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SUN-209 Clinical Hypogonadism Related to Incidentally Discovered Adrenal Insufficiency: Case Report

Introduction Hypogonadism can be primary or secondary. There are several causes of hypogonadism that include but are not limited to, congenital abnormalities, infections, systemic diseases, radiation therapy and glucocorticoid use. Addressing the primary cause tends to resolve the sex hormone defici...

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Detalles Bibliográficos
Autores principales: Darquea Leoro, Andres, Negron, Maria, Penaherrera, Carlos, Anushka, Chadha, Nisha, Giyanani, Patel, Ronak
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553196/
http://dx.doi.org/10.1210/js.2019-SUN-209
Descripción
Sumario:Introduction Hypogonadism can be primary or secondary. There are several causes of hypogonadism that include but are not limited to, congenital abnormalities, infections, systemic diseases, radiation therapy and glucocorticoid use. Addressing the primary cause tends to resolve the sex hormone deficiency. Case presentation Patient is a 46-year-old man with a history of HIV (on therapy), treated syphilis, and rheumatoid arthritis who presented to the office due to low testosterone levels found on laboratory tests done the prior year as well as complain of decreased libido and erectile dysfunction. He was sexually active with one male partner only and denied taking any testosterone-augmenting agents in the past. Physical exam was pertinent for truncal obesity, normal hair distribution, normal penis and testicles with no masses. Patient also endorsed taking a short course of steroids (prednisone) a few months before due to joint pain. On laboratory studies, patient had a normal prolactin, growth hormone, IGF-1 and thyroid function. Morning cortisol was low at 0.8 ug/dL (6.2 - 19.4 ug/dL) on two separate occasions, with borderline low ACTH. He also had low total and free testosterone at 203 ng/dL and 1.8 pg/ml, respectively. FSH and LH were inappropriately normal for the level of testosterone deficiency, and CD4 count was within normal limits. MRI of the brain showed a small 2.5 mm microadenoma, which was most likely a non-functional adenoma. Given low cortisol levels, the patient was started on hydrocortisone with subsequent transition to prednisone. After three months of treatment for adrenal insufficiency, his testosterone levels improved to normal range with no need for androgen replacement therapy, and his symptoms also improved significantly. Discussion Secondary hypogonadism has several causes, including but not limited to hyperprolactinemia, testosterone supplementation, opiate abuse, or glucocorticoid treatment. In this case, our patient developed adrenal insufficiency, possibly due to previous steroid administration. Glucocorticoid use is an uncommon but known cause of secondary hypogonadism, as it alters FSH and LH secretion. Low testosterone and hypogonadism have been studied and are relatively common in men with HIV (1), although how much of a role the HIV infection played in our patient’s findings is unclear, given that he was well controlled. Since the patient responded to steroid treatment with correction of his testosterone levels, his hypogonadism was most likely due to hypothalamic-pituitary axis dysfunction, also resulting in adrenal insufficiency. Reference: Mirza, F. S., Luthra, P., & Chirch, L. (2018). Endocrinological aspects of HIV infection. Journal of Endocrinological Investigation, 41(8), 881-899. doi:10.1007/s40618-017-0812-x