Hypogonadotropic hypogonadism after bleeding prolactinoma in a 15 year old male: Permanent or transient?

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 167-198-Hypothalamus-Pituitary Development & Biology
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-172
Melissa Anne Buryk*1, Ediz Yesilkaya2 and Oscar Escobar3
1Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, 2Gülhane Military Medical Academy, ANKARA, Turkey, 3Univ of Pittsburgh Sch of Med, Pittsburgh, PA
Background: A variable pattern of pituitary hormone deficits can be seen in patients with pituitary adenoma from compromise of the pituitary cells by tumor mass effect, intratumoral bleed, or postsurgical changes.  We present a patient with a bleeding prolactinoma with both transient and permanent endocrine manifestations.

Clinical case: A 15 year old male presented with one month of headache, hyperprolactinemia and MRI finding of enlarged pituitary with fluid level. He was found to have hypogonadotropic hypogonadism, central adrenal insufficiency and central hypothyroidism and was later diagnosed with growth hormone (GH) deficiency.

Initial physical exam was significant for delayed puberty: testicular volume 3mL bilaterally, pre-pubertal phallus, Tanner 2 pubic hair, no axillary or facial hair.  Laboratory evaluation revealed: Prolactin (PRL) 882.1 ng/mL (N: <20 ng/mL), FSH 1.1 IU/mL, LH: undetectable and low TSH, free T4 and morning cortisol. Medical treatment was begun with cabergoline (initiated at 0.25mg twice weekly and gradually titrated to 1mg twice weekly) as well as hydrocortisone and levothyroxine replacement.  GH deficiency was confirmed 2 years later and GH replacement subsequently started.

PRL level normalized after 8 months of therapy. One year after treatment began, despite normalization of PRL, he remained prepubertal both physically and by biochemical evaluation. He was given one course of 4 monthly IM injections of 80 mg of testosterone enanthate. Pubertal changes were noticed afterwards and puberty subsequently progressed at a normal pace with no further injections; LH, FSH, and testosterone levels rose to pubertal ranges. His central hypothyroidism, adrenal insufficiency, and GH deficiency persisted and continued to be managed with hormone replacement therapy. 

Conclusion: The hormone impairments for this patient were both acute and permanent (pituitary bleed leading to thyrotroph, corticotroph and somatotroph dysfunction) as well as chronic and reversible (long standing hyperprolactinemia leading to suppression of gonadotroph function manifested as delayed puberty). Despite lack of recovery of other pituitary hormones, gonadotropin levels returned to normal after normalization of PRL and a “jump start’ with a short course of exogenous testosterone. This underscores the importance of understanding the mechanism of deficiency of each pituitary hormone and its implications in the mode of therapy: transient or permanent replacement.

Nothing to Disclose: MAB, EY, OE

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