Clinical Considerations in Returning Pediatric and Young Adults With Cancer to Physical Activity.

ABSTRACT: There is a gap in the literature on the best treatment of clinical sequelae within adolescent and young adult pediatric cancer populations. Children, adolescents, and young adults are at risk for a multitude of immediate and late effects of their disease and treatment that warrant a comprehensive, multidisciplinary team approach to optimize care. Sports medicine providers are well-equipped with their background to join the oncology rehabilitation team in diagnosing and managing cancer-related impairments to help these populations live a healthier and more active lifestyle. In this manuscript, four essential clinical components to consider when returning children, adolescents, and young adults with cancer history to physical activity are discussed: chemotherapy-induced peripheral neuropathy, cardiotoxicity, nutritional deficiencies, and deconditioning.

SOCS1 Haploinsufficiency Presenting as Severe Enthesitis, Bone Marrow Hypocellularity, and Refractory Thrombocytopenia in a Pediatric Patient with Subsequent Response to JAK Inhibition.

Haploinsufficiency of suppressor of cytokine signaling 1 (SOCS1) is a recently discovered autoinflammatory disorder with significant rheumatologic, immunologic, and hematologic manifestations. Here we report a case of SOCS1 haploinsufficiency in a 5-year-old child with profound arthralgias and immune-mediated thrombocytopenia unmasked by SARS-CoV-2 infection. Her clinical manifestations were accompanied by excessive B cell activity, eosinophilia, and elevated IgE levels. Uniquely, this is the first report of SOCS1 haploinsufficiency in the setting of a chromosomal deletion resulting in complete loss of a single SOCS1 gene with additional clinical findings of bone marrow hypocellularity and radiologic evidence of severe enthesitis. Immunologic profiling showed a prominent interferon signature in the patient's peripheral blood mononuclear cells, which were also hypersensitive to stimulation by type I and type II interferons. The patient showed excellent clinical and functional laboratory response to tofacitinib, a Janus kinase inhibitor that disrupts interferon signaling. Our case highlights the need to utilize a multidisciplinary diagnostic approach and consider a comprehensive genetic evaluation for inborn errors of immunity in patients with an atypical immune-mediated thrombocytopenia phenotype.