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.

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Patients with Cushing’s disease (CD) present with a variety of symptoms and comorbidities including central obesity, hypertension, hyperglycemia, fatigue, weakness, insomnia and mood changes. Proximal myopathy is one of the classical signs of hypercortisolism and patients typically report difficulty rising from a seated position or climbing stairs. Due to variability in clinical presentation, with some patients showing subtle or few symptoms, the diagnosis of CD can be delayed. We describe a patient with late recurrent CD whose primary symptom was proximal myopathy. A 63 yr. old man presented to our clinic with complaints of progressive muscle weakness and fatigue. He had been successfully treated for CD at age 35 with transsphenoidal pituitary adenomectomy. He had been on hormonal replacement therapy for panhypopituitarism since surgery including levothyroxine, testosterone and glucocorticoids. He noted progressive weakness for several years prior to presentation in our clinic. Earlier evaluations revealed vitamin B12 and vitamin D deficiency, but supplementation did not lead to significant symptom improvement. He suffered two episodes of unprovoked deep venous thrombosis with pulmonary embolism and developed a left biceps tear that required hospital admission. During admission, his muscle weakness was exacerbated by immobility and he was subsequently referred to endocrinology for consideration of steroid induced myopathy. He had been on physiologic glucocorticoid replacement since diagnosed with panhypopituitarism. At the time of our evaluation, he was able to ambulate with a walker, but was unable to climb stairs, drive a car and required assistance with activities of daily living. His only other symptoms were fatigue and insomnia. Laboratory testing after holding prednisone revealed: morning cortisol 31.7 mcg/dl (reference interval [RI], 4.0-22.0), ACTH 128 pg/mL (RI 6 - 50), FSH <0.7 mIU/mL (RI 1.6 - 8.0), LH <0.2 mIU/mL (RI 1.6 - 15.2), testosterone 85 ng/dL (RI 250 - 827), IGF-1 55 ng/mL (RI 41 - 279), prolactin 4.9 ng/mL (RI 2.0 - 18.0), TSH 0.01 mIU/L (RI 0.40 - 4.50), free T4 1.5 ng/dL (RI 0.8 - 1.8), HbA1c 6.8% (RI <5.7%). Prednisone was discontinued and hypercortisolism was confirmed by 1 mg overnight dexamethasone (dex) suppression test (Cortisol 32.4 mcg/dL, dex 517 ng/dL, RI 180-550 ng/dL) and elevated 24 h urine free cortisol 315.4 mcg/24h (RI 4.0 - 50.0). 8 mg DST showed mild cortisol suppression (Cortisol 21.2 mcg/dL, dex >1000 ng/dl). MRI confirmed recurrent tumor (1.2 x 0.8 x 1.3 cm) extending into the right cavernous sinus and the patient underwent repeat transsphenoidal tumor resection. Pathology confirmed ACTH adenoma. Our case report highlights that patients with CD can have late recurrences and require long term monitoring for return of hypercortisolism, even in cases of prior panhypopituitarism.

Background: Continuous Glucose Monitoring (CGM) is useful in the management of patients on insulin therapy. In late 2017 a diagnostic CGM clinic was implemented in our VA hospital to aid in the management of diabetes. Our aim is to measure the impact of CGM technology in the veteran population. Methods: Retrospective chart review of all the patients who received a diagnostic CGM (Libre Pro) between January 2018 through October 2019. Patients underwent a diagnostic CGM (blind) if they were on insulin therapy or had an A1c > 7%. We evaluated: glycemic control and travel distance to the VA hospital. A total of 208 patients with diabetes were included in the study (males 91%). The most common diagnosis was T2D 86%, followed by T1D 14%. The mean A1c was 8.4% +/- 1.8. CGM data was examined by an endocrinologist and necessary medication adjustments were recommended. Results: Patients wore the CGM on an average of 10.3 days +/- 4.6, the glucose average was 174.7 +/- 56. In 20 patients, the sensor did not recorded data. The time in range (70-180 mg/dL) was 45% +/- 26, the time above the range was 26 +/- 27. Hypoglycemia (<70 mg/dL) was seen more than 5% of the CGM wore in 32% of patients. In 65% of patient, the CGM prompted a change in treatment regimen. Because CGM results and physician recommendations were communicated via telephone, patients saved an average travel distance of 60 miles SD 38.5, or roughly 120 of roundtrip travel time. Of the patients whose insulin regimen changed after CGM placement, the average HbA1c decreased from 8.2% to 7.5% (p < 0.05). 100% of participants surveyed rated their satisfaction at highest and reported they would wear the CGM device again. Conclusion: A diagnostic CGM clinic significantly improved glycemic control and reduced travel time in the studied veteran population. The diagnostic CGM was well accepted. A rational use of CGM technology may therefore lead to improved diabetes management. Disclosure G. Barsamyan: None. A. da Silva: None. L. Whyte: None. M. Amole: None. H. Ghayee: None. J.A. Leey: None.