The features of liver lesions in children at the time of diagnosis of inflammatory bowel disease. Observations from one medical center

Wstęp: W przebiegu nieswoistych zapaleń jelit stosunkowo często procesem chorobowym objęte są inne narządy, w tym wątroba.Cel pracy: Ocena częstości występowania biochemicznych cech uszkodzenia wątroby w momencie rozpoznania nieswoistego zapalenia jelit (NZJ) u dzieci.Materiał i metody: Analizą objęto 49 dzieci z NZJ w wieku 2–18 lat. U wszystkich chorych przeprowadzono badanie kliniczne oraz diagnostykę laboratoryjną [między innymi aktywność aminotransferazy alaninowej (ALT) i asparaginowej (AST), gammaglutamylotranspeptydazy (GGTP) i stężenie bilirubiny w surowicy krwi]. Rozpoznanie choroby podstawowej ustalono na podstawie badania endoskopowego przewodu pokarmowego oraz oceny histopatologicznej wycinków błony śluzowej jelita. Jako podstawowe kryterium uszkodzenia wątroby przyjęto wartości aktywności ALT powyżej 45 j./l.Wyniki: Podwyższoną aktywność ALT stwierdzono u 16 badanych dzieci (32%) z nieswoistymi zapaleniami jelit. Aktywność ALT mieściła się w granicach 45–157 j./l; średnio 75,8 ± 40 j./l.Wnioski: U pacjentów pediatrycznych z nieswoistymi zapaleniami jelit stosunkowo często, już w momencie rozpoznania, obserwuje się cechy uszkodzenia wątroby. U wszystkich chorych z nieswoistymi zapaleniami jelit należy monitorować parametry funkcji wątroby w celu wczesnego rozpoznania współistniejących powikłań hepatologicznych. Obserwacje poczynione w niniejszym badaniu mają jedynie charakter wstępny i zobowiązują do pogłębienia diagnostyki „hepatologicznej” w celu ustalenia szczegółowego rozpoznania i wdrożenia właściwego leczenia. Konieczne są dalsze badania obejmujące liczniejsze grupy dzieci chorych na nieswoiste zapalenia jelit.Introduction: Patients with inflammatory bowel diseases (IBD) often develop complications involving other organs, including the liver.Aim of study: To assess the prevalence of elevated liver enzymes in children suffering from inflammatory bowel disease (IBD).Material and methods: We analyzed a group of 49 patients with IBD from 2 to 18 years old. Each patient had physical examination done, medical history taken and laboratory tests performed [alanine transaminase (ALT), aspartate transaminase (AST), gamma gluthamylotranspeptydase (GGTP), bilirubin]. The diagnosis of IBD was based on endoscopic and histopathological criteria.The liver damage was recognized when activity of ALT was above 45 U/l.Results: Increased liver enzymes activity was found in a group of 32% of patients with IBD. The activity of ALT ranged from 54 to 157 U/l.Conclusions: 1. In pediatric population with inflammatory bowel diseases the liver damage might be present at the very beginning of the IBD. 2. In all the patients with IBD liver enzymes activity ought to be monitored in order to recognize hepatic complications. 3. Observations of this study oblige to extend diagnostic procedures enabling accurate recognition and appropriate treatment

Long-term effects of vitamin D supplementation in vitamin D deficient obese children participating in an integrated weight-loss programme (a double-blind placebo-controlled study) – rationale for the study design

Abstract Background Obesity is associated not only with an array of metabolic disorders (e.g. insulin resistance, hiperinsulinemia, impaired tolerance of glucose, lipid disorders) but also skeletal and joint abnormalities. Recently, a pleiotropic role of vitamin D has been emphasized. Obese children frequently present with vitamin D deficiency, and greater fat mass is associated with lower serum concentration of this vitamin. Although some evidence suggests that weight loss may affect vitamin D status, this issue has not been studied extensively thus far. The aim of a double-blind placebo-controlled study is to assess long-term health effects of vitamin D supplementation in vitamin D deficient obese children participating in an integrated weight-loss programme. Methods A randomized double-blind, placebo-controlled trial analysing the effects of vitamin D3 supplementation in overweight or obese vitamin D deficient (<30 ng/ml) children participating in an integrated weight-loss programme. Children are randomized to receive either vitamin D (1200 IU) or placebo for 26 weeks. Primary endpoints include changes in BMI (body mass index), body composition and bone mineral density at the end of the study period, and secondary endpoints – the changes in laboratory parameter reflecting liver and kidney function (transaminases, creatinine) and glucose homeostasis (glucose and insulin levels during oral glucose tolerance test). Discussion The effects of vitamin D supplementation in obese individuals, especially children, subjected to a weight-loss program are still poorly understood. Considering physiological processes associated with puberty and adolescent growth, we speculate that supplementation may enhance weight reduction and prevent bone loss in obese children deficient in this vitamin. Trial registration NCT 02828228 ; Trial registration date: 8 Jun 2016; Registered in: ClinicalTrials.gov. The trial was registered retrospectively

Transforming growth factor β1 protein and mRNA levels in inflammatory bowel diseases: towards solving the contradictions by longitudinal assessment of the protein and mRNA amounts

Previously published studies on levels of the transforming growth factor-β1 (TGF-β1) protein and mRNA of the corresponding gene in patients suffering from inflammatory bowel diseases (IBD) gave varying results, leading to contradictory conclusions. To solve the contradictions, we aimed to assess longitudinally TGF-β1 protein and mRNA levels at different stages of the disease in children suffering from IBD. The study group consisted of 19 pediatric patients with IBD at the age between 3.5 and 18.4 years. The control group consisted of 42 children aged between 2.0 and 18.0 years. The plasma TGF-β1 concentration was measured with ELISA. mRNA levels of the TGF-β1 gene isolated from samples of the intestinal tissue were assessed by reverse transcription and real-time PCR. Levels of TGF-β1 protein in plasma and corresponding mRNA in intestinal tissue were significantly higher in IBD patients than in controls. TGF-β1 and corresponding transcripts were also more abundant in plasma and intestinal tissue, respectively, in patients at the active stage of the disease than during remission. In every single IBD patient, plasma TGF-β1 level and mRNA level in intestinal tissue was higher at the active stage of the disease than during remission. Levels of TGF-β1 and corresponding mRNA are elevated during the active stage of IBD but not during the remission. Longitudinal assessment of this cytokine in a single patient may help to monitor the clinical course of IBD

Association between uridin diphosphate glucuronosylotransferase 1A1 (UGT1A1) gene polymorphism and neonatal hyperbilirubinemia

Objective: To assess the prevalence of UGT1A1*28 and UGT1A1*60 polymorphisms of UGT1A1 gene and their association with hyperbilirubinemia. Study design: The study was performed at a single centre - at the Department of Obstetrics of the Medical University of Gdansk in Poland. DNA was isolated from Guthrie cards of 171 infants. Only full term newborns (gestational age 38-42 weeks) were included in the study. Fluorescent molecular probes were used for UGT1A1 promoter variation analysis. The presence of UGT1A1*28 polymorphism was detected with a dual-probe system, and UGT1A1*60 with a SimpleProbe™. Result: Homozygous UGT1A1*28 and UGT1A1*60 genotypes were detected in 14.6% and 20.5% of the newborns, respectively. Homozygous (G/G) genotypes of UGT1A1*60 polymorphism were found in all of the UGT1A1*28 (i.e. (TA)7/(TA)7) homozygotes. More than 80% (55/66) of the children with "wild" type UGT1A1*28 genotype (where no polymorphism was detected) (i.e. (TA)6/(TA)6) carried the "wild" (T/T) genotype of UGT1A1*60 as well. The UGT1A1*28 polymorphism was detected more often among neonates with elevated bilirubin. Hyperbilirubinemia was diagnosed more frequently in boys. Conclusion: Polymorphisms of the UGT1A1 gene frequently co-exist in neonates. The presence of UGT1A1*28 polymorphism and male gender seem to predispose to neonatal hyperbilirubinemia