These results suggest that high BMI, regular vaccination and scheduled visits may have beneficial effects on the survival of bronchiectasis. Besides, presence of hypoxemia, hypercapnia, dyspnea level and radiographic extent were more closely correlated with mortality.
Background: Patients with asthma incur the risk of steroid-induced myopathy, which is a well-known side effect of treatment with corticosteroids. However, the adverse effect of long-term steroid treatment on respiratory muscle function remains controversial. Objective: We aimed to evaluate the effects of long-term moderate dose of systemic corticosteroids and high-dose inhaled beclomethasone on maximal inspiratory and expiratory pressures (PImax and PEmax, respectively) in two groups of asthmatic patients exhibiting comparable levels of hyperinflation. Methods: Twelve steroid-dependent asthmatic patients requiring 10–20 mg/day of prednisone-equivalent corticosteroids for an average of 9.83 ± (SD) 9.86 years; 14 subjects with moderate to severe asthma who have used inhaled beclomethasone for at least 1 year at a daily dose higher than 1,000 μg and 15 healthy controls were included to the study. Results: No significant difference in pulmonary function tests and arterial blood gases appeared between two asthmatic groups with different treatment modalities. PImax as an absolute value was significantly lower in steroid-dependent asthmatics than in patients treated with inhaled beclomethasone and controls (p < 0.01). %PImax was also lower in steroid-dependent asthmatics than in control groups (p < 0.01). A significant correlation was found between %PImax and hyperinflation assessed by %RV, %FRC, %FRC/TLC (p < 0.05) in all asthmatic patients. Conclusions: We believe that hyperinflation plays a major role in inspiratory muscle dysfunction in asthma, but the finding of significantly decreased PImax values in steroid-dependent asthmatics when compared with patients on high-dose inhaled beclomethasone with a comparable level of hyperinflation points to a deleterious effect of long-term, moderate-dose systemic corticosteroid but not high-dose beclomethasone on inspiratory muscle function in asthmatics.
Endothelin-1 (ET-1) has been described to have crucial effects in the initiation and evolution of pulmonary hypertension (PH) secondary to cardiac disorders. However, the precise role of ET-1 in PH induced by chronic obstructive pulmonary disease (COPD) is not yet clear. The objective of this cross-sectional study was to determine the local and peripheral plasma ET-1 profile of COPD patients with or without PH. Twenty-six COPD patients with clinical and/or laboratory findings suspicious of PH, and 20 healthy smoker volunteers constituted the study population. Patients were allocated to PH (n = 17) and non-PH (n = 9) groups according to their pulmonary artery pressures determined by right-heart catheterization. Plasma ET-1 samples, obtained from the main pulmonary artery (mixed venous blood) and peripheral blood (radial artery and brachial vein), were assessed by radioimmunoassay. Brachial vein ET-1 levels were within normal ranges in PH (2.7 ± 0.5 pg/ml) and non-PH (3.2 ± 0.7 pg/ml) COPD patients compared with that of the controls (4.4 ± 0.1 pg/ml). Likewise, radial artery ET-1 levels in PH (3.3 ± 0.7 pg/ml) and non-PH (2.9 ± 0.8 pg/ml) groups, and in controls (3.4 ± 1.1 pg/ml) were also comparable. The pulmonary artery ET-1 concentration of the PH group (13.6 ± 3.7 pg/ml) was higher than that of the non-PH group (2.2 ± 0.4 pg/ml) and that of the peripheral blood levels of controls. Elevated pulmonary artery ET-1 in the PH group was inversely correlated only with PaO2 levels. These results could be taken as an evidence of a local role of ET-1 in COPD-induced PH, but it remains to be clarified whether ET-1 is a marker or a mediator of PH in COPD.
The impairment of pulmonary function (mainly disturbance in airflow rates and air trapping) and pulmonary hypertension may be present, even in a simple form of CWP. The pulmonary function impairment in patients with CWP is likely to be attributable to the occurrence of emphysema. However, pulmonary hypertension was directly related to the profusion of pneumoconiotic nodules, which may result in obliteration of the vascular bed.
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