Treatment Bone Mineral Density Research Articles

Bone Mineral Density and Body Composition in Short Children Born SGA during Growth Hormone and Gonadotropin Releasing Hormone Analog Treatment

Postponement of puberty by GnRH analog (GnRHa) in addition to GH treatment might increase adult height (AH) in short adolescents born small for gestational age (SGA). GnRHa treatment is thought to have negative effects on bone mineral density (BMD) and body composition. The objective of the study was to assess the BMD of total body (BMD(TB)), lumbar spine (BMD(LS)), bone mineral apparent density lumbar spine (BMAD(LS)), lean body mass, fat mass, and fat distribution during GH treatment, with or without an additional 2 yr of GnRHa. This was a prospective GH trial involving short SGA adolescents (≥8 yr). Eighty-eight children (50 girls) were treated until AH (GH randomized 1 or 2 mg/m(2) · d during puberty); 52 of these children received additional GnRHa. BMD and body composition were longitudinally assessed by dual-energy X-ray absorptiometry. Baseline BMD(TB) sd score (SDS) and BMD(LS) SDS were significantly reduced (both P < 0.001), but BMAD(LS) SDS was comparable with zero (P = 0.129). BMD(TB) SDS and BMD(LS) SDS improved (both P < 0.001) from the start until AH, whereas BMAD(LS) SDS remained similar (P = 0.168). At AH, 93% of patients had a normal BMD(TB), 99% a normal BMD(LS), and 98% a normal BMAD(LS) (> -2 and < +2 SDS). From the start until AH, lean body mass SDS(height) and fat mass SDS increased significantly toward zero (both P <0.001). Multiple regression analyses showed that additional GnRHa treatment had no adverse effect on the changes in BMD and body composition during GH treatment, also after correction for influencing variables. Untreated short SGA adolescents had reduced BMD(TB) and BMD(LS) but normal bone size-corrected BMAD(LS). During GH treatment, BMD(TB) and BMD(LS) increased significantly, leading to a normal adult BMD in almost all patients. Two years of GnRHa in addition to GH treatment had no adverse effect on BMD or body composition.

Are changes in bone mineral density different between groups of early rheumatoid arthritis patients treated according to a tight control strategy with or without prednisone if osteoporosis prophylaxis is applied?

SummaryAddition of 10 mg prednisone daily to a methotrexate-based tight control strategy does not lead to bone loss in early rheumatoid arthritis (RA) patients receiving preventive treatment for osteoporosis. A small increase in lumbar bone mineral density (BMD) during the first year of treatment was recorded, regardless of use of glucocorticoids.IntroductionThis study aims to describe effects on BMD of treatment according to EULAR guidelines with a methotrexate-based tight control strategy including 10 mg prednisone daily versus the same strategy without prednisone in early RA patients who received preventive therapy for osteoporosis.MethodsEarly RA patients were included in the CAMERA-II trial: a randomized, placebo-controlled, double-blind 2-year trial, in which effects of addition of 10 mg prednisone daily to a methotrexate-based tight control strategy were studied. All patients received calcium, vitamin D and bisphosphonates. Disease activity was assessed every 4 weeks. Radiographs of hands and feet and dual-energy X-ray absorptiometry of lumbar spine and left hip were performed at baseline and after 1 and 2 years of treatment.ResultsBMD increased significantly over time in both treatment groups at the lumbar spine with a mean of 2.6 % during the first year (p < 0.001), but not at the hip; at none of the time points did BMD differ significantly between the prednisone and placebo group. Higher age and lower weight at baseline and higher disease activity scores during the trial, but not glucocorticoid therapy, were associated with lower BMD at both the lumbar spine and the hip in mixed-model analyses.ConclusionAddition of 10 mg prednisone daily to a methotrexate-based tight control strategy does not lead to bone loss in early RA patients on bisphosphonates. A small increase in lumbar BMD during the first year of treatment was found, regardless of use of glucocorticoids.

Bone mineral density of the lumbar spine in psoriatic patients with long term etretinate therapy.

Etretinate has been known to produce a variety of skeletal manifestations when administered for prolonged periods. To study whether osteoporotic changes occurred during the treatment bone mineral density (BMD) was measured by dual energy X-ray absorptiometry in 13 psoriatic patients who received long term etretinate therapy (average 3.7 yrs). The values of BMD of the lumbar spine in these patients were decreased from those of age-matched controls (92.3 +/- 9.7%), p < 0.01), while those in psoriatic patients who received topical corticosteroid applications alone showed no significant decrease. Our findings suggest that long term etretinate intake induces an increased risk of osteoporotic changes.

Effect of Long-Term Administration of Progestogen on Post-Menopausal Bone Loss

Summary OBJECTIVE We determined whether a progestogen given alone to post-menopausal women may prevent bone loss. STUDY DESIGN Thirty-five early post-menopausal women who had not received any form of treatment to prevent bone loss were randomly assigned to a 2-year regimen of 500 μ g/day of a gestagen derived from 19-norprogester-one (Promegestone) or a placebo for 21 days out of a 28-day treatment cycle. Bone mineral density of the spine was measured by dual photon absorptiometry. RESULTS After 2 years of treatment bone mineral density decreased significantly in the placebo group by a mean of 4.5%. In the gestagen group, the rate of bone change was significantly lower as compared to the placebo group (-1.3%± 1.2% vs −4.5%± 2% (mean ± SEM), P & lt; 0.05). There were no changes in the biochemical bone turnover parameters in the placebo group but in the gestagen group a significant decrease was observed in the urinary calcium excretion after 2 years. CONCLUSION The results suggest that a gestagen with no androgenic action can partly counteract early post-menopausal bone loss.