Metanephrines, GH, cortisol may predict severe, short-term outcome in women with anorexia nervosa

In a new study, critical states occurred in women with restrictive anorexia nervosa who had multiple hormonal abnormalities, suggesting the utility of a complementally hormonal assessment in this group, researchers concluded.

Specifically, the study identified metanephrines, growth hormone and cortisol as independent predictors of severe, short-term outcome in women with restrictive anorexia nervosa.

Researchers in France evaluated the hormonal profiles of 210 young women with restrictive type anorexia nervosa compared with 42 age- and sex-matched control women. They measured thyroid hormones, GH, insulin-like growth factor I, cortisol, estradiol, follicle-stimulating hormone, luteinizing hormone, sex hormone-binding globulin, dehydroepiandrosterone sulfate, plasma metanephrines and bone markers.

The study confirmed hormonal abnormalities previously reported in restrictive anorexia nervosa, including low triiodothyronine syndrome; decreased levels of free thyroxine, IGF-I and free testosterone; and increased GH release, hypercortisolism, SHBG and bone uncoupling. However, data revealed a normality of mean values of metanephrines and DHEA, similar to those of controls.

The hormonal abnormalities manifested below different BMI levels, ranging from 17 to 15. A significant percentage of normal values for each parameter was observed for very low BMI levels.

Women who developed critical states during the three months after the hormonal assessment had a BMI less than 15 and a significant increase in cortisol, GH and metanephrine values.

“These results address a major question concerning the notion of normality of hormonal profile in anorexia nervosa,” the researchers wrote.

They proposed increased metanephrines (>2,000 pg/mL), GH (24-hour mean >20 IU/L) and/or cortisol levels (24-hour mean >400 ng/mL) as “alert signals for physical risk in anorexia nervosa subjects that could lead to specific medical care independently of BMI.”

Estour B. J Clin Endocrinol Metab. 2010;95:2203-2210.