Background: The majority of Polish smokers declare their will to quit smoking and many of them attempt to quit. Although morbidity and mortality from tobacco-related diseases are among the highest in the world, there is a lack of comprehensive cessation support for smokers. We aimed to investigate how Poles, including the medically ill, cope with quitting cigarettes and what their motivations to quit are.

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Background There is controversy whether taking β‐blockers or ACE inhibitors (ACEI) is a risk factor for more severe systemic insect sting reactions (SSR) and whether it increases the number or severity of adverse events (AE) during venom immunotherapy (VIT). Methods In this open, prospective, observational, multicenter trial, we recruited patients with a history of a SSR and indication for VIT. The primary objective of this study was to evaluate whether patients taking β‐blockers or ACEI show more systemic AE during VIT compared to patients without such treatment. Results In total, 1,425 patients were enrolled and VIT was performed in 1,342 patients. Of all patients included, 388 (27.2%) took antihypertensive (AHT) drugs (10.4% took β‐blockers, 11.9% ACEI, 5.0% β‐blockers and ACEI). Only 5.6% of patients under AHT treatment experienced systemic AE during VIT as compared with 7.4% of patients without these drugs (OR: 0.74, 95% CI: 0.43–1.22, p = 0.25). The severity of the initial sting reaction was not affected by the intake of β‐blockers or ACEI (OR: 1.14, 95% CI: 0.89–1.46, p = 0.29). In total, 210 (17.7%) patients were re‐stung during VIT and 191 (91.0%) tolerated the sting without systemic symptoms. Of the 19 patients with VIT treatment failure, 4 took β‐blockers, none an ACEI. Conclusions This trial provides robust evidence that taking β‐blockers or ACEI does neither increase the frequency of systemic AE during VIT nor aggravate SSR. Moreover, results suggest that these drugs do not impair effectiveness of VIT. (Funded by Medical University of Graz, Austria; Clinicaltrials.gov number, NCT04269629).

PurposeYKL-40 is a chitinase-like protein found to correlate with asthma as well as numerous infectious and autoimmune diseases or cancer. The aim of the present study was to investigate the role of YKL-40 as a possible marker of asthma and its associations with factors differentiating phenotypes of asthma.MethodsThe study group comprised 167 patients, including 116 women and 51 men aged 18–88 years with chronic asthma. The control group comprised 81 healthy individuals, including 50 women and 31 men aged 19–86 years. In every participant, medical history was taken; spirometry and skin prick tests were performed. YKL-40 was determined in sera by means of ELISA test.ResultsMean serum YKL-40 level was 59.7 ng/ml (53.6–65.7 ng/ml; 95 % CI) with significant difference between asthmatics and healthy controls (mean values: 66.8 ± 53.8 vs. 44.9 ± 29.4 ng/ml; p < 0.001). In asthmatics, the level was significantly higher in subgroup with poor control of symptoms and exacerbations (91.8 ± 57.1 ng/ml) compared to stable asthmatics (59.6 ± 50.8 ng/ml; p < 0.001) as well as in atopic compared to non-atopic asthmatics (77.2 ± 53.9 vs. 61.1 ± 57.8 ng/ml; p < 0.001). Mean YKL-40 level in obese asthmatics was 135.6 ng/ml compared to 50.0 ng/ml in non-obese (p < 0.001). When phenotypes of early-onset atopic, late-onset non-atopic, and obesity-related asthma were compared, YKL-40 levels were 80.62 ± 46.9, 51.5 ± 24.9, and 168.1 ± 71.5 ng/ml, respectively (p < 0.05).ConclusionAlthough YKL-40 is not a specific marker for asthma, it correlates with some clinical features such as exacerbation, level of control, atopy, and obesity.

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