SUN-205 Pseudo-Cushing Syndrome Secondary to Malnutrition and Gluco-Toxicity Mimicking Type 1 Diabetes Mellitus

Abstract

Background: Pseudo-Cushing Syndrome (PCS) is an under-recognized clinical entity that is a reversible consequence of alterations in cortisol production. We present a case of a patient with presumed type 1 Diabetes Mellitus (DM) who was found to have PCS secondary to malnutrition. Once the nutritional status normalized, the patient’s glycemic control remarkably improved and became well-controlled on metformin alone. Clinical case: A 54-year-old female with poorly controlled insulin-dependent DM for 10 years was referred for concern for adrenal insufficiency after an ACTH came back elevated in the setting of intractable nausea, vomiting and considerable weight loss over 1 year. Prior HbA1c was 16.2% (RR 4.4–6.7). On exam her vitals were normal, body mass index (BMI) was 15 kg/m2. Workup confirmed an elevated ACTH of 100 pg/ml (RR 6–50 pg/ml), however, random PM cortisol was unexpectedly elevated at 26.58 ug/dL (RR 4.46 – 22.7). 8 AM labs for ACTH and cortisol were similarly elevated at 91 pg/ml and 28.33 ug/dl, respectively. She had no evidence of classic Cushingoid features. Subsequent low dose dexamethasone suppression test and 24-hour urine free cortisol were negative. Over 18 months, with optimization of her insulin therapy, BMI improved to 19 kg/m2, ACTH and cortisol started to downtrend spontaneously. After 30 months, her BMI improved to 20 kg/m2. Repeat blood work showed A1C 6.5%, ACTH and cortisol completely normalized to 42 pg/dl and 8 ug/dL, respectively. After being adherent to insulin for a few years, her gluco-toxicity state resolved. A month prior to following up, she self-discontinued insulin due to hypoglycemia but continued on metformin. Currently she continues to remain off insulin. Discussion: PCS is a challenging diagnosis to recognize and differentiate from Cushing Disease (CD) especially due to overlap in biochemical profile. It is important to be aware of this clinical condition to avoid misdiagnosis, delay in treatment or over-treatment. Common etiologies causing PCS include depression, chronic alcoholism, obesity, physical stress, malnutrition, eating disorders, uncontrolled DM, obstructive sleep apnea. PCS occurs due to chronic activation of the hypothalamic-pituitary-adrenal axis, it is usually mild and resolves with treatment of underlying etiology. In our case, first-line screening tests could differentiate between PCS and CD hence she did not require late-night salivary cortisol testing or corticotropic-releasing hormone testing. Conclusion: In our patient, PCS occurred secondary to malnutrition and severe gluco-toxicity which mimicked insulin-dependent type 1 DM. Interestingly, once her nutritional status and insulin compliance improved, cortisol levels normalized, gluco-toxicity state resolved and she no longer required exogenous insulin therapy.