SAT166 Elevated Insulin Autoantibody During COVID19 Illness Associated With Significant Hypoglycemia In A Type 1 Diabetic

Disclosure: D.A. Shewmon: None. D.C. Preston: None. Background: Insulin antibodies are a rare cause of hypoglycemia in diabetes mellitus type 1 (DM1). Exacerbation of this phenomenon by COVID-19 has not been previously reported. Clinical Case: A 46 year old, 60 kg female with DM1 of 19 year duration with hypoglycemic unawareness and retinopathy, who was admitted for flu-like symptoms, a blood glucose of 600 mg/dL in the absence of DKA, and COVID-19 by RT-PCR test. Hospitalization was complicated by 48 hours of hypoglycemia in the absence of insulin treatment, requiring continuous 10% dextrose infusion. Four months earlier the patient had been admitted for an undiagnosed non-COVID flu-like illness, with hypoglycemia for 60 hours in the absence of insulin treatment. Her glucose control was stable on 5 units of insulin per day at five and nine days after admission, and 25 units per day at 35 days after admission. At both admissions, the workup included a normal cortrosyn stimulation test, an undetectable C-peptide, a normal IGF-2 level, and a careful investigation to rule out evidence for self-administration of insulin. However insulin antibodies were elevated at 1.17 +/- 0.56 U/mL (n=4, normal <0.4) during the non-COVID illness, and 5.0 U/mL and 5.4 U/mL, during and 35 days after the COVID-19 illness, respectively. Thus insulin antibodies were 13 times the upper limit of normal during COVID-19 illness versus 2.9 times the upper limit of normal during the non-COVID-19 illness. Viral infection is one of the most significant environmental factors that may cause overstimulation of the immune system and has been shown to be associated with autoantibody generation and increase, in addition to autoimmune diseases. Known cytokine profiles on COVID-19 infections include IL-1, IL-6, IL-12, IFN-gamma, and TNF-alpha. The presence of IL-1 and TNF-alpha in particular, are known to be key pro-inflammatory cytokines in myriad autoimmune disorders. In vitro data suggest that IL-1 is also an important effector cytokine in DM1, through a number of direct (i.e., beta cell toxicity) and indirect means (i.e., by marking beta cells for Fas-dependent destruction by autoreactive cytotoxic T-lymphocytes). Conclusion: Our data could represent another example of the exacerbation of autoimmunity associated with COVID-19. The increases in the incidence of both autoantibodies and autoimmune diseases seen with COVID-19 suggest one of the conceptual frameworks for creating hypotheses regarding the nature of the Long COVID syndrome. Presentation: Saturday, June 17, 2023