When Hyperprolactinemia Fails to Suppress: The Silent Gonadotroph in a Pituitary Macroadenoma
https://doi.org/10.15605/jafes.041.S1
- Author:
Min Jing Choo
1
;
Liang Wei Wong
2
Author Information
1. Department of Internal Medicine, Hospital Taiping
2. Endocrine Institute, Hospital Putrajaya
- Publication Type:Journal Article
- MeSH:
Gonadotrophs;
Hyperprolactinemia
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):85-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Pituitary macroadenomas may present with mass effects,
hypopituitarism, or hormone hypersecretion. Hyperprolactinemia, resulting from a prolactin-secreting tumor
or stalk compression, typically suppresses gonadotropins.
Thus, elevated follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) with low testosterone in this
context are unusual. We report a macroprolactinoma with
a clinically non-functioning gonadotroph adenoma.
Case:A 69-year-old male presented with acute giddiness and
headache while in Vietnam. He reported reduced libido
but no visual symptoms or galactorrhea. Examination
showed no neurological deficits, normal visual fields, and
secondary sexual characteristics; bilateral testes volume of
25 mL. Magnetic resonance imaging (MRI) brain revealed
a 1.6 × 2.2 × 2.1 cm pituitary macroadenoma compressing
the optic chiasm and pituitary stalk.
Initial pituitary evaluation demonstrated hyperprolactinemia (prolactin >200 µg/L; normal 2.4–13.1), central hypothyroidism (T4 6.8 pmol/L [7.8–14.4], thyroid-stimulating
hormone 2.3 mIU/L [0.38–5.3]), elevated FSH (21.5 IU/L
[1.2–19.2]) and LH (191 IU/L [1.24–8.62]), low testosterone
(8.88 nmol/L), normal insulin-like growth factor 1 (IGF-1)
(68 µg/L [46.5–191.9]), and cortisol 237 nmol/L. Cabergoline
was initiated at 0.25 mg twice weekly and titrated to 1
mg twice weekly over 4 months, alongside levothyroxine
25 µg daily.
Repeated MRI brain 2 months after cabergoline initiation
showed a persistent macroadenoma (1.7 × 2.2 × 2.2 cm) with
bilateral cavernous sinus extension. Prolactin decreased to
<170 µg/L, central hypothyroidism persisted; levothyroxine
was optimized, and hydrocortisone was initiated.
At the 5-month follow-up, prolactin further improved to
57 µg/L. Central hypothyroidism and borderline adrenal
function persisted, requiring continued replacement
therapy. Testosterone remained low-normal (10.2 nmol/L)
despite elevated FSH (15.4 IU/L) and LH (92 IU/L). Followup MRI and hormonal reassessment were planned in
May 2026.
Conclusion:Profoundly elevated prolactin level >200 µg/L and response
to cabergoline reflect true prolactinoma rather than stalk
effect. Persistently low testosterone with discordant high
FSH/LH suggests a non-functioning gonadotroph component producing biologically inactive gonadotropins. Definitive diagnosis requires histopathological confirmation,
while serial biochemical and radiological follow-up guides
management and clarifies tumor subtype.
- Full text:2026080414220478514EP_A119.pdf
