{'fraction_non_alphanumeric': 0.03672220333219993, 'fraction_numerical': 0.019041142468548114, 'mean_word_length': 5.206751054852321, 'pattern_counts': {'":': 0, '<': 3, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
SUN-380 A Case of Cushing Syndrome

Abstract Introduction: Cushing's syndrome is characterized by over-secretion of cortisol. Etiologies of Cushing’s syndrome can be ACTH dependent or independent. This highlights a case of ACTH independent Cushing’s secondary to an adrenal lesion. Clinical case: A 28 year old lady presents to Endocrine clinic for evaluation of secondary amenorrhea for 2 years. She was previously evaluated by a gynecologist who performed a progesterone challenge test with no response. The patient reports mild acne during adolescence but denies excess hair growth, or voice deepening. She notes weight gain primarily distributed in her abdomen and face. She reports fatigue, anxiety, easy bruising, intermittent headaches as well as some polydipsia and polyuria. She is not experiencing peripheral muscle weaknessm galactorrhea, or problems with peripheral vision. Her medications are fish oil, multivitamin, and probiotic. Physical exam is notable for BMI of 21.7 kg/m2, round face with increased facial plethora, and an increased posterior fat pad. Significant labs include DHEA sulfate 15mcg/dL (18-391mcg/dL), FSH 6.3mlU/mL, estradiol <15pg/mL for a non-premenopausal woman (19-357pg/mL), total testosterone 3ng/dL (2-45ng/dL), prolactin 25.9 ng/dL (3.0-30 ng/dL). Her ACTH is <5pg/mL (6-50pg/mL) and AM cortisol followed by 1 mg dexamethasone of 22.9mcg/dL (<2.0mcg/dL). Repeat low dose dexamethasone suppression test is significant for AM cortisol 20.7 mcg/dL (4-22mcg/dL) and dexamethasone 258ng/dL. CT Abdomen is performed revealing a left sided adrenal mass. The patient undergoes unilateral adrenalectomy with pathology demonstrating an adrenal cortical adenoma. Her post-operative midnight salivary cortisol levels are appropriately low. Given some symptoms of adrenal insufficiency of dizziness and weakness she undergoes a slow hydrocortisone taper. Her menstrual cycles gradually return, facial plethora and sites of abnormal fat deposition resolve. She reports a significant improvement in her psychological wellbeing with decreased anxiety and increased functionality. Conclusion: The signs and symptoms of Cushing’s syndrome are attributable to the presence of hypercortisolism. While there are signs highly suggestive of Cushing’s syndrome including central obesity with wasting of the extremities, increased dorsocervical fat pad, easy bruising and wide purple striae, symptoms can be subtle, leading to a delay in diagnosis. Our patient presented with a complaint of amenorrhea. Menstrual irregularities are very common in women with Cushing’s syndrome. These symptoms are due to suppression of gonadotropin-releasing hormone secretion secondary to hypercortisolemia, with resultant decrease in levels of FSH and LH. A high level of suspicion is important in order to diagnose Cushing’s syndrome as curative treatment leads to a significant improvement in morbidity and the patient’s quality of life.