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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.

Introduction Adrenal glands are highly vascularized organs and can be the foci of metastatic disease. Incidentally discovered adrenal nodules should be evaluated with CT or MRI imaging and biochemical testing. Metastatic lesions do not have a specific clinical presentation or imaging features but are suspected when there is attenuation greater than 10 HU, presence of calcification, hemorrhage, or abnormal enhancement signals in CT scan or MRI. However, malignant lesions can be present along with benign ones as described here. Clinical Case A 74-year-old female initially presented with uncontrolled hypertension in 2002, at which time she was found to have a left adrenal incidentaloma. MRI/MRA of the abdomen with and without gadolinium contrast showed a 2.5 x 2.6 cm left adrenal nodule, described as a benign lipid rich adrenal adenoma. Biochemical testing revealed no evidence of pheochromocytoma, hyperaldosteronism, or hypercortisolism. Follow-up CT scan in 2003 showed the left adrenal nodule was slightly larger (3.0 x 2.5 cm) but remained lipid rich (