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 Euglycemic diabetic ketoacidosis (DKA) is a challenging diagnosis since near normal blood sugar levels can be misleading. In the present case, we describe a patient with Type 1 Diabetes (T1D) on SGLT2 who underwent a strict low carb diet. Case Report A 70-year-old female with past medical history of unspecified diabetes mellitus and primary hypothyroidism presented to emergency room complaining of nausea and dizziness of four days with decreased oral intake. She was alert and oriented, normal weight (52 kg, BMI 20 kg/m2) with stable vital signs, except for mild tachypnea (22/min). Initial labs showed serum glucose 136 mg/dL, bicarbonate 10 mmol/L (normal 20-31), anion gap of 27, venous blood gas pH 7.1, B-hydroxybutyrate 8.8 mmol/L (normal 0.02-0.27), glucosuria > 500 mg/dL, and moderate ketonuria. Screening for ethyl alcohol and ethylene glycol was negative. Lactic acid, cardiac enzymes, renal and liver function tests were normal. She was diagnosed with diabetes mellitus at age 37, on insulin since then. No alcohol use. Her new primary care physician found an A1C of 9.0% for which metformin 1000mg oral twice a day and empagliflozin 12.5 mg oral daily were added and aspart insulin was discontinued. Daily glargine remained at 20 units daily. She was advised to lose weight for which she started a keto-diet 4 weeks prior to this presentation. She had lost 15 pounds since then accompanied by polyuria and polydipsia. Upon admission, she received IV insulin and IV fluids. An endocrinology consultation was requested for euglycemic DKA secondary to SGLT2 complicated by starvation ketosis. Antibodies against glutamic acid decarboxylase were positive at 250 IU/mL (normal < 5). She was discharged on glargine, aspart insulins and oral medications were discontinued. Conclusion This case shows the importance of identifying the specific type of diabetes for appropriate individualization of therapy. Following a keto-diet in unrecognized T1D can trigger ketoacidosis in the setting of SGLT2 inhibitors leading to euglycemic diabetes ketoacidosis.

Introduction: About 20–40% of patients with Cushing’s syndrome present with cyclic Cushing’s Syndrome characterized by episodes of cortisol excess interspersed with periods of normal cortisol secretion. A high degree of suspicion is needed to identify patients with cyclical hypercortisolism. Fluctuations in cortisol levels can make this a diagnostic challenge. Rarely, hypocortisolemia and frank adrenal insufficiency can occur. Case Report: A 77-year-old female with history of Cushing’s syndrome and transsphenoidal surgery with no adenoma identified on pathology presented with fatigue and concern for recurrence with ACTH of 358 pg/mL (6–50 pg/mL) and morning serum cortisol of 41.4 mcg/dL. Brain MRI showed a possible 4 mm pituitary adenoma. However, when she was transferred to our hospital, there was no evidence of hypercortisolism with cortisol of 9.5 mcg/dL, ACTH of 33pg/mL, 24 hr urine free cortisol (UFC) of 4.4ug/d (<45ug/d) and she was discharged home after neurosurgery recommended no surgical intervention. A week later, the patient returned to the hospital with nausea and weakness, and found to have cortisol of 4.4mcg/dL, ACTH of 12 pg/mL and UFC of 2.8 ug/d requiring short course of hydrocortisone for adrenal insufficiency. One year later, she presented with hip fracture, worsening weakness, plethora, and facial swelling. UFC was 1,338.3mcg/24 hr(4.0–50.0 mcg/24 hr), AM serum cortisol 58.8mcg/dL and ACTH 304.7 pg/mL. In addition to severe osteoporosis with hip fracture, she had hypertension and impaired fasting glucose. She was treated with Ketoconazole 200mg daily which was titrated until AM cortisol levels decreased from 58.8 mcg/dL to 20 mcg/dL. Patient was discharged on Ketoconazole with plan to complete a Dotatate scan to evaluate for ectopic ACTH production which resulted negative. Shortly thereafter, she returned with hypotension, nausea, and fatigue. Repeat cortisol level was 2.3 mcg/dL with ACTH of 27.6 pg/ml. Ketoconazole was discontinued and patient was started on hydrocortisone for adrenal insufficiency. Hydrocortisone was gradually tapered off. Pituitary MRI and IPSS are planned for further evaluation. Discussion: Cyclic Cushing’s syndrome is diagnosed with three peaks and two troughs of cortisol production. Diagnosis and treatment are challenging since the cycles of hypercortisolism can occur sporadically and rapid fluctuations in cortisol makes it difficult to localize a source. Cortisol fluctuations can affect quality of life and result in complications such as diabetes, hypertension, and osteoporosis. Prompt identification of the source of the Cyclic Cushing’s syndrome is vital to pursue definitive therapy. However, in 9% of cases, there is no identifiable source. In such cases, medical therapy is warranted.

A 70-year-old female with unspecified diabetes presented to the emergency department complaining of nausea, dizziness, and anorexia for 4 days. She was diagnosed with diabetes at age 37 years. In her record, both type 1 diabetes and type 2 diabetes were listed as diagnoses. No prior C-peptide or serum antibodies were available. She had peripheral neuropathy and early stage 3 chronic kidney disease without proteinuria.