Selective interference with the functioning of the immune system consisting of the selective blockade of pro-inflammatory factors is a modern, promising, and developing strategy for the treatment of diseases resulting from dysregulation of the immune system, including inflammatory bowel disease. Inhibition of the TNF alpha pathway, group 12/23 cytokines, and lymphocyte migration is used in the treatment of severe or moderate ulcerative colitis and Crohn’s disease. Intracellular signal transduction by influencing the phosphorylation of SAT (signal transducer and activator of transcription) proteins remains in clinical trials.
The disease caused by coronavirus SARS-CoV-2 (COVID-19) can affect almost all organs of the human body, including kidneys. We conducted a one-center study to comprehensively analyze the effects of kidney involvement on the course and outcomes in patients hospitalized with COVID-19, depending on the estimated glomerular filtration rate (eGFR) at admission. Out of the 1958 patients, 1342 (68.54%) had eGFR ≥ 60 mL/min/1.73 m2 (group A) and 616 (31.46%) had eGFR < 60 mL/min/1.73 m2 (group B). Group B was additionally divided into subgroups B1, B2, and B3 based on eGFR. We found that mortality rates during hospitalization, as well as after 90 and 180 days, were much higher in group B than group A. The highest mortality was observed in the B2 subgroup with eGFR of 15–29. The mortality of B patients was associated with comorbidities, respiratory dysfunction, immunological impairment, and more frequent development of AKI. AKI had a negative impact on patients’ survival, regardless of the initial renal function. At discharge, 7.4% of patients had serum creatinine levels 30% higher, or more, as compared to admission. The disease course and outcomes in COVID-19 patients are associated with baseline eGFR; however, AKI during hospitalization is a more significant predictor of poor prognosis regardless of the initial renal function.
Introduction: Lower gastrointestinal bleeding (LGIB) is not a rare clinical problem in children. The aetiology of LGIB varies according to age. Likewise, experiences in different countries reflect the disparities in the frequency of various causes of LGIB in children. Although some cases can be diagnosed clinically, choosing the appropriate diagnostic methods in children is challenging. The aim of the study was to determine the aetiology of LGIB in children and analyse the diagnostic procedures needed to make a diagnosis. Material and methods:The medical records of children with chronic LGIB admitted to the Paediatric Gastroenterology Department were reviewed. The diagnoses and diagnostic procedures were analysed according to age groups (< 5 with subgroups < 2 and 2-5, 5-10, and > 10 years old). Results: 227 patients were enrolled in the study. The most important causes of LGIB among all patients were constipation associated with anal fissures (36.6%) and inflammatory bowel disease (IBD) (33.5%). According to age groups, the main causes of LGIB were: up to 5 years old -constipation (39.62%) and food allergy (28.3%), in the youngest age subgroup up to 2 years old -food allergy (52.38%), between 5 and 10 years old -constipation (44%) and ulcerative colitis (14%), over 10 years old -IBD ulcerative colitis (36.29%), Crohn's disease (13.71%), and constipation (32.26%). Patients with IBD were more likely to have anaemia and weight loss. The level of faecal calprotectin was significantly elevated in children with IBD and colorectal polyps. Conclusions: Constipation is a common cause of LGIB in all age groups of children. Food allergy should be considered in infants and young children, but it is rarely seen in children over 5 years old. In children older than 5 years old, diagnostics for IBD should be carried out, especially in patients with weight loss, high levels of faecal calprotectin, and anaemia. Colorectal polyps and Meckel's diverticulum are less common causes of LGIB.
Type 1 diabetes (T1D) and celiac disease (CD) coexist very often. Identification of the human leukocyte antigen (HLA) DQ2/DQ8 can confirm the genetic predisposition to CD. Negative result of this test allows to exclude CD with a high probability. It was suggested that in individuals with higher risk of CD, including T1D patients, the implementation of genetic testing should reduce the number of patients requiring systematic immunological screening. The aim of this study was to analyze the prevalence of different haplotypes predisposing to CD in children and adolescents with previously diagnosed T1D. Material and methods: A retrospective analysis was performed on 166 T1D children (91 girls) in whom HLA DQ2/DQ8 alleles were tested. In 9.6% CD was also diagnosed. Results: In 12.7% both HLA DQ2/DQ8 were negative. In 87.3% patients HLA DQ2 and/or DQ8 was positive, including 27.7% patients with both haplotypes DQ2.5 and DQ8 positive. In all CD patients the disease predisposing alleles were positive, while none of the HLA DQ2/DQ8 negative children were diagnosed with CD. Conclusions: The prevalence of HLA DQ2.5 and the HLA DQ2.5 / HLA DQ8 configuration is higher in patients with T1D, and CD compared to children with T1D alone. The combination of HLA DQ2 and HLA DQ8 most significantly increases the risk of developing CD. The group of HLA DQ2/DQ8 negative patients with improbable CD diagnosis, is relatively small. Most of T1D patients HLA DQ2/DQ8 positive need further regular antibody assessment. In patients with T1D, who are at high risk of developing CD, genetic testing may be considered to select those who require further systematic serological evaluation. Due to its retrospective nature, the study was not registered in the database of clinical trials and the Clinical trial registration number is not available.
Background: The incidence of acute pancreatitis (AP), acute recurrent pancreatitis (ARP) and chronic pancreatitis (CP) in pediatric population is rising and becomes common clinical problem in gastroenterology. The assessment of morbidity risk factors is necessary to improve the quality of diagnosis, to determine further treatment and to identify groups with poor prognosis of the evolution of AP into ARP and CP. Objectives: The assessment of etiological factors in acute and acute recurrent pancreatitis in children. Material and methods: From January 2015 to November 2017, data on etiological factors responsible for the onset of AP and ARP were collected in a group of pediatric patients hospitalized at the Department of Paediatrics, Gastroenterology and Nutrition, Medical University of Wroclaw, Poland. The study group consisted of 39 patients (27 patients with AP, 11 patients with ARP and 1 with CP). Results: The potential etiological factor was established in 85.2% of children with AP and in 100% of children with ARP. Mutations in the SPINK1 gene were found in 44.4% of children from the ARP group, no mutations in the PRSS1 gene were found in this group. In all patients with a genetic predisposition (SPINK1 mutation) during the first episode of the ARP, coexistence of an additional predisposing factor was found. Conclusions: Patients with ARP require diagnostics towards mutations predisposing to the transition of AP into a chronic disease. The interaction of additional triggers plays a role in the development of pancreatitic inflammatory disease in genetically predisposed individuals.
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