xRead - Nasal Obstruction (September 2024) Full Articles

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International consensus statement on rhinosinusitis

RV inoculation. 370,371 Both studies found early increases in IL-10 in controls exposed to RV. Koch et al. also showed increases in IL-6 and interferon gamma-induced protein 10. 370 These studies suggest viral infection induced alter ation of the immunologic homeostasis of the sinonasal mucosa, which could promote secondary bacterial infec tion. Interestingly, Koch et al. also found repeated inoc ulation with RV 1 week after initial exposure had atten uated cytokine response. 370 This is consistent with anti inflammatory and immunosuppressive functions for IL 10 seen in overexpression experiments by Stanic et al. and could provide a mechanism for ABRS following RV infection. 372 In vitro RV models. In vitro experiments have focused on the effect of RV inoculation on markers of immunoreg ulation, as RV accounts for most viral URIs. 373 These studies suggest that viral infection provokes alterations to immunologic homeostasis, consistent with invivo studies. Wang et al. determined that RV infections invitro resulted in increased bacterial adhesion on subsequent exposure to common bacterial pathogens, likely explained by RV induced expression of enhanced bacterial host cell adhe sion molecules. 374 This finding is consistent with the trend toward increased bacterial load noted in Hofstra et al. 368 In summary, the epidemiologic studies show that a subset of patients with viral URI will develop clinical ARS. Viral challenge experiments with RV support previ ous data showing increased bacterial populations in natu rally occurring viral infection. Invitro studies provide evi dence that viral infection (particularly RV) leads to altered immunologic homeostasis that could underly previously proposed mechanisms of ostial obstruction or disrupted MCC. Further longitudinal studies are needed to evaluate why only a small percentage of patients with viral infec tion develop ARS, and if there are specific virome-genome interactions that result in these susceptible populations.

medications in allergic adults with ARS. Moreover, there is no evidence that treatment of AR reduces the incidence of ARS.

Allergy as a Contributing Factor for ARS Aggregate Grade of Evidence: C (Level 2: 5 studies; level 3: 4 studies; level 4: 2 studies; Table VII-6).

VII.C.3 Contributing Factors for ARS: Viruses It has been hypothesized that viral URI predisposes to development of ARS. Autio et al. noted 84% nasopharyn geal viral prevalence by multiplex PCR in ARS patients. 363 Maxillary infundibulum occlusion in viral infection 216 and increased nasal or ostiomeatial complex (OMC) bacterial loads in viral URI compared to healthy controls 364,365 have also been suggested as contributing factors. Several lines of evidence have been published, including epidemiologic studies, prospective viral challenges, and in vitro experiments. Epidemiologic studies . There have been several stud ies estimating the prevalence of RS and co-occurrence of viral infection as a complication of URI in children and adults. In cohort studies by Demuri et al., 7.1% of chil dren with URI symptoms developed ARS. 366 Rhinovirus (RV: 45%), coronavirus (CoV: 6%), and respiratory syncy tial virus (RSV: 3%) were detected in patients with uncom plicated URI. In patients with ARS, 76% showed early PCR evidence of virus (35% RV, 13% CoV, 10% RSV). One limita tion of this study is that diagnoses of ARS were based solely on clinical criteria alone. RV is the predominant virus detected in the majority of epidemiologic studies. 363,366,367 Prospective RV challenges . Prospective viral challenges have examined the impact of experimentally-induced RV inoculation. Hofstra et al. utilized 16s rRNA sequenc ing to evaluate bacterial populations in 6 healthy par ticipants with confirmed, experimentally-induced RV-16 infections. 368 Trends were observed toward increased H. parainfluenzae, S. aureus , and N. subflava , suggesting increased bacterial populations after RV infection. Allen et al. inoculated 10 healthy volunteers with RV-39. No increase in bacterial load was found. 369 Both studies were underpowered to demonstrate a statistically significant change. Koch et al. and Heymann et al. evaluated changes in inflammatory cytokine levels in healthy volunteers upon

Viruses as a Contributing Factor for ARS Aggregate Grade of Evidence: C (Level 3: 4 studies; level 4: 8 studies; level 5: 6 studies; Table VII-7).

VII.C.4 Contributing Factors for ARS: Odontogenic Infections Odontogenic rhinosinusitis (ORS) results from diseases arising from the dental or dentoalveolar structures. Dur ing development, the adult maxillary sinus expands toward