Inhaled and Systemic Corticosteroid Therapies: Do They Contribute to Inspiratory Muscle Weakness in Asthma?

Abstract

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.

High serum levels of tumour necrosis factor‐α and interleukin‐8 in severe asthma: markers of systemic inflammation?

“…Probably, this class of drugs may enhance neutrophil function through increased leukotrienes and superoxide production, as well as inhibition of apoptosis [29]. In addition, high levels of sTNF-a and systemic corticosteroid therapy could be involved in determining the skeletal muscle weakness, a feature of chronic severe asthma [30][31][32]. We did not find any difference in the sIL-16, marker of T cell recruitment, levels among the healthy controls and mild-moderate or severe asthmatics.…”

Tulobuterol Patch Maintains Diaphragm Muscle Contractility for Over Twenty-four Hours in a Mouse Model of Sepsis

“…It is well known that β 2 -adrenergic receptor agonists, such as isoproterenol (Howell and Roussos 1984), fenoterol (Suzuki et al 1986), terbutaline (Cairns and Dulhunty 1993) and clenbuterol (Heijden et al 1997), increase diaphragm muscle contractility. It has also been reported that diaphragm weakness occurs in patients with mild to moderate bronchial asthma (Akkoca et al 1999;Barbarito et al 2001;Weiner et al 2002). We have recently reported that transdermal tulobuterol treatment increases the force-frequency curves of normal diaphragm muscle for 24 hours (Shindoh et al 2007).…”

How and Why Exercise Is Impaired in COPD

“…Clearly, disuse cannot be ignored, but other factors must cause it in the first place. Steroid myopathy is unlikely to be a common cause of skeletal muscle dysfunction in COPD as it occurs with oral therapy [25, 26, 27], whereas most patients with COPD receiving steroids are given aerosols. Furthermore, steroids cause atrophy of type 2 fibers [28]while in COPD type 1 fibers are primarily affected [16].…”