Effects of obesity and bariatric surgery on airway hyperresponsiveness, asthma control, and inflammation

Abstract

Background: Asthma in obese subjects is poorly understood, and these patients are often refractory to standard therapy.

Objectives: We sought to gain insights into the pathogenesis and treatment of asthma in obese subjects by determining how obesity and bariatric surgery affect asthma control, airway hyperresponsiveness (AHR), and markers of asthmatic inflammation.

Methods: We performed a prospective study of (1) asthmatic and nonasthmatic patients undergoing bariatric surgery compared at baseline and (2) asthmatic patients followed for 12 months after bariatric surgery.

Results: We studied 23 asthmatic and 21 nonasthmatic patients undergoing bariatric surgery. At baseline, asthmatic patients had lower FEV(1) and forced vital capacity and lower numbers of lymphocytes in bronchoalveolar lavage fluid. After surgery, asthmatic participants experienced significant improvements in asthma control (asthma control score, 1.55 to 0.74; P < .0001) and asthma quality of life (4.87 to 5.87, P < .0001). Airways responsiveness to methacholine improved significantly (methacholine PC(20), 3.9 to 7.28, P = .03). There was a statistically significant interaction between IgE status and change in airways responsiveness (P for interaction = .01). The proportion of lymphocytes in bronchoalveolar lavage fluid and the production of cytokines from activated peripheral blood CD4(+) T cells increased significantly.

Conclusions: Bariatric surgery improves AHR in obese asthmatic patients with normal serum IgE levels. Weight loss has dichotomous effects on airway physiology and T-cell function typically involved in the pathogenesis of asthma, suggesting that obesity produces a unique phenotype of asthma that will require a distinct therapeutic approach.

Figure 1

Enrollment and follow-up of study participants. Participants were initially enrolled prior to bariatric surgery, though only participants who actually went through bariatric surgery were included in the analysis. There were six asthmatics and no control participants who did not have bariatric surgery. This was related to the fact that asthmatics were enrolled at presentation to the bariatric clinic whereas control participants were only enrolled once their surgery had been scheduled.

Figure 2

Change in AHR in patients with normal IgE (A) (P = .001), n = 11 and elevated IgE (B) (P = .89). Squares represent median values. A significant interaction term exists between IgE status and change in AHR (P = .01 for interaction term).

Figure 3

Cytokine production from CD3–CD28 stimulated CD4⁺ T lymphocytes before, and 12 months after, bariatric surgery in controls (n=15) and asthmatics (n=10). P values shown for comparison of asthmatics at 0 and 12 months, no significant differences between asthmatics and control at visit 0.