Environmental factors and allergic diseases

An objective of this article is a review of contemporary knowledge on various environmental factors, that influence prevalence and course of allergic diseases, like asthma, allergic rhinitis, atopic dermatitis and also contact dermatitis. Surrounding climate may directly influence each patient, but also determines type of flora and fauna within particular geographical regions and thus affects sources of airborne and food allergens. Epidemiological studies suggest that there is a strong relationship between air pollution and development and exacerbation of asthma and other allergic diseases – main attention has been concentrated on gaseous materials such as ozone (O3) and nitrogen dioxide (NO2), as well as particulate matter (PM), generated by car traffic and industry. Diesel exhaust particulate (DEP) has the ability to bind proteins and may serve as a potential carrier of allergens, penetrating deep into respiratory tract. Among the most extensively studied environmental factors influencing allergy are airborne allergens: dust mites, pollens, fungi and animal dander. Foods may elicit both true IgE-mediated allergy and also various non-immunological reactions, associated with direct release of mediators or toxic activity. It has been estimated, that over 85 000 chemicals are recognized in the human environment and they may act as contact allergens or irritants, causing allergic or non-allergic contact dermatitis. Among them metals, fragrances, preservatives, botanicals and paraphenylenediamine are considered as the most significant. Infections have always been associated with etiopathogenesis of allergic diseases and they may contribute to exacerbation of their course

Circulating Tumor Cells as a Marker of Disseminated Disease in Patients with Newly Diagnosed High-Risk Prostate Cancer

The aim of this study was to investigate whether the enumeration of circulating tumor cells (CTCs) in blood can differentiate between true localized and metastatic prostate cancer. A cross-sectional study of 104 prostate cancer patients with newly diagnosed high-risk prostate cancer was conducted. In total, 19 patients presented metastatic disease and 85 were diagnosed with localized disease. Analyses included intergroup comparison of CTC counts, determined using the CellSearch® system, EPISPOT assay and GILUPI CellCollector®, and ROC analysis verifying the accuracy of CTC count as a maker of disseminated prostate cancer. The vast majority (94.7%) of patients with advanced-stage cancer tested positively for CTCs in at least one of the assays. However, significantly higher CTC counts were determined with the CellSearch® system compared to EPISPOT assay and GILUPI CellCollector®. Identification of ≥4 CTCs with the CellSearch® system was the most accurate predictor of metastatic disease (sensitivity 0.500; specificity 0.900; AUC (95% CI) 0.760 (0.613–0.908). Furthermore, we tried to create a model to enhance the specificity and sensitivity of metastatic prediction with CTC counts by incorporating patient’s clinical data, including PSA serum levels, Gleason score and clinical stage. The composite biomarker panel achieved the following performance: sensitivity, 0.611; specificity, 0.971; AUC (95% CI), 0.901 (0.810–0.993). Thus, although the sensitivity of CTC detection needs to be further increased, our findings suggest that high CTC counts might contribute to the identification of high-risk prostate cancer patients with occult metastases at the time of diagnosis