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Introduction -Clinical presentation of Pituitary macroadenoma and Lymphocytic hypophysitis may mimic each other. It is necessary to be cautious when one treats these patients and follow up with clinical response and hormonal and radiological evaluation is important to differentiate between the two pathologies. Case presentation Sixty years lady with no comorbidities presented with giddiness and vomiting for three days. She was found to have high blood pressure and was started on betablocker. This was followed by hypotension and bradycardia for which patient required admission. On admission she had persistent hypotension and bradycardia required inotropes for 48 hours. Her routine investigations were unremarkable but S. sodium was 117 (135-145 mEq/L). Endocrine reference was for persistent hyponatremia. History did not reveal any significant medical or surgical problems. She did not have headaches, visual complaints or polyuria. Clinical examination was unremarkable. Her hormonal profile was done and started on intravenous steroids. There was dramatic response to the steroid treatment. Her investigations - Urine spot Na 40 (more than 20meq/L), Urine specific gravity 1. 015 (1. 005-1. 030), Urine osmolarity 210.6mosm/kg of water (500-850) Serum osmolarity of 257.7 moms/kg(275- 295), Random bloodsugar 106 mg/dl(less than 140), Cortisol 1.91 mcg/dl (10-20), ACTH 5.59 pg/ml(10-60), Ft3 1.67pg/ml(2.3-4.1) Ft4 0.7 ng/dl(0.7-1.9) TSH 0. 05mIU/L(0.5-5. 0), Prolactin 12.5 ng/ml(less than 25), LH 1.58 IU/L(19.3-100) FSH 11.85 IU/L(25-130), uric acid 3.2 mg/dl (3.5-7.2), Glycosylated Hb 5.7% (less than 5.7),serum sodium 117 mEq/L(135-145), serum K+ 4.5 meq/L (3.6-5.2), serum creatinine 0.8 mg/dl (0.6-1.3), ACE levels 21.32 mcg/L(less than 40), antiTPO antibodies 1.82 IU/mL (less than 9), IGF1 23.6 ng/ml (55-165) . MRI pituitary showed a pituitary macroadenoma. Patient improved dramatically with intravenous steroids and thyroxine 50 mcg per day. She was discharged on oral steroids prednisolone 5 mg twice a day and thyroxine 50 mcg daily. Patient followed up after 6 weeks and was clinically stable and her Ft3 was 2.46 pg/ml and FT4 was 1. 06 ng/dl with 8 am Cortisol (without steroids) 16.3 mcg/dl and ACTH 54.4 pg/ml. Her MRI pituitary after 3 months showed a normal pituitary and clinically she was stable off steroids . She is coninued on thyroxine 50 mcg and is under regular follow up. Conclusion - A female patient who presented in adrenal crisis with central hypothyroidism with radiological evidence of a pituitary macroadenoma which vanished on treatment of steroids. Retrospectively it was probably Lymphocytic hypophysitis which recovered over 3 months. Her hormonal profile improved. It is important to have a clinical index of suspicion while treating a Pituitary macroadenoma which may masquerade a Lymphocytic hypophysitis as the natural course of disease and treatment is different in both. Presentation: No date and time listed

Introduction-: Postmenopausal hirsutism is a rare presentation. The presentation of clinical hyperandrogenism , its severity and the pace of presentation along with the hormonal profiles help in determining the cause. Once iatrogenic cause is ruled out, one has to assess for the endocrine causes of postmenopausal hirsutism. There are various benign and malignant causes of ovarian hyperandrogenism. Case Presentation- A 62 years post menopausal lady came with complaints of increasing facial hair, coarseness of facial skin and alopecia for two years. She had no significant medical illness and had not received androgens in any form. She had a normal menstrual history during her reproductive years and has two children born of natural conception. Clinically there was no evidence of other endocrine causes of hyperandrogenism like Acromegaly, Cushing’s syndrome, Late onset CAH. Her hormonal profile showed significantly elevated testosterone levels with normal DHEAS levels. Investigations - TSH 1.898 uIu/ml (NR 0.5-5.0); Testosterone 216.10 ng/dl ( NR 20-90); DHEAS 40 mcg/dl ( NR 17-90); USG abdomen and pelvis showed thickened endometrium 8 mms in size and submucosal fibroid. Further investigations-Serum Testosterone 145 ng/dl (NR 20-90); DHEAS 23.8 mcg/dl ( NR 17-90); 17 OH Progesterone 0.86 ng/ml ( NR 0.2- 0.5); Post Dexamthasone 1 mg cortisol < 1.0 mcg/dl (normal response< 1.8- 2.0); Alpha Fetoprotein 2.08 ng/ml ( NR <10 ng); IGF1 71 ng/ml ( NR 70-140) ; Estradiol 10 pg/ml ( NR <30). Her assessment for other causes of hirsutism ruled out Acromegaly, Late onset CAH and Cushing syndrome. MRI abdomen and pelvis revealed normal ovaries and uterus for her menopausal status. In view of persistent symptoms and very high levels of testosterone along with endometrial hyperplasia, patient was counselled to get her ovaries and uterus removed.She underwent a total hysterectomy with bilateral oophorectomy. Postoperatively the patients symptoms have improved, her skin hue is better and the facial hair growth has significantly reduced. The testosterone levels have returned to normal. Postoperative Total Testosterone 16.12 ng/dl ( NR 20-90) and Free Testosterone 1.63pg/ml ( NR 0.3-2). The histopathology showed bilateral ovarian hyperthecosis along with benign endometrial hyperplasia. Conclusion: Polycystic ovaries is a common cause of hirsutism in young women of reproductive age group. It is not commonly seen in the post menopausal state. Even though the hormonal profile points towards an ovarian cause, localisation of an ovarian pathology is sometimes difficult. Diagnostic and therapeutic bilateral oophorectomy points towards the diagnosis which can be unusual and curable like bilateral ovarian hyperthecosis. This was an unusual , curable and rewarding case of postmenopausal hirsutism. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news confer...

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