Traumatic brain injury (TBI) is one of the leading causes of death and neurological disability worldwide. The search for biomarkers that indicate TBI severity and prognosis with greater accuracy is ongoing. This study aimed to evaluate the significance of several neuroinflammatory cytokines and chemokines, assessing their potential as biomarkers in pediatric TBI (pTBI). This was an exploratory analysis of inflammatory cytokines and chemokines measured in a subset of 26 children aged 0–18 years with TBI and 21 controls. TBI severity was determined by GCS. The functional outcome was measured via the GOS-E score at 6 weeks and 3, 6, 9, and 12 months post-injury. Serum samples were analyzed for ICAM-1, VCAM-1, SAA, CRP, IFN-g, IL-10, IL-12p70, IL-13, IL-1b, IL-2, IL-4, IL-6, IL-8, TNF-a, TNF-b, eotaxin, eotaxin-3, IP-10, MCP-1, MCP-4, MDC, MIP-1a, MIP-1b and TARC. Levels of IL-6, IL-10, IL-13, IL-16, MDC, and GM-CSF were increased, and IFN-γ, IL-5, IL-8, and eotaxin-3 were decreased at enrollment when compared with controls. Elevated IL-6 and IL-10 at enrollment were associated with severe TBI (AUC of 1, p = 0.0002 and p = 0.8, suggesting biomarker potential. Our data indicate that several cytokines and chemokines measured after TBI may aid in the assessment of pTBI severity and prognosis. IL-6, IL-10, and IL-16 may show potential as biomarkers for pTBI severity and outcomes.

Purpose: To report a case of polydrug ingestion involving levothyroxine and insulin in an adolescent, demonstrating potential protective effects of insulin co-ingestion against symptomatic thyrotoxicosis. Methods: A 14-year-old female with type 1 diabetes and Hashimoto thyroiditis presented following intentional ingestion of 6.75 milligrams levothyroxine, 60 units insulin aspart, and 80 units insulin degludec. Laboratory studies revealed severe biochemical thyrotoxicosis with free thyroxine greater than 7.77 nanograms per deciliter and total triiodothyronine 220.5 nanograms per deciliter. She required glucose infusion at 2.3 to 3.7 milligrams per kilogram per minute to maintain normoglycemia, with hypoglycemic episodes lasting up to 17 h post-ingestion. Throughout her 12-day admission, she maintained normal vital signs with no clinical evidence of sympathetic overactivity despite prolonged biochemical thyrotoxicosis. Conclusions: Co-ingestion of insulin and levothyroxine appears to minimize symptomatic thyrotoxicosis risk, potentially through inhibition of thyroxine to triiodothyronine conversion and glucose homeostasis maintenance. This case highlights complex interactions in polydrug ingestions and suggests insulin may provide protection against thyroid storm in mixed overdoses.