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Abstract Context While individuals with diabetes appear to be at similar risk for SARS-CoV-2 infection to those without diabetes, they are more likely to suffer severe consequences, including death. Diabetic ketoacidosis (DKA) is a common and potentially lethal acute complication of diabetes arising from a relative insulin deficiency, which occurs more often in those with type 1 diabetes and in the setting of moderate to severe illness. Early reports indicate that among patients with pre-existing diabetes, DKA may be a common complication of severe COVID-19 and a poor prognostic sign. Case Description This clinical perspective explores the key elements of caring for individuals with DKA during the COVID-19 pandemic through 2 cases. Topics addressed include diagnosis, triage, and the fundamental principles of treatment with a focus on the importance of characterizing DKA severity and medical complexity to determine the best approach. Conclusions As discussed, some tenets of DKA management may require flexibility in the setting of COVID-19 due to important public health goals, such as preventing transmission to highest risk individuals, reducing healthcare worker exposure to infected patients, and preserving personal protective equipment. Evidence for alternative treatment strategies is explored, with special attention placed on treatment options that may be more relevant during the pandemic, including use of subcutaneous insulin therapy. Finally, DKA is often a preventable condition. We include evidence-based strategies and guidance designed to empower clinicians and patients to avoid this serious complication when possible.

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Testosterone (T) is the principal male sex hormone, secreted primarily by the testes and transported in the blood by the carrier protein, sex-hormone binding globulin (SHBG). Only 1% to 2% of testosterone circulates in blood as unbound "free" testosterone, but this fraction exhibits the most potent biological activity. Dihydrotestosterone (DHT), the most biologically active androgen, is synthesized from testosterone by 5a-reductase and exerts its effects via a family of androgen receptors. Some biological effects of testosterone may result from its aromatization to estradiol and subsequent interaction with the estrogen receptor. In addition to developing primary and secondary sex characteristics, androgens have diverse anabolic functions such as increasing muscle mass and bone density.1 Testosterone has also demonstrated a number of important effects on the cardiovascular system. In men, T levels begin to decrease after age 40, and this decrease has been associated with an increase in all-cause mortality and cardiovascular risk.2,3 However, whether low T causes negative cardiovascular events or is simply associated with them has yet to be determined. 4 This review highlights the evidence underlying the major interrelationships between androgens and the cardiovascular system. Testosterone Actions on Cardiovascular CellsTestosterone and the more potent DHT bind to cytoplasmic androgen receptors (AR) that are chaperoned by heat shock proteins. Once bound, the DHT-AR complex migrates to the nucleus, dimerizes with another DHT-AR complex, associates with coactivator proteins, and transactivates a family of genes with androgen response elements that alter myocardial and vascular cell behavior.1 Evidence also supports a direct rapid membrane effect of T on G-protein-coupled receptors, with an increase in inositol trisphosphate and diacylglycerol and subsequent alterations in cytoplasmic calcium and potassium channel activity. 5 Cardiovascular Risk in Testosterone Deficiency DefinitionTestosterone deficiency (TD) is a well-established major medical condition that negatively impacts male sexuality, general health, and quality of life. Symptoms include decreased libido, erectile dysfunction, decreased energy, depressed mood, irritability, and decreased sense of well-being. In the correct clinical setting, the diagnosis of TD is usually confirmed by low serum concentrations of total T (e.g., < 200 ng/mL) drawn in the early morning. However, there is no specific value that reliably distinguishes men who experience signs and symptoms of TD from those who do not nor those who will likely respond to treatment. Interpretation of total T concentrations is confounded by variation between individuals, variation in serum SHBG, and variation in androgen sensitivity. 6 Furthermore, considerable controversy has arisen regarding the accuracy of currently available commercial testosterone assays, especially those showing T levels at the lower end of the "normal" range. 4 Free testosterone level may be a more reliable indicator of androg...