In a previous paper, I hypothesized that hypoxic stress could be a risk factor for post-concussive hypopituitarism (PCH) [1]. Essentially, the suggestion was that post-concussive patients with systemic hypoxic stress from various sources (smoking, sleep apnea, etc) could experience elevated inflammation at the already compromised hypothalamic infundibulum. This elevated inflammation would constitute an increased risk for autoimmunity, leading to hypopituitarism. Recently, a small number of puzzling cases of pediatric multi-system inflammation have emerged in association with COVID-19 infection. This suggests an extension of my previous hypothesis: is history of concussion a risk factor for COVID-19 related pediatric multi-system inflammation? A respiratory infection of any sort, including COVID-19, represents a temporary risk of hypoxic stress. This could activate an already incipient PCH. If the PCH manifests as hypoadrenia, the lack of glucocorticoid secretion would make it difficult for the patient to control inflammation. This inflammation could in turn aggravate the PCH. A vicious cycle is then established ...
Language: en
LA - en SN - 0306-9877 UR - http://dx.doi.org/10.1016/j.mehy.2020.109921 ID - ref1 ER -