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Objective Periostin is an extracellular matrix protein that is elevated in the sinonasal tissues of patients with chronic rhinosinusitis (CRS). The purpose of this study was to determine whether serum periostin could serve as a molecular biomarker of nasal polyp burden in sinonasal disease. Study Design Prospective cohort study. Setting Academic medical center. Subjects and Methods Serum periostin levels were measured by ELISA on blood samples collected from patients undergoing sinus surgery for CRS (n = 71), further stratified by phenotype as defined by nasal polyps and asthma. Results were compared with assays performed on control subjects (n = 62). Results Mean serum periostin levels were markedly elevated in patients with CRS versus controls (66.1 ng/mL [95% CI, 51.6-80.6] vs 38.7 ng/mL [95% CI, 34.4-42.9], respectively, P = .004). In addition, mean periostin levels were significantly higher in CRS patients with nasal polyps as compared with those without polyps (94.8 ng/mL [95% CI, 67.3-122.4] vs 41.1 ng/mL [95% CI, 35.2-47.0], respectively, P < .001). Periostin levels did not correlate with sex ( P = .473), smoking history ( P = .748), aspirin-exacerbated respiratory disease status ( P = .136), oral steroid use within 1 month of surgery ( P = .281), use of topical steroid nasal spray ( P = .864), or number of prior sinus operations ( P = .973). Conclusion Serum periostin appears to be a novel molecular biomarker for the presence of nasal polyps and may serve as an indicator of CRS endotypes.

Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) have been shown to suppress expression of periostin, a matricellular protein that is markedly elevated in nasal polyp tissue. The purpose of this study was to determine whether use of these antihypertensive agents affects the time to revision sinus surgery in patients with polyp regrowth.Case series with chart review.Academic medical center.Records were reviewed for 330 patients who underwent ≥2 operations for chronic sinusitis with nasal polyps from April 1987 through August 2015. The time between surgical interventions was compared with patient demographics and clinical characteristics, including use of ACEIs and ARBs.Sixty patients were taking ACEIs or ARBs during the study period, of which 32 had concurrent asthma. The mean interval between polyp operations was 61.0 ± 45.2 months (range, 2-228.6 months). Among patients with asthma (n = 197), the mean time to revision surgery was prolonged by2 years for those taking ACEIs or ARBs (81.0 vs 54.5 months, P = .006). A similar impact on time to revision surgery was not observed for nonasthmatics taking these medications (61.0 vs 65.2 months, P = .655).Use of ACEIs and ARBs is associated with an increased time to revision sinus surgery among patients with concurrent nasal polyps and asthma. A possible mechanism of this observed effect is suppression of periostin expression through inhibition of the angiotensin pathway.

To determine whether variations in gene expression exist at multiple subsites along the sinonasal tract in patients with chronic sinusitis with polyps and in healthy controls.Prospective, controlled study.Academic medical center.Tissue expression levels of 5 genes, previously found to be characteristic of ethmoid polyps, were measured using real-time quantitative polymerase chain reaction in 100 sinonasal tissue samples. Specimens harvested from 5 regions--the ethmoid sinus, septum, inferior turbinate, middle turbinate, and lateral nasal wall--in 10 patients with chronic sinusitis and ethmoid polyps were compared to tissue from similar regions in 10 control patients without sinusitis. Western blot analysis was performed to validate differential gene expression at the protein level.Gene expression levels of ethmoid polyps differed significantly from those of healthy ethmoid mucosa, as well as tissue from 4 surrounding anatomical sites in both patients with chronic sinusitis and controls. Alterations specific to the polyp tissue included downregulated genes, prolactin-induced protein (fold change 377.2 ± 169.0, P.0001), and zinc α2-glycoprotein (fold change 72.1 ± 26.5, P.0001), as well as upregulated genes, met proto-oncogene (fold change 2.5 ± 0.7, P = .029), and periostin (fold change 7.5 ± 3.4, P = .003). No significant differences in gene expression was found for neurabin 2 (fold change 1.0, P = .99).The transcriptional pattern of ethmoid polyps appears to be unique compared with other subsites in the sinonasal cavity of patients with chronic sinusitis. Care must be taken when collecting specimens for molecular studies of the sinonasal tract to differentiate polyp from nonpolyp tissue in chronic sinusitis.

Objective: Etiologies for Meniere’s disease and sudden sensorineural hearing loss remain unknown. Indirect evidence exists for allergy-mediated or autoimmune process. The purpose of this study is to determine whether immunogenic proteins share similar sequences with inner ear proteins, which may lead to cross-reactivity and immune activation in inner ear disorders.Method: Comprehensive bioinformatic primary sequence analyses of intact and mutated proteins associated with human syndromic and nonsyndromic hearing loss and proteins expressed in the human inner ear was performed. Comparison of sequences to epitopes in the Immune Epitope Database was performed by exact match, BLAST, and BLOSUM62 score computational algorithms.Results: Computational analysis of primary protein sequence for 81 known inner ear proteins, 102 proteins from genes identified in syndromic and non-syndromic hearing loss, and 438 protein sequences with known mutations that contribute to sensorineural hearing loss was compared to 151,086...