ODP308 Does This Patient Have Sheehan's Syndrome Due to Thrombosis?

Abstract

Abstract Background Sheehan syndrome (SS) is the necrosis of the anterior pituitary cells due to ischemia. The most common etiology is the result of postpartum hemorrhage, causing hypovolemia and decreased blood supply to an already enlarged pituitary gland, which occurs during pregnancy. Other less common causes are thrombosis, vasospasm, or compression on hypophysial arteries. Clinical Case A 35-year-old lady G1P1 was referred to Endocrinology Clinic for evaluation of secondary amenorrhea and infertility, and a desire for a second child. Prior to birth of her daughter, she had irregular menses every 30-90 days. She did not have excessive bleeding with delivery. However, she developed postpartum deep vein thrombosis, and was treated with enoxaparin for 1 year after delivery. Although she had no symptoms of hypopituitarism, she has not had a menstrual period since delivery of her child and does not exercise vigorously. She did not have symptoms or signs of PCOS. Upon evaluation, Factor V Leiden showed a heterozygous mutation, Estradiol14.98L[19.5-144.2 pg/mL], LH 2.3[ 1.9 - 26.2 mIU/mL], FSH 7.4[2.3 - 12.6 mIU/mL], FT4 1.3 [0.76 - 1.46 ng/dL],TSH 1.10[ 0.358 - 3.74uIU/mL], IGFI 182[ 53 - 331ng/mL], ACTH 12[ 0–47 pg/mL], am Cortisol 15.2[5.3 - 22.5 ug/dL],Testosterone18 [ 2–45 ng/dL],DHEA Sulfate58[35-430mcg/dL] Prolactin 5.7[<25 ng/ml],with normal fallopian tubes on HSG. Pituitary MRI was done due to low estradiol with inappropriately normal FSH and LH and was normal. The patient was diagnosed with Hypogonadotropic deficiency leading to secondary amenorrhea, of unclear etiology, in the setting of possible hereditary caused thrombosis. The concern for hormonal therapy for a second pregnancy was whether this is safe and effective, given her history of DVT and factor V Leiden mutation. Discussion and Conclusion Previous studies have found that 82% of cases with SS were due to postpartum hemorrhage, but also suggests that there are other etiologies for SS. In addition, failure of lactation occurs in 67% of patients and secondary amenorrhea in 73% of patients, as in our case. However, the extent of pituitary involvement can vary, with abnormal GH and prolactin in 90-100% of cases, while abnormal TSH, Cortisol and GnRH in 50-100%. Although anti-phospholipid syndrome has been described as a possible etiology for hypopituitarism, related to formation of thrombi, our case suggests that other coagulopathies should be considered as a cause of partial pituitary dysfunction leading to hypogonadotropic hypogonadism, due to thrombus formation. Presentation: No date and time listed