1 - Department of Endocrinology, Armed Forces Hospital, Lisbon, Portugal
2 - Paediatric Endocrinology Unit, Hospital Dona Estefânia, CHULC, Lisbon, Portugal
- Congresso internacional
- Apresentado como poster
Resumo:
Background: SARS-CoV-2 acts on the beta cell function through multiple pathways including a direct effect on the ACE2 receptors and insulin resistance associated with the cytokine storm. This may lead to beta cell exhaustion and overall glucometabolic distress caused by islet hyperstimulation and glucose toxicity. We present a case of new onset type 1 diabetes following a SARS-CoV-2 infection with late insulin resistance.
Case Report: A post pubertal previously normoglycaemic fourteen-year-old girl was admitted with severe new-onset diabetic ketoacidosis (glycaemia 668 mg/dL, ketones 4.5 mmol/L, pH 6.8, HCO3 3.8 mmol/L, HbA1c 11.2%, C-peptide 0.3 ng/mL, positive anti-IA2 and anti-GAD) complicated with refractory septic shock, pilonidal sinus with extensive infection and neurological deterioration associated with posterior reversible encephalopathy syndrome. SARS-CoV-2 PCR was negative, but IgG was positive (546 U/mL), indicating a previous coronavirus infection, supported by a confirmed positive contact. She underwent IV fluids and insulin, triple antibiotic scheme, invasive ventilation and aminergic support, with progressive clinical and neurological improvement. After clinical stability and transition to subcutaneous insulin she had two relapses of ketoacidosis needing to reinitiate IV insulin. Surgical debridement and hyperbaric oxygen therapy were also performed, and she was discharged on day 62. Over the first two months of follow-up, the insulin needs increased from 0.73 U/Kg/day to 1.13 U/Kg/day with a shift in body-mass index from 27.82 Kg/m(2) to 29.92 Kg/m(2). One month after starting metformin it was possible to reduce insulin to 0.95 U/Kg/day.
Discussion: In this case report, our patient had a previous SARS-CoV-2 asymptomatic infection which, as it happens with other viruses, may have triggered type 1 diabetes onset. On top of that, the proinflammatory milieu initiated by a cytokine storm might have disrupt both the beta cell function and the insulin signaling. As reported in the literature, these glycaemic alterations can be observed not only in the acute phase of COVID-19, but also after the disease remission.