© Borgis - Postępy Nauk Medycznych 3/2014, s. 210
A significant increase in both incidence of inflammatory bowel disease (IBD) in children and in its severity has been observed over the past years. The novel biologic therapy gives a chance for better and more effective treatment in pediatric patients. The two published cases report the use of biologic therapy in both Crohn’s disease (CD) and ulcerative colitis (UC).
Wiernicka shows in her original paper the outcomes of biologic treatment with adalimumab in small group of children with UC. In her review paper, the author summarizes previous experiences with biologic therapy for UC.
Szymańska in her review paper describes clinical utility of different scales for the assessment of Crohn’s disease activity, and in her original paper, the author summarizes a considerable group of children qualified to biologic therapy.
I would also like to pay attention to the original paper by Szczepański et al.: “Fecal calprotectin is a good biomarker of mucosal healing in monitoring of children with IBD”. This paper is a summary of our initial experience with new noninvasive biomarkers for IBD. The results of our observations demonstrate a good correlation between calprotectin and intestinal inflammation in patients with IBD.
In the original paper “Clinical characteristics of children with cholelithiasis – experience of the two center” the authors have described the population of 113 children with cholelithiasis analyzed according to their demographics, risk factors, the course of their disease and complications. The outcomes of this study have led to a conclusion that cholelithiasis occurs in 30% of children under 3 years of age. While the risk factors analysis has shown a significant impact of genetic factors in the pathogenesis of the disease.
There are several papers on pancreatology in this edition. The original paper by Wejnarska refers to a poorly penetrated issue of genetically acquired pancreatitis in children. The author compares a clinical course of pancreatitis in children with mutation in SPINK1 and CFTR genes to a course of disease in patients with chronic pancreatitis of other etiology demonstrating no differences in the course of pancreatitis between the groups. This is one of the first papers ever published on that subject.
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