7071 Cushing disease presenting with Dilated Cardiomyopathy

Abstract Disclosure: H. Majeed: None. C. Nguyen: None. R. Galagan: None. D. Lovre: None. Background: Hypercortisolism manifests with numerous ways due to the wide distribution of glucocorticoid receptors. Here we describe a case of Cushing’s disease presenting with reversible non-ischemic cardiomyopathy. Case Presentation: A 30-year-old male presented to ER with palpitations, dyspnea, and atypical chest pain. His exam was notable for a BMI of 30.26 kg/m2, HR 76 bpm and BP of 200/110 mm Hg. His EKG revealed Left ventricular hypertrophy. Echocardiogram (ECHO) showed an EF of 25-30% with diffuse hypokinesis. An angiogram demonstrated normal coronary anatomy. He was started on Lisinopril, Carvedilol, and Spironolactone for non-ischemic cardiomyopathy. He also complained of a 40 lb weight gain, loss of libido, hot flashes and breast tenderness. He was referred to endocrinology. Initial evaluation demonstrated total testosterone (TT) of 171 ng/dl (286-1511 ng/dl), FSH 3.8 IU/L (2-12 IU/L), LH 5.6 IU/L (2-9 IU/L) consistent with secondary hypogonadism. Further pituitary workup revealed AM cortisol level 31.22 mcg/dl (4.3-22.4mcg/dl), ACTH 79 pg/ml (7.2 - 63.3pg/ml), IGF-1 257 ng/mL (88-246 ng/mL), Prolactin 23.7 ng/dl (2.1- 17.7ng/dl), TSH 0.54 mIU/l (0.35-3.74mIU/l) and FT4 0.6 ng/dl (0.76-1.46 ng/dl). A 24hr urine cortisol was 167 ug(0-50ug/24h) and midnight salivary cortisol 0.160 ug/dl (<0.010-0.090 ug/dl). An overnight 1mg dexamethasone suppression test (DST) resulted in AM cortisol of 20.95 mcg/dl (<1.8mcg/dl) and 8mg DST cortisol fell from 34 mcg/dl to 4.16 mcg/dl. A pituitary MRI revealed a left 6 mm x 4 mm microadenoma. He was treated with levothyroxine pre-op for central hypothyroidism. He underwent transsphenoidal resection of the pituitary adenoma. Post-op AM cortisol was 1.1 mcg/dl. His steroid withdrawal syndrome was treated with a prolonged course of tapered hydrocortisone. Two months post-op ECHO showed EF of 55-60%. His BP normalized on carvedilol alone. Eighteen months post-op he no longer required any hormone replacement. Repeat ACTH 24.4 pg/ml, Total Testosterone 584ng/dl, TSH 0.57 mIU/l and FT4 0.93 and 24hr urine cortisol was 24ug/dl, MN salivary cortisol <0.10 ug/dl confirming remission of his cushing's disease and resolution of secondary hypogonadism and hypothyroidism. Conclusion: Prolonged hypercortisolism can cause abnormal cardiac remodeling resulting in cardiomyopathy. Surgical remission of Cushing’s disease reverses hypercortisolism which may restore normal cardiac function. Presentation: 6/2/2024