What are the endocrinologic and metabolic effects of anorexia nervosa?

Updated: Jun 10, 2019
  • Author: Bettina E Bernstein, DO; Chief Editor: Caroly Pataki, MD  more...
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Answer

Foremost in the gamut of endocrinologic complications is amenorrhea, although, as previously mentioned, the DSM-5 no longer includes this condition as part of the diagnostic criteria of anorexia nervosa. [21] Amenorrhea results from disorders in the hypothalamic-pituitary-ovarian axis in which levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are low despite low levels of estrogen. Reversion to the prepubertal state occurs; the LH response to gonadotropin-releasing hormone (GnRH) is blunted. This blunted response is insufficient to maintain menstrual integrity, and amenorrhea results.

Weight loss and emotional instability play a role in amenorrhea, although amenorrhea persists in 5-44% of patients in whom weight gain has been documented. The explanation for this wide range has not been elucidated.

Other changes related to endocrine function include a reduction in fertility, multiple small follicles in the ovaries, and decreased uterine volume and atrophy.

Thyroid function is also affected in patients with anorexia nervosa, with laboratory data revealing a decrease in triiodothyronine (T3) and thyroxine (T4) and an increase in reverse T3. These changes are characteristic of the euthyroid sick syndrome and, similar to the cardiac changes, represent an adaptive mechanism; hormonal replacement is not necessary.

An associated impaired release of vasopressin consistent with diabetes insipidus is present. This defect is of the neurogenic type; concentration of urine is observed after administering vasopressin. This condition affects 40% of persons with anorexia nervosa and is reversible with weight gain.

Osteopenia is a serious complication. Cortical and trabecular bone are affected, and osteopenia persists despite estrogen therapy. Low levels of progesterone (accelerates remodeling) formation and decreased insulinlike growth factor-1 (IGF-1) levels, which stimulate type 1 collagen biosynthesis, contribute to bone loss.

Treatment of osteopenia with bisphosphonates is not routinely indicated in adolescents, because of concerns about osteonecrosis of the jaw; however, if this therapy is used, close monitoring is critical. [21, 22] Supplementation with 1000-1500 mg/d of dietary calcium and 400 IU of vitamin D is recommended to prevent further bone loss and to maximize peak bone mass. Although exercise and hormonal replacement therapy have some benefit in perimenopausal women, exercise may be deleterious in patients with anorexia nervosa who have amenorrhea, and hormonal replacement may induce premature closure of bone epiphysis. [21]


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