Q: Increased prolactin in anorexia nervosa A: In anorexia nervosa, mildly increased prolactin can occur, but it is not the classic hormonal pattern. Typical endocrine pattern in anorexia nervosa includes: - Hypogonadotropic hypogonadism low LH/FSH, low estradiol/testosterone - Low T3 euthyroid sick pattern - Hypercortisolemia - Sometimes altered GH/IGF-1 axis Why prolactin may be elevated Possible mechanisms: 1. Hypothalamic dysregulation/stress from severe undernutrition 2. Reduced dopaminergic inhibition of prolactin secretion 3. Coexisting factors common in these patients: - Antipsychotics, SSRIs, metoclopramide, etc. - Primary hypothyroidism - Pregnancy - Pituitary adenoma if marked elevation Clinical interpretation - Mild elevation: can be functional in severe illness/malnutrition. - Marked elevation especially 100 ng/mL, lab-dependent: should trigger evaluation for prolactinoma or drug causes. - In anorexia, amenorrhea is usually from low GnRH/LH/FSH, not prolactin alone. What to do if prolactin is high 1. Repeat fasting morning prolactin avoid stress/nipple stimulation before test 2. Review medications 3. Check TSH, pregnancy test, renal function 4. If persistent/significant elevation, consider pituitary MRI and endocrine referral If you want, I can give a quick workup algorithm based on the actual prolactin value range. Q: Reason for hypogonadotropic hypogonadism A: In anorexia nervosa, hypogonadotropic hypogonadism is mainly due to functional hypothalamic suppression from energy deficiency. Mechanism 1. Low energy availability / low fat mass 2. ↓ leptin, ↑ cortisol, altered ghrelin/NPY and stress signaling 3. Reduced pulsatile GnRH release from hypothalamus 4. ↓ pituitary LH and FSH secretion 5. ↓ ovarian/testicular sex steroid production estradiol/testosterone So it is a central hypothalamic-pituitary adaptive shutdown of reproduction during starvation, not primary gonadal failure. Why this happens biologically The body prioritizes survival over reproduction when nutrition is inadequate. Reproductive axis is one of the first to downregulate. Clinical consequences - Amenorrhea/oligomenorrhea, infertility, low libido - Bone loss low estrogen/testosterone plus malnutrition Reversibility Usually improves with nutritional rehabilitation and weight restoration and reduction in physiologic stress.