Although many of these studies were done in adults, the results are applicable to children. Exercise increases GH levels in normal subjects, an effect inhibited by naloxone, atropine and oral glucose administration (23). Elevated plasma GH levels are seen following acute trauma, major surgery, and electroconvulsive therapy, with mild increases observed following venipuncture (20). Twenty-four-hour GH secretory profiles during severe illness are characterized by higher basal levels of GH and reductions in serum IGF-1, but no differences in mean GH concentration or number of GH pulses (24). The dissociation between GH and IGF-1 is similar to that seen in catabolic states including prolonged fasting, nutritional dwarfing and anorexia nervosa.
Major depression is associated with increased GH secretion and higher 24-h urinary cortisol measurements (25). Differences in cortisol and GH response to cardiac catheterization appears to correlate best with individual coping behavior. Calm, depressed patients show no increase in plasma GH or cortisol, whereas anxious subjects have elevations of both GH and cortisol (26).
GH concentrations are increased in subjects with inflammatory disease or experimental endotoxemia (27). Receptors for the interleukins, or inflammatory cytokines, are found in nearly all endocrine glands, specifically in the hypothalamus, pituitary, adrenal, thyroid, testis/ovary, and islet cells. Through a complex feedback system unique to each cytokine, GH secretion is influenced via autocrine, paracrine or endocrine mechanisms. Growth retardation, however, is a common feature of most chronic inflammatory diseases, which suggests some interference in GH or IGF action at the level of peripheral tissues.
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