A prospective study of heparin-induced osteoporosis in pregnancy using bone densitometry

Barbour, Linda A.; Kick, Steven D.; Steiner, John F.; LoVerde, Mary E.; Heddleston, Les N.; Lear, James L.; Barón, Anna E.; Barton, Phoebe Lindsey

doi:10.1016/s0002-9378(94)70299-3

Cited by 260 publications

(115 citation statements)

References 25 publications

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“…Longer-term use of highdose heparin was avoided because of anxiety about the increased risk for osteoporosis, although the association between duration or dose of heparin and risk for osteoporosis is unclear. 9,10 The injections were well tolerated and no dif®culties were reported with selfadministration and no patients developed thrombocytopaenia. Prednisolone therapy in patients who did not require surgery was reduced from 40 mg/day after the second week.…”

Section: Resultsmentioning

confidence: 97%

Treatment of corticosteroid‐resistant ulcerative colitis with heparin —a report of 16 cases

Evans

Wong

Morris

et al. 1997

Aliment Pharmacol Ther

135

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Background:Heparin, a group of sulphated glycosaminoglycans, in addition to its anticoagulant activity, has a wide range of potentially anti‐inflammatory effects. These include inhibition of neutrophil elastase and inactivation of chemokines. Previous reports of fortuitous improvement in ulcerative colitis patients treated with heparin for prophylaxis of venous thrombosis, prompted us to perform a pilot study in patients with corticosteroid‐resistant ulcerative colitis.Methods:Sixteen hospitalized patients in relapse from ulcerative colitis and unresponsive to high‐dose corticosteroid therapy were treated with intravenous standard heparin (subcutaneous in two patients), the dose was adjusted to provide standard anticoagulant activity. Five patients continued with subcutaneous injections on discharge, with a gradual reduction in the frequency of doses.Results:Within 1 week of starting heparin, 12/16 patients had shown a considerable reduction in stool frequency. After 2 weeks of heparin therapy median stool frequency had improved from 8.0/day (range 6.3–10.0) pre‐treatment to 3.5/day (2.5–5.25) (P=0.008), and by 4 weeks 12/16 achieved clinical remission. Four patients required elective colectomy. Three patients were treated with heparin on a second occasion during a relapse, two failed to respond and required subsequent colectomy. Nine remain well. No serious complications were seen due to the anticoagulant activity, apart from bruising at subcutaneous injection sites.Conclusion:The response to heparin in patients with ulcerative colitis resistant to standard therapy is encouraging and supports the previous uncontrolled evidence for a therapeutic effect. A controlled trial of heparin in ulcerative colitis is clearly indicated.

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Section: Resultsmentioning

confidence: 97%

Treatment of corticosteroid‐resistant ulcerative colitis with heparin —a report of 16 cases

Evans

Wong

Morris

et al. 1997

Aliment Pharmacol Ther

135

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“…Rats treated once daily by subcutaneous injections of heparin exhibited decreased trabecular bone volume both by decreasing the rate of bone formation and increasing the rate of bone resorption (Muir et al, 1996). Similarly, Barbour et al (1994) showed that 36% of pregnant women undergoing long-term treatment with heparin had a 10% reduction in femoral bone mineral density. However, the mechanism sustaining this osteoporosis was unclear and it was difficult to determine if these effects on bone resorption were due to the direct effect of heparin on osteoclasts or indirectly via its osteoblast activity.…”

Section: Discussionmentioning

confidence: 96%

Glycosaminoglycans inhibit the adherence and the spreading of osteoclasts and their precursors: Role in osteoclastogenesis and bone resorption

Baud’huin

Ruiz-Velasco

Jégo

et al. 2011

European Journal of Cell Biology

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The bone microenvironment (e.g. glycosaminoglycans (GAGs), growth factors) plays a major role in bone resoption, especially in the formation of osteoclast which differentiate from the hematopoietic lineage in the presence of RANKL. Previous studies revealed that GAGs may influence osteoclastogenesis, but data are very controversial, some studies showing an inhibitory effect of GAGs on osteoclastic differentiation whereas others demonstrated a stimulatory effect. To clarify their activities, we investigated the effect of 5 families of GAGs in three different models of human/mouse osteoclastogenesis. The present data revealed that heparin inhibited osteoclastogenesis in these 3 models, which was confirmed by a decrease in mRNA expression of osteoclastic markers and by an inhibition of the bone resorption capacity. We also demonstrated in RAW 264.7 cells that other families of GAGs different from heparin inhibited RANKL-induced osteoclastogenesis, and that this inhibition was dependent on the length and the level of sulfation of GAGs. In the present work, heparin did not bind to RANKL and did not modulate RANKL signaling. Heparin acted at 2 distinct steps of osteoclastogenesis from human CD14 + cells: first, heparin strongly decreased the adherence of osteoclast precursors, and secondly inhibited osteoclasts to spread and to be active. Furthermore, the second action of heparin was reversible as the removal of heparin at the end of the culture time allowed the condensed cells to spread out and showed the formation of morphological active osteoclasts. The present work clearly evidences that GAGs inhibit osteoclastogenesis in vitro and strengthens the therapeutic interest of defined GAGs in osteolytic diseases.

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“…Ten women were recruited for study via a recurrent miscarriage clinic (mean age, 30 years; range [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40]; all had at least two previous miscarriages. Investigations into the possible maternal cause of the miscarriages revealed normal results including estrogen levels, thyroid function tests, follicle-stimulating hormone, and luteinizing hormone.…”

Section: Patientsmentioning

confidence: 99%

A Detailed Assessment of Alterations in Bone Turnover, Calcium Homeostasis, and Bone Density in Normal Pregnancy

Black

Topping

Durham

et al. 2000

Journal of Bone and Mineral Research

268

118

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The effects of pregnancy on bone turnover and the potential risk of developing an osteoporotic fracture in pregnancy are controversial. Utilizing biochemical markers of bone formation and resorption and dual-energy X-ray absorptiometry (DEXA), bone turnover before, during, and after pregnancy was studied in detail. Ten women (mean age 30 years; range 23-40) were recruited. Prepregnancy data were obtained and then a review was performed at 2-week intervals , once pregnancy was confirmed, until 14 weeks of gestation and thereafter monthly until term. Bone mineral density (BMD) was estimated by DEXA scanning of hip, spine, and forearm preconception and postpartum. In addition, BMD of the forearm at 14 weeks and 28 weeks gestation was obtained. All pregnancies had a successful outcome. Urinary free pyridinium cross-links, free pyridinoline (fPyr) and free deoxypyridinoline (

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A prospective study of heparin-induced osteoporosis in pregnancy using bone densitometry

Cited by 260 publications

References 25 publications

Treatment of corticosteroid‐resistant ulcerative colitis with heparin —a report of 16 cases

Treatment of corticosteroid‐resistant ulcerative colitis with heparin —a report of 16 cases

Glycosaminoglycans inhibit the adherence and the spreading of osteoclasts and their precursors: Role in osteoclastogenesis and bone resorption

A Detailed Assessment of Alterations in Bone Turnover, Calcium Homeostasis, and Bone Density in Normal Pregnancy

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