Background: Among the extraintestinal manifestations of inflammatory bowel disease (IBD), those involving the lungs are relatively rare and often overlooked. There are only scarce data on the prevalence of IBD-associated lung involvement in children. Objectives: The aim of our study was to assess pulmonary function in IBD children by different methods and to evaluate the influence of immunosuppressive therapy on disease severity. Methods: Seventy-two children with IBD (mean age of 14.45 ± 2.27 years) and 40 age-matched healthy controls (mean age of 14.17 ± 2.82) were included in the study. Pulmonary function tests (PFTs) were carried out by means of spirometry, oscillometry (IOS) and fractional exhaled nitric oxide (FeNO) to assess the pulmonary involvement. Results: Certain differences were observed between the study group and the control group, regarding the spirometric and oscillometry parameters. The fractions of exhaled nitric oxide did not differ between the group with IBD patients and the control group with regards to disease activity, the duration of illness and the administered immunosuppressive treatment. Conclusions: The mean spirometry results were significantly different in the study group compared to the controls, although they were still within the normal limits. The pulmonary function abnormalities did not depend on either the disease activity or the immunosuppressive therapy. Oscillometry could be a supplementary method to assess pulmonary resistance. In turn, FeNO does not appear to be useful either in screening IBD children for pulmonary involvement or for the evaluation of disease activity. It appears then that only general screening of asymptomatic patients is a suitable method and a necessary recommendation in this population, prompting a revision of the current diagnostic approach.

An increasing morbidity of atopic diseases (atopic dermatitis, food allergy, asthma and allergic rhinitis) documented in large cohort epidemiological studies is at least partially determined by high hygienic standards of living. Over the last 40 years, the accepted concept of pathogenesis of atopic diseases, the so-called atopic march, was proposed by Fouchard in 1973. It referred to the natural history of atopy manifestation, with a typical sequence of symptoms presented as atopic dermatitis in early childhood for subsequent development of allergic respiratory symptoms in late childhood and adolescence. New data suggests that the leading role of atopic dermatitis in atopic march might be less pronounced than previously expected, indicating coexistence rather than succession of atopic symptoms. The objective of this paper is to present the currently discussed concepts of atopic dermatitis – its pathogenesis, etiology, course and role in the development of other allergic diseases. More widely, we will present: 1. The genetic factors involved in skin barrier disruption with the leading role of loss-of-function gene for filaggrin mutation, 2. Genetic defects and epigenetic regulation of the immune system 3. Epidermal changes with physical barrier dysfunction as well as 4. Skin microbiome disturbances with Staphylococcus aureus colonization leading to abnormalities of the epidermal protective barrier.