Cyclical etidronate plus ergocalciferol prevents glucocorticoid-induced bone loss in postmenopausal women

Diamond, Terrence; McGuigan, L; Barbagallo, S.; Bryant, Carl

doi:10.1016/s0002-9343(99)80345-3

Cited by 88 publications

(37 citation statements)

References 24 publications

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“…There was a similar, nonsignificant trend in distal radial bone loss, but no evidence whatsoever of reduced bone loss in the proximal femur (3% in all groups). While there was clearly a benefit from the use of calcitriol, it was less than that seen in a comparable trial in which etidronate was administered from the time of introduction of steroid treatment (71); several other groups have also documented that etidronate prevents femoral bone loss (64,65). In contrast, when the effects of alphacalcidol and etidronate were compared in a recent study of bone loss after cardiac transplantation (72), neither treatment completely prevented bone loss, though the vitamin D metabolite was superior to the bisphosphonate.…”

Section: Vitamin D and Its Metabolitesmentioning

confidence: 96%

“…There is now a number of studies showing that cyclic etidronate is effective in steroid-treated patients (63)(64)(65), and this treatment has high patient acceptability, as medication is taken for only 2 weeks every 3 months. The other widely available oral bisphosphonate, alendronate, is now well established as an effective treatment for postmenopausal osteoporosis.…”

Section: Bisphosphonatesmentioning

confidence: 99%

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Glucocorticoid osteoporosis--mechanisms and management

Reid

1997

European Journal of Endocrinology

252

148

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Glucocorticoids are potent osteopenic agents, producing negative calcium and bone balance via actions at many sites. The most significant adverse effects of glucocorticoid drugs on the skeleton are probably a direct inhibition of matrix synthesis by the osteoblast, reductions in calcium absorption in both the gut and the renal tubule, and the production of hypogonadism, particularly in men. Reductions in bone density of 10-40% result, the loss being more marked in trabecular bone and in patients receiving a high cumulative dose of the steroid. Fractures occur in about 30% of individuals who take these drugs for an average of 5 years. Bone loss is reversible when glucocorticoid treatment is withdrawn. Bone density can also be increased by sex hormone replacement in those with demonstrable deficiency, by bisphosphonates, and possibly by vitamin D metabolites. All patients treated with glucocorticoids for more than 6 months should be considered for bone densitometry and be offered appropriate drug treatment if values are towards the lower end of the young normal range or if there is already evidence of fractures occurring after minimal trauma. With this approach, the significant morbidity associated with steroid osteoporosis might be substantially avoided.

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Section: Vitamin D and Its Metabolitesmentioning

confidence: 96%

Section: Bisphosphonatesmentioning

confidence: 99%

Glucocorticoid osteoporosis--mechanisms and management

Reid

1997

European Journal of Endocrinology

252

148

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“…In the prospective study, 15 of the 25 patients with stage II and III myeloma were re-evaluated after 12 months of follow-up. Their data were compared to a group of glucocorticoid-treated controls who had rheumatoid and respiratory disorders and had been treated with prednisolone (5-20 mg/d) for a minimum period of 6 months and up to a maximum period of 14 years (Diamond et al, 1995).…”

mentioning

confidence: 99%

Biochemical, histomorphometric and densitometric changes in patients with multiple myeloma: effects of glucocorticoid therapy and disease activity

Diamond¹,

Levy²,

Day³

et al. 1997

Br J Haematol

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Summary.It is unknown whether bone changes which can occur in multiple myeloma (MM) are due to cytokineinduced osteoclastic bone resorption from a clone of abnormal plasma cells or high-dose glucocorticoid therapy.We studied 25 MM patients treated for 1-12 years with combination chemotherapy, subdivided into two groups. Group 1 consisted of 12 patients with stage I and II myeloma and group 2 consisted of 13 patients with stage III MM. Their serum biochemistry, tetracycline-labelled bone histomorphometry and bone densitometry were compared to age-and sex-matched controls.Patients with MM demonstrated increased indices of bone resorption (P < 0 : 001 versus controls) and, to a lesser extent, increased indices of bone formation (P < 0 : 01 versus controls). No patient had evidence of a mineralization defect.Lumbar spine, femoral neck and total body bone mineral density measurements (BMD) were significantly lower in group 2 compared with group 1 (P < 0 : 05). Following 12 months of therapy, lumbar spine BMD decreased by 6 : 6% (95% CI, 2 : 7% to ¹9 : 3%) and femoral neck BMD decreased by 9 : 5% (95% CI, ¹3 : 2% to ¹15 : 9%). In a stepwise regression analysis, cumulative prednisolone dosage (B Coef: ¼ ¹0 : 39; P ¼ 0 : 03) and plasma cell infiltrate (B Coef: ¼ ¹0 : 08; P ¼ 0 : 05) were the most important predictors of lumbar spine bone loss, whereas serum paraprotein (B Coef: ¼ ¹0 : 35; P ¼ 0 : 02) and plasma cell infiltrate (B Coef: ¼ ¹0 : 20; P ¼ 0 : 04) were the most important predictors of femoral neck bone loss.We conclude that MM is characterized by high bone turnover with osteoblast-osteoclast uncoupling. Both disease activity and high-dose glucocorticoid therapy may be responsible for the ongoing bone loss seen with MM.

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“…Diamond et al reported that cyclical etidronate prevented glucocorticoid-induced bone loss of the lumbar spine and femoral neck in postmenopausal women commencing glucocorticoids for the first time or recommencing therapy. 18 In a recent double blind, placebo controlled trial by Adachi et al, 20 a significant diVerence in the mean percentage change from baseline in the bone mineral density of the lumbar spine (3.72%) and trochanter (4.14%) was detected between patients randomised to receive cyclical etidronate or placebo. Patients recently starting treatment with glucocorticoids maintained their bone mineral density of the lumbar spine and trochanter when randomised to receive preventive therapy with etidronate; in contrast, those in the placebo group experienced a 3.23% and 2.74% decrease from baseline, respectively.…”

mentioning

confidence: 97%

“…Previous investigations have been conducted predominantly in patients with rheumatoid arthritis where the absolute risk of bone loss may be unique due to additive eVects from the underlying disease process and diVerences in the cumulative glucocorticoid dose. 2 15 Moreover, epidemiological studies enrolling patients with respiratory diseases to assess the use of etidronate in glucocorticoid-induced osteoporosis have used non-randomised [16][17][18] or unblinded 16 18 19 designs, short follow up periods, 19 and historical controls. 18 By demonstrating the usefulness of etidronate for treating glucocorticoid-induced osteoporosis, Pitt et al have confirmed the results of this preliminary research.…”

mentioning

confidence: 99%