Development of Diabetes Type 3 After SARS-COV-2 Pancreatic B Cell Injury

SARS-COV-2 has caused millions of deaths in less than one year, yet little is known about the long-term consequences survivors may suffer. The novel coronavirus uses the ACE2 receptor to infect human cells, allowing it to target organ systems with such receptors including the respiratory, cardiovascular, gastrointestinal and endocrine system. The purpose of this case report is to describe the long-term implications COVID-19 may cause in the endocrine system. A 46-year-old woman was referred to our clinic due to abrupt uncontrolled blood glucose levels ranging from 200-550mg/dL after being infected with COVID-19 for approximately 10 weeks. She has a past medical history of Diabetes Mellitus Type 2 which was diagnosed 3 years ago and was well controlled with diet. Present history reveals polyuria, polydipsia, tiredness and a decreased appetite. Laboratory values show HbA1C 12, negative islet cell antibodies/GAD antibodies, low C-peptide, high TSH, normal FT4 and positive anti-TPO antibodies/thyroglobulin antibodies. The sudden loss of blood glucose control along with low c peptide levels without evidence of autoimmunity support the diagnosis of Pancreatic Diabetes. SARS-COV-2 infection may cause Diabetes Type 3, rendering a patient dependent on insulin use for life. Covid-19 survivors, with or without a previous history of endocrinopathy, should be evaluated for possible long-term sequels of infection as the virus targets tissues throughout the body.