Are there any interactions between replacement hormones?
Because GH therapy can decrease circulating free T 4 levels in adults with GH deficiency, free T 4 should be measured 6 weeks after initiation of GH replacement and after each dose escalation to rule out a mild case of central hypothyroidism. This also applies to those patients with central hypothyroidism already receiving LT 4 who are being started on GH therapy. Patients with GH deficiency have increased activity of 11-beta hydroxysteroid dehydrogenase type 1, resulting in increased conversion of cortisone to cortisol. Thus, GH replacement, by decreasing the conversion of cortisone to cortisol, may expose occult central adrenal insufficiency in patients with borderline ACTH reserve or those receiving subtherapeutic doses of glucocorticoids. Gonadal steroids influence GH-mediated hepatic IGF-1 generation. Because oral estrogens decrease IGF-1 levels, women on estrogen replacement therapy need higher doses of GH to reach their target IGF-1 concentrations. Commencement of glucocorticoid replacement therapy can unmask central diabetes insipidus. Finally, because thyroid hormone increases the metabolic clearance rate of cortisol, initiating LT 4 in patients with coexistent but unrecognized adrenal insufficiency can precipitate an adrenal crisis.