Endocrine Abstracts (2004) 7 P19

Changes in bone mineral density in response to growth hormone replacement in adults with isolated growth hormone deficiency compared with multiple pituitary hormone deficiencies

M Waterhouse, R Loureiro, D Walker, GM Besser & JP Monson


Department of Endocrinology, Bart's and the London Hospital NHS trust, London, UK.


The contribution of conventional hormone replacement to the clinical features attributed to adult growth hormone deficiency (GHD) is poorly defined. We measured baseline bone mineral density (BMD/DXA) at the lumbar spine and femoral neck in patients with isolated GHD (IGHD, 16 patients, 14 female, 4 childhood onset, mean age 39, range 19- 63 years) and patients with multiple pituitary hormone deficiencies (MPD, 135 patients, 94 female, 14 childhood onset, mean age 44, range 19-62 years). We observed the change in BMD in response to titrated GH replacement, (serum IGF-I of 0-2 SD), in both groups at 1 and 2 years. At baseline, both groups had reduced BMD compared to age matched subjects (Z score L2-L4, mean ± SD: MPD -0.43 ± 1.4, IGHD -0.22 ± 1.9; femoral neck: MPD -0.46 ± 1.2, IGHD -0.06 ± 0.67), with no significant differences between the groups. On maintenance GH replacement, serum IGF-I concentrations were in the normal range (MPD: 247 ± 94.7 ng/mL; IGHD: 271 ± 101.6 ng/ml). At one year, neither group demonstrated significant changes in BMD. After two years, BMD had significantly improved in both groups compared to baseline but was discordant in terms of site: (delta Z score L2-L4: MPD + 0.01 ± 1.3, P NS; IGHD +0.4 ± 1.8, P <0.05; femoral neck: MPD +0.23 ± 1.1, P <0.05; IGHD +0.18 ± 0.66, P NS). Analysis of female patients yielded similar results. We conclude that baseline BMD is compromised by GHD irrespective of additional pituitary hormone deficiencies. The delayed improvement in BMD in both groups after a year of GH replacement could be due to the effects of GH on increasing bone remodelling space. Subsequently, potentially important improvements BMD were observed in both IGHD and MPD patients. These data provide a further rationale for GH replacement in adult IGHD.

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