Risk factors precipitating exacerbations in adult asthma patients presenting at Kalafong Hospital, Pretoria

BACKGROUND: Research into asthma is proceeding at an unprecedented rate and yet we live with a disease that escalates in prevalence and severity, despite a greater understanding of its pathophysiology and the necessary therapy. The total prevalence of asthma is estimated to lie at 7.2% of the world’s population (6% in adults, 10% in children). Data from Australia, Canada and Spain report that acute asthma accounted for 1 to 12% of all adult emergency department visits. The prevalence of asthma in South Africa lies at 5% for adults and 10% for children. Asthma is reported as taking up 1 to 2% of the total health budget in direct costs, with equally large indirect costs being incurred for time lost from work and reduced productivity. It has also been reported that approximately one-third of the direct care costs of asthma are attributable to emergency department visits and hospitalisations. In some cases, exposure may be unavoidable (for example exposures to cold air, exercise or the asthma-inducing effects of pregnancy). Many studies have been done in other countries on specific triggers, especially allergens and viral respiratory infections. However, circumstances differ in the public sector in South Africa and other factors such as compliance and under-treatment, which may be applicable, should be studied in contention. METHODS: A matched case-control study was undertaken matched on age and gender between December 2003 and May 2005. Known asthma patients with exacerbations presenting at Kalafong Hospital’s emergency unit were chosen as cases. Controls were stable asthma patients recruited from the outpatient departments. A structured questionnaire was used to interview patients concerning their possible exposure to certain triggers and risk factors. Univariate and multivariate analyses with conditional logistic regression were done to determine any significant exposures. Participants were between 18 and 65 years of age. RESULTS: In total, 356 patients were evaluated. Fifty cases and 100 controls were enrolled. Cases were shown to be more non-compliant than controls (OR = 2.18; 95% Confidence interval (CI): 1.09 to 4.38, p = 0.03). Missing follow-up doctor’s appointments for the last six months were statistically significant with an OR of 2.39 (95% CI 1.08 to 5.27) and p = 0.03. CONCLUSIONS: Non-compliance was a strong predictor of exacerbations in adult asthma patients at Kalafong Hospital

Effects of repeated respiratory syncytial virus infections on pulmonary dendritic cells in a murine model of allergic asthma.

BACKGROUND: Primary and secondary respiratory syncytial virus (RSV) infection differentially regulates preexisting allergic airway inflammation. OBJECTIVES: The present study was designed to determine the effects of primary and secondary low-grade RSV infections on pulmonary dendritic cell (DC) functions. METHODS: Eight groups of BALB/c mice were used: one group each for control primary and secondary sensitization, primary and secondary sensitization to Dermatophagoides farinae (Derf) allergen, primary and secondary infection with RSV, and primary and secondary sensitization to Derf plus infection with RSV. CD11c+ pulmonary DCs were isolated from these mice and then transferred to naive mice followed by intranasal Derf challenge. Furthermore, either anti-IL-12 monoclonal antibody (alphaIL-12 mAb) or anti-IL-10 (alphaIL-10) mAb were injected into donor mice after Derf challenge and during RSV infection to determine the involvement of IL-12 and IL-10. RESULTS: Primary RSV infection failed to induce polarization in DCs since it failed to induce IL-10 and IL-12 production in Derf-sensitized donor lung. In contrast, secondary RSV infection significantly enhanced IL-12 production from Derf-sensitized donor lung, thereby enhancing both Th1 and Th2 responses. During RSV infection, alphaIL-12 but not alphaIL-10 mAb treatment blocked these immunological effects. CONCLUSION: Via IL-12, DCs may play a critical role in shifting the immune response in this experimental model of repeated respiratory viral infection in allergic asthma