SUN-LB037 Encephalitis as a Cause of Acquired Hypogonadotropic Hypogonadism

Introduction:The diagnosis of hypogonadism, either primary or secondary, is centered on the presence of signs and symptoms of hypogonadism along with low testosterone levels. AM fasting total testosterone level is the test of choice, along with other investigations to determine the cause. LH and FSH are performed to distinguish between primary or secondary hypogonadism. Both should be supranormal to indicate primary hypogonadism; otherwise, it is indicative of secondary hypogonadism. For those with secondary hypogonadism, other pituitary hormones should be performed, followed by brain imaging, MRI being the modality of choice. Case: 57 year old male with past medical history of diabetes mellitus type 2, hypertension, hyperlipidemia, was referred to endocrinology clinic after findings of a stable nonfunctional adrenal incidentaloma. Patient had history of viral encephalitis 1 year prior to presentation. During the visit, patient reported symptoms of hypogonadism that started after his hospital discharge. Prior to hospitalization patient had normal libido and erectile function. He has six biological children, worked as a pharmacist, and no history of head trauma, alcoholism or drug abuse. Initial test, showed total testosterone level of 149.9ng/dL (348-1197ng/dL) with a free testosterone level of 3.1pg/ml (7.2-24.0pg/ml). Subsequently, LH and FSH levels were performed, revealing 3.46 U/L (1.5-9.3 U/L) and 3.2U/L (1.0-14 U/L), respectively. Other hormone levels were measured, including: ACTH 11 pg/ml (0-40pg/ml), AM fasting cortisol 7.6 ug/dL (6-21ug/dL), prolactin 5.0 ug/L (0-20 ug/L), TSH 1.079 uIU/ml (0.35-4.80 uIU/ml), free T4 by direct dialysis 0.92 ng/dL (0.9-1.9 ng/dL). ACTH stimulation was done, fasting cortisol level was 9.7 ug/dL, ACTH level was 13 pg/mL, repeat cortisol level after one hour of cosyntropin administration was 34.1 ug/dL which ruled out adrenal insufficiency. Later, MRI brain showed sella turcica of normal caliber with no evidence pituitary adenoma, structural or vascular disease. Patient was then diagnosed with hypogonadotropic hypogonadism and started on androgen patch. With treatment, patient symptomatically improved, and testosterone levels were maintained at a normal range. Learning point: Although very rare, CNS infections are not only a cause of hypopituitarism, but can also lead to acquired hypogonadotropic hypogonadism. For this particular case, hormonal levels prior to encephalitis were not performed to confirm past normal gonadal function; however, since the symptoms and time of onset clinically correlate with our diagnosis, and based on our reviews of current available data, this may be the first recorded case of acquired isolated hypogonadotropic hypogonadism secondary to encephalitis. 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 conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.