Preliminary Trial of Low Doses of Human Parathyroid Hormone 1–34 Peptide in Treatment of Osteoporosis

Reeve, J.; Parsons, J. A.; Tregear, Geoffrey W.; Darby, A. J.; Hesp, R.; Hulme, P.; Klenerman, L.; Williams, D.; Potts, John T.

doi:10.1042/cs050014pa

Cited by 6 publications

(48 citation statements)

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“…This had occurred in one patient and had been successfully treated 35 years before the trial. At the time of acceptance into the study no patient had received pharmacological doses of any vitamin D preparation within two years, although one patient in Boston (case 21) was treated with vitamin D3 50 mg (2000 IU) daily for two years before entering the trial, and all the British patients (cases [1][2][3][4][5][6][7][8] were given vitamin D. 12-5 mg (500 IU) daily from three months before their baseline values were determined. These doses were maintained throughout the study.…”

Section: Methodsmentioning

confidence: 99%

Anabolic effect of human parathyroid hormone fragment on trabecular bone in involutional osteoporosis: a multicentre trial.

Reeve¹,

Meunier²,

Parsons³

et al. 1980

BMJ

549

202

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Section: Methodsmentioning

confidence: 99%

Anabolic effect of human parathyroid hormone fragment on trabecular bone in involutional osteoporosis: a multicentre trial.

Reeve¹,

Meunier²,

Parsons³

et al. 1980

BMJ

549

202

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“…The anabolic effect of human PTH(1-34) in osteoporosis has been a major focus of interest since the 1970s. (1–8) Intermittent use of PTH(1-34) (once daily for 18–24 months) decreases vertebral and non-vertebral fracture risk in patients (5,9,10) and improves bone microstructure and strength in animal models.…”

Section: Introductionmentioning

confidence: 99%

“…(1–8) Intermittent use of PTH(1-34) (once daily for 18–24 months) decreases vertebral and non-vertebral fracture risk in patients (5,9,10) and improves bone microstructure and strength in animal models. (11–15) Further, PTH(1–34) administration has been found in animal models to facilitate bone repair after fracture (16–20) and spinal fusion. (21) …”

Section: Introductionmentioning

confidence: 99%

Parathyroid hormone treatment improves the cortical bone microstructure by improving the distribution of type I collagen in postmenopausal women with osteoporosis

Ascenzi

Liao

Lee

et al. 2011

Journal of Bone and Mineral Research

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Although an important index, the level of bone mineral density (BMD) does not completely describe fracture risk. Another bone structural parameter, the orientation of type I collagen, is known to add to risk determination, independently of BMD, ex vivo. We investigated the Haversian system of transiliac crest biopsies from postmenopausal women before and after treatment with parathyroid hormone (PTH). We used the birefringence of circularly polarized light and its underlying collagen arrangements by confocal and electron microscopy, in conjunction with the degree of calcification by high-resolution micro-X-ray. We found that PTH treatment increased the Haversian system area by 48.28±38.78%; decreased bright birefringence from 0.45±0.02 to 0.40±0.01 (scale zero to one, p=0.0005); increased the average percent area of osteons with alternating birefringence from 48.15±10.27 to 66.33±7.73 (p=0.034), decreased non-significantly the semi-homogeneous birefringent osteons (8.36±10.63 vs. 5.41±9.13, p=0.40) and birefringent bright (4.14±8.90 vs. 2.08±3.36, p=0.10) osteons. Further, lamellar thickness significantly increased from 3.78±0.11μm to 4.47±0.14μm (p=0.0002) for bright, and from 3.32±0.12μm to 3.70±0.12μm (p=0.045) for extinct, lamellae. This increased lamellar thickness altered the distribution of birefringence and therefore the distribution of collagen orientation in the tissue. With PTH treatment, a higher percent area of osteons at initial degree of calcification was observed, relative to intermediate-low degree of calcification (57.16±3.08 vs. 32.90±3.69, p=0.04), the percentage of alternating osteons at initial stages of calcification increasing from 19.75±1.22 to 80.13±6.47, p=0.001. In conclusion, PTH treatment increases heterogeneity of collagen orientation, a starting point to study the reduction in fracture risk when PTH is used to treat osteoporosis.

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“…Entretanto, experimentos realizados in vitro em cultura de tecido (calvaria de ratas) demonstraram que a adição do PTH ao meio de cultura inibia a síntese de colágeno e aumentava a reabsorção óssea, trazendo certa confusão sobre o assunto (5). São desta mesma época estudos preliminares utilizando PTH como agente terapêutico para osteoporose (6).…”

Section: Históricounclassified

Paratormônio e osteoporose: encontrando o fio da meada. Bases fisiológicas para utilização do PTH no tratamento da osteoporose

Gracitelli¹,

Vidoris²,

Luba³

et al. 2002

Arq Bras Endocrinol Metab

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RESUMOO paratormônio (PTH) estará disponível em breve em nosso mercado como uma possibilidade terapêutica eficiente para a osteoporose. Esta revisão tem por objetivo apresentar os resultados das pesquisas clínicas e experimentais que justificaram tal fato, assim como procurar esclarecer por quais mecanismos o PTH pode ter ações diferenciadas sobre o esqueleto. Os trabalhos bastante recentes demonstram que existem vias diferentes para a atuação do PTH no osteoblasto, e que isto depende da dose, do tempo de exposição e dos fragmentos de PTH utilizados. Seu uso em dose única diária, por via subcutânea, tem demonstrado resultados surpreendentes em termos de ganho de massa óssea e prevenção de fraturas, superando em muito os resultados obtidos com as terapêuticas anti-reabsortivas. Sua disponibilização trará grandes modificações nos conceitos e atuais formas de tratamento da osteoporose. Parathyroid hormone (PTH) will be available in a few months for the treatment of osteoporosis. When used as a single daily subcutaneous injection for at least 1 year, it increases bone mass and reduces fracture rate more efficiently than the usual anti-resorptive therapy. Recently published articles show that PTH can act through different intracellular signaling pathways, depending on its concentration, time of exposure and molecular fragments. High concentration and prolonged exposure to amino-terminal PTH fragments stimulate bone resorption. On the other hand, in an intermittent way and in low concentrations, PTH administration increases bone formation. This review aims to present the principal results of clinical and experimental researches on PTH actions, while trying to explain the rationale for its dual effect on bone remodeling. O EXCESSO DE HORMÔNIO da paratiróide (PTH) ativo é clinicamente diagnosticado como hiperparatiroidismo e está relacionado dentre as causas de osteoporose na densitometria óssea, associado a elevado risco de fraturas e a uma doença óssea com substrato anátomo-patológico característico denominada de osteíte fibrosa cística (1). Uma elevação dos níveis plamáticos de PTH está envolvida na fisiopatologia da perda óssea na osteoporose senil, como consequência à deficiência de vitamina D (2). Estes conceitos já tão bem estabelecidos na literatura científica dificultam nossa compreensão sobre os recentes relatos do uso do PTH como tratamento da osteoporose, e que em breve estará comercialmente disponível no Brasil.

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Preliminary Trial of Low Doses of Human Parathyroid Hormone 1–34 Peptide in Treatment of Osteoporosis

Cited by 6 publications

References 0 publications

Anabolic effect of human parathyroid hormone fragment on trabecular bone in involutional osteoporosis: a multicentre trial.

Anabolic effect of human parathyroid hormone fragment on trabecular bone in involutional osteoporosis: a multicentre trial.

Parathyroid hormone treatment improves the cortical bone microstructure by improving the distribution of type I collagen in postmenopausal women with osteoporosis

Paratormônio e osteoporose: encontrando o fio da meada. Bases fisiológicas para utilização do PTH no tratamento da osteoporose

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