Journal of Psychiatric Practice Vol. 18, No. 2 126 March 2012
Hyperprolactinemia is a common consequence
of treatment with an antipsychotic medication.
It can result in hypogonadism due to the
inhibitory effect of elevated prolactin levels on
the hypothalamic-pituitary-gonadal hormonal
axis. We present a case of hypogonadism sec-
ondary to hyperprolactinemia in a patient tak-
ing antipsychotic medication, with radiological
evidence of a pituitary microadenoma. The rel-
evance and investigation of hyperprolactinemia
in patients being treated with antipsychotic
medications are discussed. (Journal of Psychiatric
Practice 2012;18:126–129)
KEY WORDS: prolactin, hyperprolactinemia, anti-
psychotics, pituitary adenoma
CASE PRESENTATION
A 35-year-old female inpatient with a diagnosis of para-
noid schizophrenia was referred to the endocrine
department for management of chronic hyperpro-
lactinemia. In the previous 7 years, she had been treat-
ed with risperidone, olanzapine, haloperidol, clozapine,
amisulpride, quetiapine, and flupenthixol. During this
period, her prolactin levels ranged from 1,203–3,193
mIU/L (normal range = 102–496 mIU/L).* At the time
of referral, her mental state was stable on a combina-
tion of amisulpride 400 mg/day and aripiprazole 20
mg/day. She was not taking oral contraceptive medica-
tion and was on no other medication. She complained of
galactorrhea, decreased libido, oligomenorrhea, back
pain, and hair thinning.
On examination, the patient had no visual field
defect, acne, goitre, or hirsutism. No clinical features
of Cushing’s syndrome or acromegaly were present.
Hormone levels were prolactin: 2,410 mIU/L (normal
102–496 mIU/L) (113.7 μg/L, normal 4.8–23.4 μg/L),
thyroid stimulating hormone: 1.24 mIU/L (normal
0.27–4.2 mIU/L), free thryoxine: 14.2 pmol/L (normal
12–22 pmol/L), follicle stimulating hormone: 6.7 IU/L
(normal 3.5–12.5 IU/L follicular phase), luteinizing
hormone: 3.7 IU/L (normal 2.4–12.6 IU/L follicular
phase), estradiol: 111 pmol/L (normal 46–607 pmol/L
follicular phase), testosterone: 1.7 nmol/L (normal
0.2–2.9 nmol/L), and sex hormone binding globulin: 60
nmol/L (normal 40–80 nmol/L). Renal function was
normal. A pituitary magnetic resonance imaging
(MRI) scan showed a new 2.5 mm microadenoma
which had not been present on a previous MRI study
7 years earlier. There was no radiological evidence of
stalk compression.
Discussion and Management Objectives
Prolactin is produced and secreted by lactotrophs of the
anterior pituitary gland. Hypothalamic dopamine acts
on the lactotroph cells to inhibit prolactin release, while
thyrotropin releasing hormone (TRH), nipple stimula-
tion, and chest wall injury stimulate prolactin secre-
tion.
1
Induction of lactation in the postpartum period is
the only functional role of prolactin described in healthy
humans; the hormone does not appear to be involved in
breast development. Prolactin levels remain relatively
stable during the day and can thus be measured at any
time.
2
Due to slight normal fluctuations, repeat testing
is advised to confirm hyperprolactinemia. The presence
of significant concentrations of macroprolactin (pro-
lactin bound to IgG rendering it detectable to the pro-
lactin assay but biologically inert) is common and
should be excluded.
3
The phenomenon of stress-induced
(e.g., venepuncture) hyperprolactinemia is well docu-
mented and clinicians should be wary of misinterpret-
ing mildly elevated prolactin levels. Moderate to severe
hyperprolactinemia produces hypogonadism, predomi-
CARROLL: Wellington Regional Hospital, Capital and Coast
DHB, New Zealand; CHRISTODOULOU and BAYNES:
Ealing Hospital NHS Trust, Southall, UK; KAHN: Columbia
University College of Physicians and Surgeons.
DOI: 10.1097/01.pra.0000413279.95843.b5
*Prolactin concentrations expressed in mIU/L can be convert-
ed to μg/L by dividing by 21.2: patient’s range = 56.7–150.6
μg/L (normal range = 4.8–23.4 μg/L).
Hyperprolactinemia in a Patient with a
Pituitary Adenoma Receiving
Antipsychotic Drug Therapy
Clinical Case Discussion
Case presentation:
RICHARD W. CARROLL, MB ChB
POLYXENI CHRISTODOULOU, MB ChB
KEVIN C. R. BAYNES, MB BS, PhD
Case discussion: DAVID A. KAHN, MD
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