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Prolactin and Osteoporosis — MRCPsych Paper B MCQ

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HardSchizophrenia & PsychosisProlactin and OsteoporosisMRCPsych Paper B

A 39-year-old woman with schizophrenia has taken risperidone for 4 years. She has had secondary amenorrhoea for 18 months and sustains a low-trauma vertebral fracture. Investigations show persistently elevated prolactin, low oestradiol and inappropriately low-normal LH and FSH. Thyroid function, renal function, adjusted calcium and 25-hydroxyvitamin D are normal. DEXA confirms markedly reduced bone mineral density. Which mechanism principally explains her bone loss?

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Correct answer: A — Prolactin-mediated suppression of GnRH, reducing gonadotropins and oestrogen

Explanation lettering: B = shown as A · A = shown as B · E = shown as C · C = shown as D · D = shown as E

B is correct. Risperidone blocks tuberoinfundibular dopamine D2 receptors, removing dopaminergic inhibition of prolactin release. Sustained hyperprolactinaemia suppresses hypothalamic GnRH signalling, producing reduced LH and FSH secretion and consequent hypo-oestrogenism. Oestrogen deficiency accelerates bone resorption, leading over time to reduced bone mineral density and fragility fractures. Her amenorrhoea, low oestradiol and inappropriately low-normal gonadotropins identify this hypogonadotropic pathway. Although experimental evidence suggests prolactin may also have direct skeletal effects, direct risperidone toxicity is not the principal established mechanism. Weight gain does not explain this endocrine pattern. Vitamin D deficiency is excluded biochemically, and risperidone is not recognised as causing osteoporosis through vitamin D catabolism. Hyperprolactinaemia therefore has a clinically important connection with bone loss.

Reference: Gloucestershire Health and Care NHS Foundation Trust. Hyperprolactinaemia Guideline, Version 2, section 'Potential Long Term Consequences—Osteoporosis', updated 2025. https://foi.ghc.nhs.uk/wp-content/uploads/2025/09/CLG082-Hyperprolactinaemia-Guideline-V2-issued-31.1.24.pdf