Anorexia nervosa is a syndrome with multifactorial etiology in which several genetic, biologic, psychological and social factors are involved. Patients affected by
anorexia nervosa (AN) may develop multiple endocrine abnormalities, e.g.
amenorrhea, hypothalamus-pituitary-adrenal axis hyperactivity,
low T3 syndrome and peculiar changes of somatotroph axis function. These endocrine abnormalities are also found after prolonged
starvation and may represent an adaptive response developed in order to save energy and
proteins. It is still a matter of debate whether these endocrine changes are etiologic or secondary. In fact, several evidences suggest the existence in AN of hypothalamus functional alterations, which may be involved in the development and maintenance of the food intake disorder; on the other hand, the increased CRH secretion seems to be secondary to
malnutrition as well as GH hypersecretion coupled to low
IGF-I levels; the latter is a common finding in AN, as well as in other
undernutrition and malabsorption conditions,
type 1 diabetes mellitus,
liver cirrhosis and catabolic states. Hypothalamic
amenorrhea, which is one of the diagnostic criteria for AN, is not linked only to the reduction of
body weight but reflects also deep alterations of
gonadotropin secretory pattern.
Low T3 syndrome is frequently found in AN; on the other hand, an
iodide-induced
hypothyroidism is quite uncommon. T3 reduction in AN seems to be an adaptive response to prolonged
starvation; however the presence of a simultaneous central dysregulation cannot be excluded. Finally, AN patients frequently show defects in urinary concentration or dilution with inappropriate secretion of
antidiuretic hormone, which may be due to intrinsic defects in the neurohypophysis or to abnormalities of its regulatory afferent neurons.