Objective

Non-Alcoholic Fatty Liver Disease (NAFLD) is reported to be the most common chronic pediatric liver disease. Little information is available on the adherence of residents in-training to the published guidelines for the evaluation and management of pediatric NAFLD.The goals of this study are: (i) to assess the consistency of screening and evaluation for NAFLD in obese and overweight children at continuity clinics by upper level residents, and (ii) to determine the residents' extent of training, knowledge, comfort and competence levels in NAFLD care.

Methods

An electronic survey developed using REDCap was emailed to accredited Pediatric Residency Programs in the United States. Program directors and coordinators were requested to forward the survey to their upper level pediatric and medicine/pediatrics residents. Statistical analysis of responses (n= 399) was performed.

Results

More than 88% of residents reported to be exposed to obese and overweight children, representing at least 25% of the patients encountered in clinics. Regardless of their training level, they inconsistently screened for (>60%), initiated evaluation of, or provided counseling on NAFLD in these patients, not following the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition guidelines. Over 80% of residents perceived to have received inadequate training resulting in insufficient knowledge on NAFLD, which they identified as their biggest barrier (25.7%). There was minimal statistically significant difference in the survey findings between training levels (PGY-2 vs PGY-3/4).

Conclusions

Educational interventions should be implemented by pediatric residency programs to enhance educational core curricula for the early detection and initiation of management of NAFLD, an emerging public health problem.

The antibody profile against autoantigens previously associated with autoimmune diseases and other human proteins in patients with COVID-19 or multisystem inflammatory syndrome in children (MIS-C) remains poorly defined. Here we show that 30% of adults with COVID-19 had autoantibodies against the lung antigen KCNRG, and 34% had antibodies to the SLE-associated Smith-D3 protein. Children with COVID-19 rarely had autoantibodies; one of 59 children had GAD65 autoantibodies associated with acute onset of insulin-dependent diabetes. While autoantibodies associated with SLE/Sjögren's syndrome (Ro52, Ro60, and La) and/or autoimmune gastritis (gastric ATPase) were detected in 74% (40/54) of MIS-C patients, further analysis of these patients and of children with Kawasaki disease (KD), showed that the administration of intravenous immunoglobulin (IVIG) was largely responsible for detection of these autoantibodies in both groups of patients. Monitoring in vivo decay of the autoantibodies in MIS-C children showed that the IVIG-derived Ro52, Ro60, and La autoantibodies declined to undetectable levels by 45-60 days, but gastric ATPase autoantibodies declined more slowly requiring >100 days until undetectable. Further testing of IgG and/or IgA antibodies against a subset of potential targets identified by published autoantigen array studies of MIS-C failed to detect autoantibodies against most (16/18) of these proteins in patients with MIS-C who had not received IVIG. However, Troponin C2 and KLHL12 autoantibodies were detected in 2 of 20 and 1 of 20 patients with MIS-C, respectively. Overall, these results suggest that IVIG therapy may be a confounding factor in autoantibody measurements in MIS-C and that antibodies against antigens associated with autoimmune diseases or other human proteins are uncommon in MIS-C.