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A 67-year-old male was admitted with shortness of breath and diarrhea. His COVID-19 polymerase chain reaction test was positive, and he was found to be in acute heart failure. Troponin levels were elevated, echocardiogram showed ejection fraction of 24%, and his electrocardiogram was normal. Inflammatory markers were elevated. Further testing revealed suppressed thyroid-stimulating hormone and elevated free thyroxine (T4). Differential diagnosis at this point included possible myocarditis from the viral illness, exacerbation of heart failure from the viral infection or from thyrotoxicosis was considered. Patient's heart failure improved with initiation of heart failure therapies; however, biochemically, his thyroid function tests (TFTs) did not improve, despite empiric methimazole. Thyroid antibody tests were unremarkable. Thyroid ultrasound showed mildly enlarged thyroid gland with no increased vascularity and 5-mm bilateral cysts. Thyroid dysfunction was attributed to subacute thyroiditis from COVID-19, methimazole was tapered, and prednisone was initiated. The patient's TFTs improved. With the ongoing COVID-19 pandemic, it is imperative that clinicians keep a broad differential in individuals presenting with heart failure, and obtaining baseline TFTs may be reasonable. Rapid treatment of the underlying thyroiditis is important in these patients to improve the cardiovascular outcomes. In our experience, steroid therapy showed a rapid improvement in the TFTs.

To characterize the expression of steroidogenic enzymes implicated in the development of ovarian steroid cell tumors, not otherwise specified (SCT-NOS). We present 4 ovarian SCT-NOS evaluated by immunohistochemical staining of steroidogenic enzymes as an approach to define this entity pathologically. All 4 ovarian SCT-NOS showed increased expression for cholesterol side-chain cleavage enzyme (CYP11A1), 17α-hydroxylase (CYP17A1), 17β-hydroxysteroid dehydrogenase 1 (HSD17B1), aldo-ketoreductase type 1 C3 (AKR1C3), 3β-hydroxysteroid dehydrogenase 2 (HSD3B2), 5α-reductase type 2 (SRD5A2), steroid sulfatase (SULT2A1), estrogen sulfotransferase (EST), and aromatase (CYP19A1). Expression was negative for 21-hydroxylase (CYP21A2) and 17β-hydroxysteroid dehydrogenase 2 (HSD17B2). 17β-hydroxysteroid dehydrogenase 3 (HSD17B3) and 5α-reductase type 1 (SRD5A1) showed variable expression. Our analysis reveals a novel finding of increased expression of AKR1C3, HSD17B1, SRD5A2, SULT2A1, and EST in ovarian SCT-NOS, which is clinically associated with androgen excess and virilization. Further studies are needed to validate these enzymes as new markers in the evaluation of hyperandrogenic ovarian conditions.

Objective: To illustrate how steroid replacement in adrenal insufficiency can influence the development of hypoglycemia in a patient with type 1 diabetes mellitus (T1D). Methods: We describe the case of a 36-year-old female patient with T1D and Addison's disease (Schmidt's syndrome) on multiple daily insulin injections who presented with recurrent hypoglycemia despite being on physiological replacement doses of hydrocortisone. Results: With the assistance of continuous glucose monitoring technology, a pattern of nocturnal hypoglycemia was clearly identified. The patient was taking her hydrocortisone 15 mg in the morning and 5 mg in the early afternoon. With the short half-life of oral hydrocortisone, the evening decline in plasma cortisol concentration led to an increased susceptibility to recurrent evening and nocturnal hypoglycemia. Hypoglycemic episodes were resolved when her morning hydrocortisone dose was changed and prednisolone was added to a later time in the evening. Conclusion: Patients with Schmidt's syndrome can be susceptible to nocturnal hypoglycemia with inadequate steroid replacement. Identifying patients at risk for hypoglycemia in Schmidt's syndrome provides an opportunity for precision management beyond the manipulation of antihyperglycemic agents., Competing Interests: Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.