Lack of Efficacy of Symptoms and Medical History in Distinguishing the Degree of Eosinophilia in Nasal Polyps

Abstract

BACKGROUND Distinguishing eosinophilic nasal polyps (NP) from noneosinophilic NP will impact prognosis and therapeutic responsiveness. OBJECTIVE To investigate the ability of clinical history and biomarkers to distinguish these conditions. METHODS A total of 74 consecutive patients undergoing surgery for NP were enrolled. Clinical presentations were evaluated using the 22-item sinonasal outcome test (SNOT-22). Biomarkers included absolute eosinophil count, IgE, and extent of tissue hyperplasia on sinus computed tomography scan. Tissue eosinophilia was quantified in 10 random hpf and data analyzed addressing both peak and average results. RESULTS No component of the SNOT-22 was predictive of tissue eosinophilia. Similarly, a medical history of allergic rhinitis, asthma, or aspirin-exacerbated respiratory disease was not predictive. An absolute eosinophil count of more than 300 was associated with NP tissue eosinophilia. In contrast, neither IgE nor extent of sinus computed tomography hyperplasia was predictive. CONCLUSIONS The ability to individualize therapies for NP is dependent on identifying clinical features or biomarkers of eosinophilia. However, with the exception of circulating eosinophilia, we could not identify a clinical feature or biomarker that robustly predicted the presence of tissue eosinophilia. Even more problematic, even the seeming “criterion standard” determination of tissue pathology was of limited value, as our cohort displayed a continuous spectrum of tissue eosinophil expression, making arbitrary any definitive cutoff distinguishing these conditions.

Neutrophils are underrecognized contributors to inflammatory burden and quality of life in chronic rhinosinusitis

“…Angiogenesis is a recognized feature of asthma, 9 and we already showed a link between bradykinin and vascular GF in asthmatic fibroblasts. 4 The present data, in line with previous reports, 4,10 support both angiogenin and VEGF as factors implicated Anna Folino and Vitina Carriero authors are first authors.…”

Chronic rhinosinusitis: Endotypes, biomarkers, and treatment response

“…17 All of these observations force consideration that the very concept of their being ''distinct'' endotypes in patients with CRS is misguided; that is, instead of being distinct phenotypes or endotypes defined by the absolute presence or absence of eosinophils, a given cytokine, or of any other specific marker, CRS needs to be approached properly as a continuum of inflammatory processes with high and variable expression of immune and inflammatory markers. Thus, in the case of eosinophilia, in our recently published studies, 18 although it was possible to define a cohort of noneosinophilic NPs (< _3 eosinophils in 10 distinct 3400 high-powered fields) and we could similarly define hypereosinophilic NPs (> _25 eosinophils), the majority of patients fell within a continuum of intermediate expression ( Fig 2) 18 without any distinct cutoff that would unambiguously separate an ''eosinophilic'' from a ''noneosinophilic'' process. These data argue that any attempt to define a distinct cutoff distinguishing eosinophilic from noneosinophilic polyps would be at best arbitrary.…”

“…For the distribution of eosinophil numbers, ''['' indicates inclusion of that number and '')'' indicates less than that number. Reproduced with permission from Steinke et al18…”

Biomarkers in Chronic Rhinosinusitis with Nasal Polyps

“…Kountakis [13] et al established a cutoff point of greater than 5 eosinophils per high power field, while Soler et al had a higher cutoff of 10 eosinophils per high power field based on a measurement of QOL improvement post-surgery [14]. Importantly, degree of tissue eosinophilia is extremely difficult to determine based on clinical symptoms, and it cannot be predicted by SNOT-22 scores or the concomitant presence of asthma or aspirin-exacerbated respiratory disease (AERD) [15]. While many studies establish that it is possible to identify a cohort of noneosinophilic nasal polyp patients and a cohort of hypereosinophilic nasal polyp patients, most patients fall along an expression continuum that makes grouping solely on eosinophilia difficult [15].…”

“…Importantly, degree of tissue eosinophilia is extremely difficult to determine based on clinical symptoms, and it cannot be predicted by SNOT-22 scores or the concomitant presence of asthma or aspirin-exacerbated respiratory disease (AERD) [15]. While many studies establish that it is possible to identify a cohort of noneosinophilic nasal polyp patients and a cohort of hypereosinophilic nasal polyp patients, most patients fall along an expression continuum that makes grouping solely on eosinophilia difficult [15]. Further experiments have utilized blood eosinophilia to predict disease relapse following surgery, but this is complicated by the fact that blood eosinophilia is not definitively correlated with that in tissue [16].…”