Abstract
We studied GH levels in 18 adolescents with AN (12-20 yrs). Our patient population differs from others studied in that our patients are younger and at an earlier stage of the disease (12 with symptoms of 1 year or less). Mean weight was 77.8 ± 11.4 Ibs. and mean height was 61.8 ± 3.3 in. All had amenorrhea (4 primary and 11 secondary). Cerebral atrophy was present in 15 of 18. The mean basal level of GH (2.3 ng/ml) was comparable to that in 10 adolescent female controls (4.1 ng/ml). A low basal GH level in AN patients contrasts to other studies which report abnormally high basal GH levels in some patients. A blunted GH response (±10 ng/ml) to clonidine stimulation was noted in 15 of 18 (83%) patients. The mean maximum GH response to clonidine was 6.0 ng/ml. There was an inverse correlation (r=-.42) between GH response and weight loss (p<.05). These low GH responses could account for our previous findings that a disproportionate number of patients with AN are short. In view of other studies which report an elevated response of GH to GRF, our results suggest that Che abnormalities in GH secretion result from an abnormal hypothalamic response to adrenergic stimuli. Low GH responses to stimuli and cerebral atrophy both correlate best with acute weight loss and are therefore findings expected in the early phase in the disease. Other reports of high GH levels may reflect changes as AN becomes chronic.
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Nussbaum, M., Shenker, I., Blethen, S. et al. LOW GROWTH HORMONE (GH) DUE TO DEFECTIVE ADRENERGIC RESPONSIVENESS IN ANOREXIA NERVOSA (AN), AN EARLY HYPOTHALAMIC DEFECT. Pediatr Res 21 (Suppl 4), 176 (1987). https://doi.org/10.1203/00006450-198704010-00060
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DOI: https://doi.org/10.1203/00006450-198704010-00060