Association Between Hypercoagulability and Severe Obstructive Sleep Apnea.

Importance: Obstructive sleep apnea (OSA) is related to the increased risk of cardiovascular disease. Although the pathogenesis of this association remains unclear, an alteration in coagulability is suspected as a link. Objective: To investigate the association between the severity of OSA and blood coagulability. Design, Setting, and Participants: A retrospective cohort study conducted at a tertiary care university hospital evaluated 146 patients with OSA from January 1, 2009, to July 31, 2015. The participants were divided into 4 groups according to the severity of OSA: control, mild, moderate, and severe. Main Outcomes and Measures: Association between the severity of OSA and coagulation test results, including platelet count, bleeding time, prothrombin time (PT) in seconds and as international normalized ratio (INR), and activated partial thromboplastin time. Results: Of the 146 patients, 135 (92.5%) were men; mean (SD) age was 34.8 (11.1) years. The control group included 41 (28.1%) patients; mild OSA, 32 (21.9%); moderate OSA, 30 (20.5%); and severe OSA, 43 (29.5%). Significant correlations were found between the apnea-hypopnea index and the PT seconds (Spearman r coefficient, -0.30; 95% CI, -0.44 to -0.14) and PT INR (Spearman r coefficient, -0.30; 95% CI, -0.44 to -0.14). There were significant differences between the OSA severity groups for PT seconds for the control group (mean, 11.26 [0.78] seconds) vs the moderate OSA group (10.74 [0.62] seconds; mean difference [MD], 0.52; 95% CI, 0.27 to 1.01) and the severe OSA group (10.67 [0.77] seconds; MD, 0.59; 95% CI, 0.14 to 1.03). Significant differences were also noted in PT INR between the control group (1.00 [0.07]) vs the moderate OSA group (0.95 [0.05]; MD, 0.04; 95% CI, 0.01 to 0.07) and the severe OSA group (0.94 [0.07]; MD, 0.05; 95% CI, 0.02 to 0.08). However, there was no significant difference between the control and mild OSA groups in PT seconds. Conclusions and Relevance: These results suggest that patients with moderate to severe OSA have elevated blood coagulability markers compared with healthy individuals, which may contribute to the occurrence of cardiovascular complications.

Increased expression of acidic mammalian chitinase and chitotriosidase in the nasal mucosa of patients with allergic rhinitis.

OBJECTIVES/HYPOTHESIS: Acidic mammalian chitinase (AMCase) has emerged as an important mediator of allergic asthma in both animal models and in humans. Recently, chitotriosidase has been suggested to play a role in innate immunity because of its phagocytic-specific expression. Thus, AMCase and chitotriosidase may play a role in the pathogenesis of allergic nasal mucosa. The expression and pattern of distribution of AMCase and chitotriosidase were, therefore, determined in normal and allergic nasal mucosa. STUDY DESIGN: Controlled, prospective study. METHODS: Normal inferior turbinate mucosa was obtained in patients who were admitted for augmentation rhinoplasty. Allergic turbinate mucosa was obtained from patients who had perennial allergic rhinitis during septo-turbinate surgery. Reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blotting were applied to the normal and allergic nasal mucosa. RESULTS: The expression of AMCase and chitotriosidase mRNAs and proteins analyzed by RT-PCR and Western blot were detected in all normal and allergic turbinate mucosa tested. The levels of expression of AMCase and chitotriosidase mRNAs and proteins were increased in allergic turbinate mucosa compared with normal turbinate mucosa. In both normal and allergic turbinate mucosa, AMCase and chitotriosidase were detected in the epithelium, inflammatory cells, and submucosal glands. The staining intensity for AMCase and chitotriosidase was stronger in allergic nasal mucosa than normal nasal mucosa. CONCLUSIONS: AMCase and chitotriosidase are constitutively expressed in normal turbinate mucosa, suggesting involvement in defense against chitin-containing pathogens. Upregulation of these chitinases in allergic condition suggests that they may play a role in the nasal allergic reaction like other inflammatory mediators in allergic rhinitis. Laryngoscope, 2010.

Upregulation of elafin and cystatin C in the ethmoid sinus mucosa of patients with chronic sinusitis.

OBJECTIVES: To investigate the expression levels and distribution patterns of elafin and cystatin C in normal and inflammatory human sinus mucosa and to evaluate their roles in chronic sinusitis. DESIGN: A controlled, prospective study. SETTING: A tertiary academic institution. PATIENTS: Normal sinus mucosa was obtained from the ethmoid sinus during surgery in 30 patients with blowout fractures. Inflammatory sinus mucosa was obtained from 30 patients undergoing endoscopic sinus surgery for chronic polypoid sinusitis. INTERVENTIONS: Reverse transcription-polymerase chain reaction, immunohistochemical analysis, and Western blotting. MAIN OUTCOME MEASURES: Expression levels and distribution patterns of elafin and cystatin C in normal and inflammatory mucosa. RESULTS: Expression of elafin and cystatin C messenger RNAs and proteins analyzed by means of reverse transcription-polymerase chain reaction and Western blot was detected in all normal and inflammatory sinus mucosa tested. Their expression levels were increased in inflammatory vs normal mucosa. Elafin in normal and inflammatory sinus mucosa was distinctly expressed in goblet cells, which are increased in inflammatory sinus mucosa. Elafin in submucosal glands was usually weak in staining intensity, except for a few scattered submucosal glands showing moderate intensity in inflammatory sinus mucosa. Cystatin C was also localized in goblet cells and submucosal glands in normal and inflammatory mucosa. Staining intensity was increased more in inflammatory vs normal sinus mucosa. CONCLUSION: Elafin and cystatin C may play an important role in the protection of normal sinus mucosa and further in regulation of the inflammatory condition in chronic sinusitis.