Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial.

Lane, Nancy E.; Sanchez, Sarah; Modin, Gunnard; Genant, Harry K.; Pierini, Elena; Arnaud, Claude D.

doi:10.1172/jci3914

Cited by 487 publications

(269 citation statements)

References 28 publications

(37 reference statements)

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“…[17][18][19][20][21][22][23][24][25][26][27][28][29][30][31] The studies included were: -Neer et al 32 Effect of parathyroid hormone (1-34) on fracture and bone min- Different intervention eral density in postmenopausal women with osteoporosis. This was a paper originating from a double-blind randomized clinical trial with 24 months of follow-up.…”

Section: Statistical Analysis and Presentation Of The Resultsmentioning

confidence: 99%

Teriparatide (recombinant human parathyroid hormone 1-34) in postmenopausal women with osteoporosis: systematic review

Trevisani

Riera²,

Imoto³

et al. 2008

Sao Paulo Med. J.

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CONTEXT AND OBJECTIVE: Osteoporosis is defined as a disease characterized by low bone mass and deterioration of the bone tissue microarchitecture. Teriparatide stimulates the formation and action of osteoblasts, which are responsible for bone formation, thus promoting bone tissue increase. The aim was to assess the effectiveness and safety of teriparatide for treating postmenopausal osteoporosis. METHODS: A systematic review was conducted using the Cochrane Collaboration methodology. RESULTS: 1) Teriparatide 20 µg or 40 µg versus placebo: there was a benefit from teriparatide, considering the following outcomes: reduction in the number of new vertebral and non-vertebral fractures, and increased whole-body, lumbar and femoral bone mineral density. 2) Teriparatide 40 µg versus alendronate 10 mg/day for 14 months: there was no statistical difference regarding the incidence of new vertebral or non-vertebral fractures, although in the group that received teriparatide there was greater bone mineral density increase in the whole body, lumbar column and femur. 3) Estrogen plus teriparatide 25 µg versus estrogen: there was a benefit, considering the following outcomes: reduction in the number of new vertebral fractures, and increased whole-body, lumbar and femoral bone mineral density after three years. CONCLUSIONS: When teriparatide is intermittently administered in low doses, it reduces the incidence of vertebral fractures (67%) and non-vertebral fractures (38%) and increases bone mineral density in the lumbar column and femur. There is a need for studies with longer observation in order to allow conclusions regarding the safety and duration of the therapeutic effects.

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Section: Statistical Analysis and Presentation Of The Resultsmentioning

confidence: 99%

Teriparatide (recombinant human parathyroid hormone 1-34) in postmenopausal women with osteoporosis: systematic review

Trevisani

Riera²,

Imoto³

et al. 2008

Sao Paulo Med. J.

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“…Yet, clinical studies have established that intermittent PTH causes a dramatic increase in bone mass in established disease [121], albeit the anabolic response is blunted in mice given prednisolone simultaneously with PTH [122]. In mice with osteoblastspecific expression of 11β-hydroxysteroid dehydrogenase, an enzyme that inactivates glucocorticoids, osteoblasts were protected against the pro-apoptotic effects of glucocorticoids and the negative effects of glucocorticoids on bone formation were ameliorated [123].…”

Section: The Therapeutic Efficacy Of Intermittent Pth On the Osteopormentioning

confidence: 99%

Molecular and cellular mechanisms of the anabolic effect of intermittent PTH

Jilka

2007

Bone

623

531

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Intermittent administration of parathyroid hormone (PTH) stimulates bone formation by increasing osteoblast number, but the molecular and cellular mechanisms underlying this effect are not completely understood. In vitro and in vivo studies have shown that PTH directly activates survival signaling in osteoblasts; and that delay of osteoblast apoptosis is a major contributor to the increased osteoblast number, at least in mice. This effect requires Runx2-dependent expression of antiapoptotic genes like Bcl-2. PTH also causes exit of replicating progenitors from the cell cycle by decreasing expression of cyclin D and increasing expression of several cyclin-dependent kinase inhibitors. Exit from the cell cycle may set the stage for pro-differentiating and pro-survival effects of locally produced growth factors and cytokines, the level and/or activity of which are known to be influenced by PTH. Observations from genetically modified mice suggest that the anabolic effect of intermittent PTH requires insulin-like growth factor-I (IGF-I), fibroblast growth factor-2 (FGF-2), and perhaps Wnts. Attenuation of the negative effects of PPARγ may also lead to increased osteoblast number. Daily injections of PTH may add to the pro-differentiating and pro-survival effects of locally produced PTH related protein (PTHrP). As a result, osteoblast number increases beyond that needed to replace the bone removed by osteoclasts during bone remodeling. The pleiotropic effects of intermittent PTH, each of which alone may increase osteoblast number, may explain why this therapy reverses bone loss in most osteoporotic individuals regardless of the underlying pathophysiology.

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“…Treatment options that were recommended by the CPG for glucocorticoid-induced osteoporosis included alendronate, risedronate and teriparatide all of which have been shown to prevent vertebral fractures in these patients [50][51][52] …”

Section: Osteoporosis In Special Circumstancesmentioning

confidence: 99%

A Review of the 2008 Singapore Ministry of Health Clinical Practice Guidelines on Osteoporosis and an Update

Tan

Bee

Chandran

2012

JAFES

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Osteoporosis is a major public health problem worldwide and it is of particular significance in a rapidly aging society such as Singapore. In order to prevent the devastating sequelae of osteoporosis, it is important, to diagnose the condition early, to identify its associated risk factors and to initiate pharmacotherapy promptly when required. In addition, it is important to increase awareness of this condition amongst both health care professionals and the public. The Singapore Ministry of Health (MOH) Clinical Practice Guidelines published in 2008 was an update of a previously published version in 2002. It aimed at providing the best evidence-based recommendations for diagnosis, classification, evaluation and multidisciplinary management of osteoporosis and osteoporotic fractures in Singapore. This article summarizes the guidelines, discusses their applicability and utilization in Singapore and briefly outlines updates in management since the publication of the CPG.

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Parathyroid hormone treatment can reverse corticosteroid-induced osteoporosis. Results of a randomized controlled clinical trial.

Cited by 487 publications

References 28 publications

Teriparatide (recombinant human parathyroid hormone 1-34) in postmenopausal women with osteoporosis: systematic review

Teriparatide (recombinant human parathyroid hormone 1-34) in postmenopausal women with osteoporosis: systematic review

Molecular and cellular mechanisms of the anabolic effect of intermittent PTH

A Review of the 2008 Singapore Ministry of Health Clinical Practice Guidelines on Osteoporosis and an Update

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