SARS-CoV-2 infection is associated with significant lung and cardiac morbidity but there is a limited understanding of the endocrine manifestations of COVID-19. Although, thyrotoxicosis due to subacute thyroiditis has been reported in COVID-19, it is unknown whether SARS-CoV-2 infection can also lead to decompensated hypothyroidism. We present the first case of myxedema coma in COVID-19 and we discuss how SARS-CoV-2 may have precipitated multi-organ damage and sudden cardiac arrest in our patient. A 69-year-old female with a history of small cell lung cancer presented with hypothermia, hypotension, decreased respiratory rate, and a Glasgow Coma Scale score of 5. The patient was intubated and administered vasopressors. Laboratory investigation showed elevated thyroid stimulating hormone, very low free thyroxine, elevated thyroid peroxidase antibody, and markedly elevated inflammatory markers. SARS-CoV-2 test was positive. Computed tomography showed pulmonary embolism and peripheral ground glass opacities in the lungs. The patient was diagnosed with myxedema coma with concomitant COVID-19. While treatment with intravenous hydrocortisone and levothyroxine were begun the patient developed a junctional escape rhythm. Eight minutes later, the patient became pulseless and was eventually resuscitated. Echocardiogram following the arrest showed evidence of right heart dysfunction. She died two days later from multi-organ failure. This is the first report of SARS-CoV-2 infection with myxedema coma. Sudden cardiac arrest likely resulted from the presence of viral pneumonia, cardiac arrhythmia, pulmonary emboli, and myxedema coma – all of which were associated with the patient’s SARS-CoV-2 infection

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We report the case of a 56 year-old Hispanic male with a 10-year history of type 2 diabetes who presented with abrupt onset of hyperglycemia resistant to escalating doses of intravenous insulin infusion (>2500 units daily). He was diagnosed with antibody-mediated insulin resistance given the presence of hyperglycemia despite receiving >200 units insulin/day, a lack of identifiable precipitants for diabetic ketoacidosis or hyperosmolar hyperglycemic state, and elevated insulin antibodies. He underwent pre-immunomodulatory therapy screening for infections, rheumatologic disorders, and malignancy, which uncovered a new diagnosis of latent tuberculosis. While concurrently being treated for latent tuberculosis, he successfully responded to immunomodulatory therapy with rituximab, dexamethasone, and cyclophosphamide. Insulin was discontinued completely, and he maintained appropriate glycemic control on oral diabetic agents (metformin and pioglitazone). This case supports the use of immunomodulatory therapy for the treatment of antibody-mediated insulin resistance and highlights the importance of pre-immunomodulatory therapy screening to uncover occult infection or identify underlying neoplastic/rheumatologic disease prior to immunosuppression.

Background : Antibody-mediated extreme insulin resistance is characterized by hyperglycemia despite the use of >200 units of insulin/day and is often divided into two subtypes, insulin receptor antibody-mediated (Type B insulin resistance) and insulin antibody-mediated insulin resistance. The National Institutes of Health (NIH) published an immunomodulatory protocol for the treatment of Type B insulin resistance (1). However, there is scarce data on immunomodulatory therapy use for insulin antibody-mediated insulin resistance, and little has been documented to guide pretreatment screening. Clinical Case : We report the case of a 56 year-old Hispanic male with a 10-year history of well-controlled type 2 diabetes, who presented with abrupt onset hyperglycemia/diabetic ketoacidosis resistant to escalating doses of intravenous insulin infusion (>2500 units daily). He was diagnosed with antibody-mediated insulin resistance due to hyperglycemia requiring very high doses of insulin, lack of identifiable precipitants for diabetic ketoacidosis or hyperosmolar hyperglycemic state, and elevated insulin antibody levels. He underwent pre-immunomodulatory therapy screening for infections, rheumatologic disorders, and malignancy, which uncovered a new diagnosis of latent tuberculosis. He was started on treatment for latent tuberculosis, and began immunomodulatory therapy using the protocol developed by the NIH with rituximab, dexamethasone, and cyclophosphamide. One month after the second therapy cycle, insulin was no longer required for glycemic control, and he maintained appropriate glycemic control on oral diabetic agents alone (metformin and pioglitazone). Conclusion : This case validates the use of immunomodulatory therapy for the treatment of insulin antibody-mediated insulin resistance. It also highlights the importance of pre-immunomodulatory therapy screening to uncover occult infection prior to immunosuppression, and to investigate for possible causal neoplastic or rheumatologic disease. We propose an algorithm for pre-immunomodulatory screening prior to therapy in patients with antibody-mediated insulin resistance. Reference: (1) Malek R, Chong AY, Lupsa BC, et al. Treatment of Type B insulin resistance: a novel approach to reduce insulin receptor autoantibodies. The Journal of Clinical Endocrinology & Metabolism . 2010;95(8):3641-3647.