Intravenous pamidronate in the treatment of osteoporosis associated with corticosteroid dependent lung disease: an open pilot study.

Gallacher, S. J.; Fenner, John; Anderson, Kenneth E.; Bryden, F.; Banham, S. W.; Logue, F. C.; Cowan, Robert A.; Boyle, I T

doi:10.1136/thx.47.11.932

Cited by 71 publications

(24 citation statements)

References 23 publications

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“…The greater increase of NTx with respect to HOP could be due to the fact that NTx is a more sensitive marker of bone resorption. In agreement with other studies [21,22], the treatment with prednisone significantly decreased BGP. Glucocorticoids have been shown to inhibit in vitro osteocalcin secretion by a direct effect at the transcriptional level, thus, osteocalcin is considered to be a sensitive index of the inhibition of the bone matrix mineralization by steroids [30].…”

Section: Discussionsupporting

confidence: 93%

“…Several studies have reported that intermittent cyclical etidronate is effective in both the prevention and treatment of corticosteroid-induced bone loss [17][18][19]. Another aminobisphosphonate, pamidronate, administered both orally [20,21] and parenterally [22], was found to increase bone mineral density (BMD) and reduced bone turnover in glucorticoid-treated patients. Oral clodronate has also been reported to be effective [23].…”

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confidence: 98%

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Prevention of Corticosteroid-Induced Osteoporosis with Alendronate in Sarcoid Patients

Gonnelli

Rottoli

Cepollaro

et al. 1997

Calcified Tissue International

111

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Prolonged corticosteroid administration, as often required in the treatment of sarcoidosis, increases the risk of osteoporosis and fracture. The aim of the present study was to evaluate the usefulness of alendronate, a third generation bisphosphonate, in preventing corticosteroid-induced osteoporosis. Forty-three consecutive, previously untreated, sarcoid patients (17 men and 26 premenopausal women) were included in the study: 13 needed no treatment and served as controls (Group 1) and 30 needed glucocorticoids (prednisone) and were randomly selected to also receive either placebo (n = 15, Group 2) or alendronate 5 mg/day (n = 15, Group 3). Bone mineral density (BMD) at the ultradistal radius by dual photon absorptiometry (Osteograph 1000, NIM, Verona, Italy) and biochemical markers of bone turnover were measured at baseline and after 6 and 12 months of glucocorticoid therapy. No significant difference was found between Groups 2 and 3 in the mean cumulative dose of prednisone (4945 +/- 1956 mg and 5110 +/- 2013 mg, respectively). At the end of the study period, BMD increased by 0.8% in the alendronate-treated group; in the placebo-treated group, BMD decreased by 4.5%. The difference between groups was significant (P < 0.01, ANOVA). A significant decrease in markers of bone formation was found in all patients treated with prednisone (Groups 2 and 3), independently of alendronate. Alendronate, however, counteracted the increase in markers of bone resorption induced by glucocorticoid therapy. Our data suggest that alendronate is effective in preventing glucocorticoid-induced bone loss in sarcoid patients. Further studies on alendronate use in steroid-induced osteoporosis are needed.

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Section: Discussionsupporting

confidence: 93%

mentioning

confidence: 98%

Prevention of Corticosteroid-Induced Osteoporosis with Alendronate in Sarcoid Patients

Gonnelli

Rottoli

Cepollaro

et al. 1997

Calcified Tissue International

111

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“…In those patients proceeding to a second year of treatment, the gains in bone density were maintained, whereas there was progressive loss in the placebo group. Oral pamidronate is not widely available, but three-monthly infusions of 30 mg of this drug appear to be comparably effective (62).…”

Section: Bisphosphonatesmentioning

confidence: 99%

Glucocorticoid osteoporosis--mechanisms and management

Reid

1997

European Journal of Endocrinology

249

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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“…Etidronate improved BMD at the lumbar spine by 5.7% and total hip by 6.8%, while the calcium supplemented group lost 3.4% BMD at the lumbar spine and 4.1% at the total hip [128]. In 15 patients with asthma and two with sarcoidosis treated with prednisolone for a range of 3-30 yrs, with a range of doses between 7.5 and 40 mg?day -1 , treatment with 30 mg of pamidronate every 3 months for 1 yr produced a mean gain in BMD at the lumbar spine of 3.4% without any change at the femoral neck [129].…”

Section: Bisphosphonatesmentioning

confidence: 99%