Factors Influencing Changes in Bone Mineral Density in Patients with Anorexia Nervosa-Related Osteoporosis: The Effect of Hormone Replacement Therapy

Department of Rheumatology, CHRU Lille, Hôpital Roger Salengro, 59037, Lille cédex, France.
Calcified Tissue International (Impact Factor: 3.27). 10/2008; 83(5):315-23. DOI: 10.1007/s00223-008-9173-y
Source: PubMed


The purpose of this longitudinal study was to evaluate factors affecting changes in bone mineral density (BMD) in patients with anorexia nervosa (AN) and osteoporosis and, more particularly, to assess the benefits of hormone replacement therapy (HRT) on BMD in these patients. Our study involved 45 AN patients, 12 of whom had been treated by HRT for 2 years following a diagnosis of osteoporosis by densitometry (WHO criteria). Patients' mean age was 25.3 +/- 6.7 years. Mean duration of illness was 5.7 +/- 5.3 years. Serum calcium and phosphate were measured at baseline, as were bone remodeling markers. Osteodensitometry by dual-energy X-ray absorptiometry was performed at inclusion and after 2 years. After 2 years, no significant differences were observed between spine, femoral neck, and total hip BMDs either in the HRT group (P = 0.3, P = 0.59, P = 0.58) or in the nontreatment group (P = 0.17, P = 0.68, P = 0.98). Moreover, there were no significant differences between the two groups when changes in spine, femoral neck, and total hip BMDs at 2 years were compared (P = 0.72, P = 0.95, P = 0.58). In both groups, change in weight at 1 year correlated with change in spine BMD at 2 years (r = 0.35, P = 0.04) and change in total-hip BMD at 2 years (r = 0.35, P = 0.04) but not with change in femoral neck BMD at 2 years. Patients with a body mass index (BMI) > or = 17 kg/m(2) at 2 years showed a significant increase in total-hip BMD when compared with patients with a BMI < 17 kg/m(2) (+4.4% +/- 6.7 vs. -0.5% +/- 6.01, P = 0.03). No significant differences were observed for spine and femoral neck BMD. In patients who had recovered their menstrual cycle, significant increases were observed in spine BMD (+4% +/- 6.3 vs. -1.9% +/- 5.6, P = 0.008), femoral neck BMD (+3% +/- 6.2 vs. -2.4% +/- 8, P = 0.05), and total-hip BMD (+3% +/- 7.1 vs. -3.7% +/- 10, P = 0.04). Prevention of bone loss at 2 years in AN patients treated by HRT was not confirmed in this study. We did confirm that increase in weight at 1 year was the most predictive factor for the improvement of spine and hip BMD at 2 years.

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    • "Furthermore, it has been reported that while moderate exercise is beneficial for bone mass, excessive exercise, which is very common in AN, may put patients at higher risk of low bone mass and lead to overuse fractures (Waugh et al., 2011). Hormone replacement therapy (HRT) and treatment with oral contraceptives have resulted in inconclusive and often disappointing outcomes (Seeman et al., 1992; Klibanski et al., 1995; DiVasta and Gordon, 2008; Legroux-Gerot et al., 2008; Mehler and MacKenzie, 2009). "
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    ABSTRACT: Since the advent on non-invasive in vivo clinical bone densitometry, investigators have reported that regional bone mineral material loss accompanies the onset and continuance of anorexia nervosa (AN). Initial single-energy photon absorptiometric (SPA) studies were followed by a succession of dual-energy x-ray absorptiometric (DXA) investigations, and a few single-energy quantitative computer assisted tomographic (SEQCT) bone densitometry vertebral measurements. Although most all DXA studies found a relatively small diminution (~3%) of bone mineral material at lumbar vertebral and proximal femoral bone-sites of AN-afflicted adolescent girls and young women, these findings have been consensually interpreted and near-universally accepted as losses of actual bone mineral material accompanying AN. It has also been claimed by some that about 50% of those beset by AN while still young adolescents were osteoporotic. Nonetheless, over the last intervening 2 decades of these studies, no specific underlying direct bone-biological causal link between AN and trabecular bone material loss has yet been uncovered. The present exposition shows that in vivo SPA, DXA, and SEQCT measurements of bone mineral material losses do not constitute evidence of actual loss of bone material, and that the attribution of osteopenia and osteoporosis to AN-afflicted younger adolescent girls is not sustainable. Rather, the full gamut of these reported bone material "losses" can be accounted for by the already well-documented AN-induced changes in the anthropometrics and compositional mixes of extra-osseous soft tissues (primarily in a very noticeable reduction of extra-skeletal fat) and intra-osseous bone marrow yellowing (marrow hypoplasia and marrow cell necrosis). These changes in soft tissue compositions and anthropometrics alone have been shown to be sufficient to cause in vivo SPA, DXA, and SEQCT to systematically mis-estimate true bone material density and erroneously register changes in bone mineral content, even when no actual changes in bone mineral material have occurred. As a result, it is seen that in vivo bone densitometry methodologies have not demonstrated that AN induces actual loss of bone mineral material. It is also demonstrated that DXA and SEQCT bone density measurements of predominantly trabecular bone-sites cannot be relied upon as gauges of heightened propensity for early (or late) osteoporotic development.
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