Anti-Calprotectin S100A8 monoclonal antibody

Purpose: To investigate whether measurement of urinary calprotectin can serve as a biomarker in the diagnosis of primary bladder cancer and to confirm its diagnostic role in determining high grade and stage disease. Materials and Methods: Urinary calprotectin was measured in spot urine samples from patients with primary bladder cancer and control subjects. To confirm levels in urine, tissue samples were also obtained from bladder tumor and healthy trigone of bladder by transurethral resection in both groups. Finally, calprotectin levels in tissue and urine of the patients and control subjects were compared and their diagnostic potential was investigated in high grade and stage bladder cancers. Results: Of 82 participants, 52 were patients with bladder cancer and 30 were control subjects. The two groups were comparable in terms of age, smoking status, and comorbidities. Tissue and urinary calprotectin levels were significantly higher in the bladder cancer group. In subgroup analyses, urinary calprotectin levels were significantly higher in patients with high-grade, muscle-invasive tumors. After receiver operating characteristic analyses, the sensitivity and specificity of urinary calprotectin was 100% and 96.7%, respectively, in the diagnosis of primary bladder cancer. High grade and stage bladder cancers were detected with sensitivity and specificity of 70% and 74.2%, and 80% and 84.8%, respectively. Conclusions: Urinary calprotectin may be a valuable parameter in the diagnosis of primary bladder cancer with high sensitivity and specificity. Furthermore, it may be useful in the prediction of high grade and stage disease. However, more investigations are needed.

Introduction: Chronic rhinosinusitis (CRS) is a common upper airway disease with a prevalence of greater than 10% of the general population. Although the pathogenesis of CRS remains poorly understood, there is growing evidence indicating that epithelial physical barrier defects play an important role in CRS pathogenesis. Areas covered: Epithelial physical barriers are maintained by various intercellular junctions, especially tight junctions (TJs). Recent studies suggest that the expression of TJ molecules and epithelial barrier function in human nasal epithelium are modulated by various internal and external factors. This review summarizes recent advances regarding the structure, function, and regulating mechanisms of the epithelial physical barrier in the context of CRS. Expert opinion: Available data indicate that epithelial physical barrier defects in CRS can result from inhaled allergens, microbial or virus infections, cytokines, hypoxia, or zinc deficiency, among other causes. Several genes/molecules, such as SPINK5, S100A7, S100A8/9, PCDH1, NDRG1, SPRR, and p63 are involved in modulating the physical barrier function in the context of CRS. The exact mechanisms and molecular pathways that lead to these barrier defects, however, require additional study. Additional work is necessary to further explore the epithelial physical barrier function in normal and pathologic sinonasal mucosa.