American journal of respiratory and critical care medicine
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Am. J. Respir. Crit. Care Med. · Jun 2019
ReviewInhaled Corticosteroid Therapy in Adult Asthma: Time for a New Therapeutic Dose Terminology.
The Global Initiative for Asthma guidelines use the traditional terminology of "low," "medium," and "high" doses of inhaled corticosteroids (ICS) to define daily maintenance doses of 100 to 250 μg, >250 to 500 μg, and >500 μg, respectively, of fluticasone propionate or equivalent for adults with asthma. This concise clinical review proposes that this terminology is not evidence based and that prescribing practice based on this terminology may lead to the use of inappropriately excessive doses of ICS. Specifically, the ICS dose that achieves 80-90% of the maximum obtainable benefit is currently classified as a low dose, with the description of two higher dose levels of medium and high, which are associated with significant risk of systemic adverse effects. ⋯ We propose a reclassification of ICS doses based on a "standard daily dose," which is defined as 200-250 μg of fluticasone propionate or equivalent, representing the dose at which approximately 80-90% of the maximum achievable therapeutic benefit of ICS is obtained in adult asthma across the spectrum of severity. It is recommended that ICS treatment be started at these standard doses, which then represent the doses at which maintenance ICS are prescribed at step 2 and within ICS/long-acting β-agonist combination therapy at step 3. The opportunity is available to prescribe higher doses within ICS/long-acting β-agonist maintenance therapy in accordance with the stepwise approach to asthma treatment at step 4.
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Am. J. Respir. Crit. Care Med. · Jun 2019
Human Rhinovirus Impairs the Innate Immune Response to Bacteria in Alveolar Macrophages in COPD.
Rationale: Human rhinovirus (HRV) is a common cause of chronic obstructive pulmonary disease (COPD) exacerbations. Secondary bacterial infection is associated with more severe symptoms and delayed recovery. Alveolar macrophages clear bacteria from the lung and maintain lung homeostasis through cytokine secretion. ⋯ The IL-10 response to H. influenzae was significantly impaired by poly I:C, IFN-β, and IFN-γ in COPD cells. Conclusions: HRV impairs phagocytosis of bacteria in COPD, which may lead to an outgrowth of bacteria. HRV also impairs cytokine responses to bacteria via the TLR3/IFN pathway, which may prevent resolution of inflammation leading to prolonged exacerbations in COPD.