BES2002 Poster Presentations Bone (11 abstracts)
Changes in parathyroid hormone sensitivity and rhythmicity and its effects on bone metabolism following growth hormone replacement in adult growth hormone deficient patients
AM Ahmad 1 , HD White 1 , J Thomas 1 , A Clewes 1 , MT Hopkins 1 , R Guzder 1 , H Ibrahim 1 , BH Durham 2 , JP Vora 1 & WD Fraser 2
1Department of Diabetes and Endocrinology, Royal Liverpool University Hospital, Liverpool, UK; 2Department of Clinical Chemistry, Royal Liverpool University Hospital, Liverpool, UK.
BACKGROUND: Adult Growth Hormone Deficiency (AGHD) is associated with reduced bone mineral density (BMD). PTH plays an important role in bone metabolism and reports have suggested target cell insensitivity to PTH as a contributor to the changes in bone turnover seen in AGHD. Although growth hormone replacement (GHR) increases BMD, the underlying mechanisms remain unclear.
OBJECTIVES: To determine the effect of GHR on 24-hour PTH profiles, phosphocalcium metabolism and bone turnover markers
METHODS: 16 AGHD patients were recruited. Half-hourly blood and 3-hourly urine samples were collected, at baseline and 1,3,6 and 12 months following GHR, for PTH, calcium, phosphate, 1,25-dihydroxyvitamin-D (1,25(OH)2D3), nephrogenous cAMP (NcAMP), a marker of PTH circulating activity, type-I collagen C-telopeptide (CTx), type-I collagen cross-linked N-telopeptide (NTx), markers of bone resorption, and procollagen type-I amino-terminal propetide (PINP), a marker of bone formation. Local Ethical Committee approval was obtained.
RESULTS: At baseline, PTH concentration was high in the presence of low NcAMP. Serum adjusted calcium and 1,25(OH)2D3 were low, while urinary calcium excretion was high. Following GHR, PTH decreased (p<0.001) with reciprocal increase in NcAMP (p<0.001) and concomitant increase in 1,25(OH)2D3, serum adjusted calcium and phosphate (all p<0.001). All bone resorption and formation markers simultaneously increased (p<0.001). The decrease in PTH and increase in 1,25(OH)2D3 and bone turnover markers was maintained after 12 months, whereas NcAMP, serum adjusted calcium, serum phosphate, urinary calcium and phosphate decreased to below pre-treatment levels after 6 months (p<0.001).
CONCLUSION: Our results suggest a possible renal and bone target cell insensitivity to PTH in AGHD. GHR appears to restore PTH sensitivity which 1) results in increased 1,25(OH)2D3 production and calcium reabsorption; and 2) may in part be responsible for the observed increase in bone turnover. These changes may, thus, explain the underlying mechanisms responsible for BMD changes before and after GHR, previously reported in AGHD.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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