Résumé
Purpose@#At the beginning of the Coronavirus disease (COVID-19) epidemic, physicians paid close attention to children with chronic diseases to prevent transmission or a severe course of infection. We aimed to measure the severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) antibody levels in children with chronic gastrointestinal and liver diseases to analyze the risk factors for infection and its interaction with their primary disease. @*Methods@#This cross-sectional study analyzed SARS-CoV-2 antibody levels in patients with gastrointestinal and liver diseases (n=141) and in healthy children (n=48) between January and February 2021. @*Results@#During the pandemic, 10 patients (7%) and 1 child (2%) had confirmed COVID-19 infection (p=0.2). The SARS-CoV-2 antibody test was positive in 36 patients (25.5%) and 11 children (22.9%) (p=0.7). SARS-CoV-2 antibody positivity was found in 20.4%, 26.6%, 33.3%, and 33.3% of patients with chronic liver diseases, chronic gastrointestinal tract diseases, cystic fibrosis, and liver transplantation recipients, respectively (p>0.05, patients vs. healthy children). Risk factors for SARS-CoV-2 antibody positivity were COVID-19-related symptoms (47.2% vs. 14.2%, p=0.00004) and close contact with SARS-CoV-2 polymerase chain reaction-positive patients (69.4% vs. 9%, p<0.00001). The use, number, and type of immunosuppressants and primary diagnosis were not associated with SARS-CoV-2 antibody positivity. The frequency of disease activation/flare was not significant in patients with (8.3%) or without (14.2%) antibody positivity (p=0.35). @*Conclusion@#SARS-CoV-2 antibodies in children with chronic gastrointestinal and liver diseases are similar to that in healthy children. Close follow-up is important to understand the long-term effects of past COVID-19 infection in these children.
Résumé
Background: The Transmembrane Activator and Calcium modulator ligand Interactor [TACI], encoded by TNFRSF13B/TACI gene, is mutated in some patients with Common Variable Immunodeficiency [CVID] and IgA Deficiency [IgAD]. The purpose of the study was to investigate for the first time in Turkish patients the prevalence of TNFRSF13B alterations in CVID, selective and partial IgAD patients
Methods: Forty two CVID, 36 selective IgAD, 34 partial IgAD and 25 healthy controls were included. All patients were examined for TNFRSF13B gene mutations by PCR
Results: The percentages of TNFRSF13B mutations in CVID, selective and partial IgAD patients were 7.1, 2.7 and 2.9%, respectively. No disease causing TNFRSF13B mutation in healthy controls was found. Patients with TACI mutations had recurrent respiratory tract infections. None of them experienced autoimmunity, bronchiectasis or granulomatous disease. In conclusion, TNFRSF13B mutations were present not only in CVID patients, but also in IgAD cases
Conclusion: Modifier genes as well as their combination with other genetic or environmental factors may play an important role in the development of the immunodeficiency phenotype