The clinical syndrome of aspirin-exacerbated respiratory disease (AERD) is a condition where inhibition of cyclooxygenase-1 (COX-1) induces attacks of upper and lower airway reactions, including rhinorrhea and varying degrees of bronchospasm and laryngospasm. Although the reaction is not IgE-mediated, patients can also present with anaphylactic hypersensitivity reactions, including hypotension, after exposure to COX-1 inhibiting drugs. All patients with AERD have underlying nasal polyps and intractable sinus disease which may be difficult to treat with standard medical and surgical interventions. This review article focuses on the management of AERD patients with a particular emphasis on aspirin desensitization and continuous treatment with aspirin.

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Exposure to cigarette smoke is associated with a significant increase in the risk for respiratory viral infections. The airway epithelium is the primary target for both cigarette smoke and respiratory viral infection. We investigated the effects of cigarette smoke on the response of airway epithelial cells to rhinovirus infection. We found that pre-exposure of BEAS-2B cells or primary normal human bronchial epithelial cells (NHBEs) to cigarette smoke extract (CSE) reduced the induction of mRNA of the chemokines CXCL10 and CCL5 by either the viral mimic polyinosine-polycytidylic acid (Poly I:C) or human rhinovirus 16 (HRV-16) infection. The HRV-16-induced release of CXCL10 and CCL5 was also significantly suppressed by CSE. Activation of the IFN mediator STAT-1 and the activation of JNK by poly I:C and HRV-16 were partially suppressed by pre-exposure to CSE. In contrast, the poly I:C-induced and HRV-16-induced phosphorylation of ERK1/2 was unaffected by CSE. HRV-16-stimulated IFN-b mRNA was also significantly reduced by CSE. Because suppression of the IFN response to viral infection was associated with increased viral production, we assessed HRV-16 RNA concentrations. Exposure to CSE resulted in an increase in HRV-16 RNA at 48 hours after the infection of BEAS-2B cells. These data demonstrate that exposure to CSE alters the response of airway epithelial cells to HRV infection, leading to decreased activation of the IFN-STAT-1 and SAP-JNK pathways, the suppression of CXCL10 and CCL5 production, and increased viral RNA. A diminished, early epithelial-initiated antiviral response to rhinovirus infection could contribute to the increased susceptibility of subjects to prolonged respiratory viral infections after exposure to cigarette smoke.

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BackgroundInfluenza causes significant morbidity and mortality; the pandemic in 2009–2010 was a reminder of the potential for novel strains and antigenic changes. Studies have shown that vitamin D deficiency may be associated with poor vaccine immunogenicity, therefore we sought to determine if there was a correlation between 25-hydroxyvitamin D [25(OH)D] and influenza vaccine response.MethodsA retrospective observational study was conducted among young, healthy military members to evaluate the association between total 25(OH)D levels with post influenza vaccination antibody titers and healthcare encounters during the 2009–10 influenza season. Univariate analyses were performed to evaluate whether 25(OH)D levels are associated with baseline characteristics and post-vaccination antibody responses. Multivariable logistic regression models were utilized to determine the associations between antibody responses and 25(OH)D levels adjusting for possible confounders.ResultsA total of 437 subjects were studied. Most participants were young adults (91% were 18–39 years of age), 50% were male, and 56% resided in the southern U.S. Overall, 152 (34.8%) were vitamin D deficient, 167 (38.2%) insufficient, and 118 (27.0%) with normal 25(OH)D levels. There were no demographic differences by 25(OH)D category. Only 224 (51.3%) demonstrated a seroprotective anti-influenza post-vaccination titer, which did not vary by categorical 25(OH)D levels [vitamin D deficient vs. normal: OR 1.10 (0.68–1.78) and insufficient vs. normal: OR 1.25 (0.78–2.01)] or continuous vitamin D levels [OR 0.98 (0.84–1.15)]. There were also no associations with increased influenza like illnesses, respiratory diagnoses and healthcare encounters between the vitamin D groups.ConclusionVitamin D insufficiency and deficiency were highly prevalent despite evaluating a young, healthy adult population. There were no significant associations between 25(OH)D levels and post-vaccination antibody titers to influenza vaccine. Further studies are required to discover strategies to improve vaccine efficacy as well as to determine the role of 25(OH)D in vaccine immunity.

Recent reports suggest US military service members who deployed in support of the recent conflicts in Iraq and Afghanistan have higher rates of new-onset asthma than those who did not deploy. However, it is unknown whether combat experiences, in addition to deployment, contribute to new-onset asthma risk. This study aimed to longitudinally determine the risk factors for developing asthma, including combat deployment (categorized as deployed with combat experience, deployed without combat experience, or nondeployed), among participants in the Millennium Cohort Study from 2001 to 2013. A total of 75,770 participants completed a baseline survey and at least 1 triennial follow-up survey on deployment experiences, lifestyle characteristics, and health outcomes. Complementary log-log models stratified by sex were used to estimate the relative risk of developing asthma among participants who reported no history of asthma at baseline. In models with adjustments, those who deployed with combat experience were 24%–30% more likely to develop asthma than those who did not deploy. Deployed personnel without combat experience were not at a higher risk for new-onset asthma compared with nondeployers. Further research is needed to identify specific features of combat that are associated with greater asthma risk to inform prevention strategies.

A penicillin allergy label is a risk to military readiness secondary to associated increases in the length of hospitalizations and emergency department and medical visits. Penicillin de-labeling is a simple intervention that can improve readiness, significantly decrease health care costs and prevent antibiotic resistance, as well as antibiotic-associated adverse events. The military allergist should be "front and center" providing expertise guidance and leadership for clinic and hospital-based penicillin de-labeling efforts which are nested within the antibiotic stewardship programs.