Endocrine Abstracts

Growth hormone deficiency leads to reduced bone turnover, mainly due to alterations in PTH circadian rhythmicity as well as to a lack of sensitivity of the kidney and bone to the effects of PTH. These mechanisms may be responsible for bone turnover changes and development of osteoporosis. Patients with GHD show abnormalities of renal phosphate metabolism, which may also contribute to the pathogenesis of bone loss in these patients. GH treatment leads to restoration of renal tubular reabsorption and sensitivity of target organs to PTH, bone turnover and improvement of BMD under GH replacement therapy.

The role of the phosphatonine FGF-23 in this complex process was investigated. We measured the relationship between parameters of calcium metabolism such as Calcium, Phosphate, Creatinine and PTH and their correlation to the phosphatonine FGF-23 and 25-OH Vitamin D levels in GDH patients before, after 6 and 12 months therapy with growth hormone.

EDTA-Plasma (due to better stability than serum samples) of 15 patients was investigated. Arithmetic means for intact FGF-23 before therapy were 17.3 pg/ml, after 6 months therapy 15.3 pg/ml and 23 pg/ml at 12 months (all P<0.001). C-terminal FGF-23 initial was 58 U/ml, at 6 months 47 U/ml and at month 12 108.6 U/ml (all P<0.001). Calcium values were 2.38, 2.44 and 2.43 mmol/l. Corresponding phosphate levels were 3.04, 3.39 and 3.08 mg/dl (all P<0.001). As expected, FGF-23 was inversely correlated to serum phosphate.

GH supplementation in GHD patients leads to normalization of tubular reabsorption of phosphate due to regulation by FGF-23 and reverses the GHD-induced relative phosphate-deficient state. Restoration of the physiological regulation of phosphate metabolism emphazises the beneficial effect of GH supplementation on bone remodeling in GHD patients.