ± 0.46 vs. 0.19 ± 0.61 L; p = 0.021). The main findings in HRCT in acromegalic patients were air trapping, airway calcification and bronchiectasis, which were observed in 60%, 40% and 35% of cases, respectively. There was no significant correlation between the levels of growth hormone and insulin-like growth factor I, the lung function and the air trapping. Conclusions Acromegalic patients show changes consistent with the involvement of the small airways and ventilation inhomogeneity, both in terms of lung function and structure. However, air trapping cannot be explained either by hormone levels or changes in lung function.