Heparin-Induced Osteopenia: An Appraisal

Avioli, Louis V.

doi:10.1007/978-1-4684-0946-8_33

Cited by 125 publications

(42 citation statements)

References 38 publications

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“…There are three case reports in the literature describing osteoporosis that can be attributed to the use of UFH although all three cases had other risk factors (Schuster et al, 1969;Avioli, 1975;Hausdorf et al, 1982;Murphy et al, 1992). Certainly, where possible, the use of prolonged exposure to UFH should be avoided in all age groups.…”

Section: Osteoporosismentioning

confidence: 99%

Aspects of anticoagulation in children

Payne

2010

Br J Haematol

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SummaryThe number of children receiving anticoagulation is increasing. Thromboembolic events are associated with significant risk of morbidity and mortality although the optimal management of asymptomatic events remains unclear. Specific challenges in paediatrics include the diagnosis of thrombosis, delivery and monitoring of anticoagulation in a wide range of ages from neonates through to adolescents. The development of the haemostatic system as children age results in changing pathophysiology of thrombosis and response to anticoagulation agents. Although registry and observational studies have provided vital information, specific paediatric, prospective anticoagulation studies have been few and limited in design. The result is that much of current practice is extrapolated from adult studies. Traditional anticoagulants have significant limitations. Both heparin and warfarin are in widespread use but many fundamental questions regarding dose, therapeutic range, efficacy and optimum duration have not been fully answered. Alternative agents, such as direct thrombin inhibitors and the selective anti-factor Xa inhibitor fondaparinux, may have advantages for children. Clinical trials in adults and preliminary data in children are promising but caution should be applied until specific paediatric studies have demonstrated safety and efficacy.

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Section: Osteoporosismentioning

confidence: 99%

Aspects of anticoagulation in children

Payne

2010

Br J Haematol

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“…The possible role of HS in bone mass regulation has been speculated for some time. For example, the frequent association of osteoporosis with the low-molecular-weight heparin therapy for venous thromboembolism (6)(7)(8) has been thought to reflect the physiological function of HS in bone mass regulation. Yet, how endogenous HS acts in bone homeostasis remains elusive because of the lack of appropriate genetic models to address the issue.…”

Section: Introductionmentioning

confidence: 99%

Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass

et al. 2018

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“…[1][2][3][4][5][6][7][8][9][10][11][12] Heparin is currently given long-term to prevent and treat venous thromboembolism during pregnancy, to prevent systemic embolism in pregnant women with mechanical heart valves, and to prevent pregnancy loss in women with antiphospholipid antibodies. Long-term heparin therapy is also indicated in nonpregnant patients with venous thromboembolism who have developed recurrences despite "adequate" oral anticoagulant therapy and in some patients who are immobilized for prolonged periods and who require ongoing thromboprophylaxis.…”

Section: Introductionmentioning

confidence: 99%

Heparin acts synergistically with interleukin-11 to induce STAT3 activation and in vitro osteoclast formation

Walton

Duncan

Deschamps

et al. 2002

Blood

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We have previously demonstrated that long-term heparin treatment causes cancellous bone loss in rats due in part to an increase in the number of osteoclasts lining the trabecular bone surface. In the present study, we investigated this phenomenon by examining the ability of heparin to synergistically enhance interleukin-11 (IL-11)-induced osteoclast formation. Treatment of murine calvaria and bone marrow cells with IL-11 was found to induce the formation of tartrate-resistant acid phosphatase-positive (TRAP ؉ ) multinucleated cells (MNCs) in a dose-dependent fashion. No effect was seen when cocultures were treated with heparin alone. However, when cocultures were treated with both IL-11 and heparin, IL-11's ability to induce TRAP ؉ MNC formation was enhanced 6-fold. In an attempt to resolve the mechanism responsible for this effect, we examined the ability of heparin to influence IL-11 signaling using murine calvaria cells. Heparin was found to enhance both IL-11-induced STAT3-DNA complex formation and transactivation without altering either STAT3 (signal transducer and activator of transcription-3) tyrosine or serine phosphorylation. Heparin was also found to enhance IL-11's ability to induce the expression of both receptor activator of nuclear factor-B ligand (RANKL) and glycoprotein (gp) 130. When taken together, these findings suggest a plausible mechanism by which heparin may cause increased osteoclastogenesis and therefore bone loss when administered longterm. (Blood. 2002;100:2530-2536)

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Heparin-Induced Osteopenia: An Appraisal

Cited by 125 publications

References 38 publications

Aspects of anticoagulation in children

Aspects of anticoagulation in children

Osteoblastic heparan sulfate regulates osteoprotegerin function and bone mass

Heparin acts synergistically with interleukin-11 to induce STAT3 activation and in vitro osteoclast formation

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