SAT-134 Postmenopausal Virilization: Rare Case of an Ovarian Tumor Not Easily Identified on Imaging

Introduction: Ovarian sex cord-stromal tumors are a rare type of ovarian tumor which can be benign or malignant. Steroid cell tumors are a subtype of these tumors, representing <0.1% of all ovarian neoplasms (1). Here, we present the case of a 58 year old post-menopausal female who presented with virilization in the setting of bilateral adrenal adenomas & pelvic ultrasound without a definitive mass. Case Report: A 58 year old post-menopausal white female presented with deepening of voice, male pattern hair loss, increased muscle mass, weight gain, clitoromegaly, acne, increased axillary & facial hair growth. This had occurred over a period of 1.5 years. Initial investigatory labs revealed markedly elevated testosterone level of 630 ng/dL (n 2-45ng/dL). Normal FSH/LH, morning ACTH and cortisol, DHEAS, 17 OHP, androstenedione, prolactin and IGF1. Exogenous intake of testosterone was excluded. A transvaginal ultrasound showed thickened and cystic endometrial lining but no cysts or masses in the ovaries. An endometrial biopsy was normal. In the absence of a definitive source of elevated androgens, CT abdomen pelvis was done & showed remarkable for bilateral adrenal adenomas. Serum metanephrines were normal. An overnight dexamethasone suppression test was abnormal; morning cortisol level 3.1 (n 4.0-22.0). With a normal DHEAS these adenomas were considered to be the less likely etiology of her virilization. Given concern for an ovarian malignancy, a hysterectomy was recommended. Her total testosterone level right before surgery was 954 ng/dL. Post-operatively, not only did the total testosterone levels drastically fall to 18 ng/dL merely on POD 4, but the patient reported new scalp hair growth, decreased abdominal girth & skin smoothing. Her surgical pathology was with that of a steroid tumor of the ovary. Conclusion Steroid cell tumors of the ovary can be benign or malignant. A prompt diagnosis is critical. In the presence of elevated testosterone levels or virilizing symptoms, an ovarian etiology must be suspected. Given the malignant potential of these tumors, if there is clinical suspicion, an expedited total hysterectomy and bilateral salpingo-oophorectomy is recommended. The objective of surgical treatment is to relieve symptoms and for staging in the case of malignancy. Timely management of the tumor can reduce metastasis and significantly improve quality of life, as seen in our case. References 1.Kurman, R. J., Ellenson, L. H., & Ronnett, B. M. (2011). Blaustein’s pathology of the female genital tract (6th ed.). New York; London: Springer.

Unusual causes of Cushing's syndrome

Although in the majority of the patients with Cushing's syndrome (CS), hypercortisolism is due to ACTH hypersecretion by a pituitary tumour or to ectopic ACTH secretion from an extrapituitary neoplastic lesion or to autonomous cortisol secretion by an adrenal tumour, in occasional patients a much rarer entity may be the cause of the syndrome. Herein, we attempted to summarise and categorise these unusual causes according to their presumed aetiology. To this end, we performed a comprehensive computer-based search for unusual or rare causes of CS. The following unusual forms of CS were identified: (i) ACTH hyperesecretion due to ectopic corticotroph adenomas in the parasellar region or the neurohypophysis, or as part of double adenomas, or gangliocytomas; (ii) ACTH hypersecretion due to ectopic CRH or CRH-like peptide secretion by various neoplasms; (iii) ACTH-independent cortisol hypersecretion from ectopic or bilateral adrenal adenomas; (iv) glucocorticoid hypersensitivity; (v) iatrogenic, due to megestrol administration or to ritonavir and fluticasone co-administration. Such unusual presentations of CS illustrate why Cushing's syndrome represents one of the most puzzling endocrine syndromes.