xRead - Nasal Obstruction (September 2024) Full Articles

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to injury even at higher pH events, and cites a higher incidence of nasopharyngeal reflux events with pH < 5 in refractory CRS patients. 676 Pepsin, which is found in higher levels in the middle turbinates of CRS patients rela tive to controls, is believed to mediate high pH injury, dam aging the epithelial barrier by digesting intercellular junc tion proteins, promoting a pro-inflammatory milieu, dam aging mitochondria, and upregulating MAP Kinase and downstream heat shock protein 70 in human nasal epithe lial cells, indicating a response to cellular damage. 696–698 H. pylori has also been implicated in CRS pathogenesis. 699,700 Vceva et al. identified H. pylori DNA in the nasal polyp tissue of 28.6% (10/35) of their study group but did not find any in the middle turbinates of their control cohort, in spite of the ubiquitous H. pylori DNA found in the gastric mucosa of all study and control patients. 699 Ozdek et al. found that 33% of patients with classic CRS were positive for H. pylori DNA, while none of their control group was positive. 701 In their meta-analyses, Leason et al. found the H. pylori prevalence in CRS was 31.7%, and that 87.5% of subjects with intranasal H. pylori hadGERD. 681 Proton pump inhibitors play a key role in manage ment of suspected reflux-associated CRS. Vaezi et al., in a DBRCT demonstrated a reduction in PND, SNOT-20, and Quality of Life in Reflux and Dyspepsia scores in PND patients treated with lansoprazole 30 mg twice daily for 16 weeks vs placebo. 679 Median symptoms score improve ment for patients treated with a PPI at 8 and 16 weeks was 55 and 50 respectively, relative to 3.5 and 5.0 for con trols. DiBaise et al. found that 67% of 19 adult patients with GER and CRS had improvements in measures of sinonasal health after reflux treatment. 702 DiBaise et al. in an open label study of 11 refractory CRS patients with GERD treated with omeprazole for 12 weeks, found that sinus and global satisfaction scores improved in most patients, peaking by week 8 and maintaining thereafter. Anzic et al. performed a DBRCT where patients with diagnosed LPR and comor bid CRS received 8 weeks of omeprazole 20 mg twice daily. They found objective reductions in reflux symptom index and scores, improved symptoms of comorbid CRSsNP, and improved endoscopy scores. 679 CRS remains a multifactorial disease, with existing data suggesting that reflux can be an important contributor in some cases, especially in refractory disease. When reflux is present, treatment should include addressing the nasal inflammatory condition as well as the reflux. The long term use of PPIs must be weighed with inherent risks of long term PPI use, including pneumonia, susceptibility to enteric infections such as Clostridium difficile , micronutri ent deficiencies, osteoporosis, rebound reflux disease after treatment cessation, and PPI-resistance. 703,704 For this reason, various other treatments have been tested for a

safer management of GERD or LPR. Alginate compounds have demonstrated, in various studies, an efficacy com parable to PPIs in the management of this disease with a comforting safety profile. 705–707 In particular, magnesium alginates showed interesting results in children with LPR and uncontrolled asthma, with a significant improvement of both reflux and airway related inflammation. 708 With this data in mind, we conclude that with the evidence available, we cannot recommend the use of PPIs for the treatment of CRS, although it may be a useful adjunct in cases where post-nasal drip is a leading symptom.

Reflux as a Contributing Factor for CRSsNP Aggregate Grade of Evidence: B (Level 1: 1 study; level 2: 2 studies; level 3: 3 studies; level 4: 9 studies; Table IX-7).

IX.C.6 Contributing Factors for CRSsNP: Vitamin D Deficiency Vitamin D (VD3) circulates in its inactive form (25VD3) and is converted to its active form (1,25VD3) by 1 α hydrox ylase. This active form has anti-inflammatory and anti bacterial actions, 710–712 thus prompting studies on its potential role in CRS. Our understanding of CRSsNP is limited, but it is thought to represent a heterogeneous disease process, characterized by the absence of nasal polyps. 154 The literature on the effects of vitamin D on CRSsNP consists primarily of studies comparing CRSsNP and controls, and is limited to case series and case-control studies looking at systemic and local sinonasal vitamin D levels and metabolism. Clinical studies investigating systemic vitamin D lev els in adult CRSsNP patients predominantly demonstrate a lack of association between CRSsNP and systemic vita min D deficiencies. 713–720 This lack of association is fur ther supported in a pediatric study (Table IX-8). 717 While systemic 25VD 3 levels appear to be normal in CRSsNP patients, active or passive smoke exposure is associated with decreased systemic 25VD 3 . 719 Active smoking was also shown to decrease serum 25VD3 and 1,25VD3 in per imenopausal women without CRS. 721 A study looking at ethnic background and its effect on CRS found that African Americans with severe CRS had significantly lower serum 25VD 3 levels than both Caucasian patients and race/sex matched controls, but a limitation of this study is that polyp status was not defined. 722 Of the reviewed studies,

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