Heparin Osteoporosis

Griffith, George C.; Nichols, George; Asher, Joe; Flanagan, Brian P.

doi:10.1378/chest.56.3.222

Cited by 41 publications

(50 citation statements)

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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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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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“…It may be thlat the mast cells are elaborating a local factor such as heparin or prostaglandin D2, that causes or promotes the osteolysis and decreases the boneforming ability (6,(12)(13)(14)(15). There is an increased incidence of osteopenia after treatment with large doses of heparin, and in systemic mast cell disease (12)(13)(14).…”

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confidence: 99%

Idiopathic familial acroosteolysis: Histomorphometric study of bone and literature review of the Hajdu‐Cheney syndrome

Udell

Schumacher

Kaplan

et al. 1986

Arthritis & Rheumatism

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We describe a 27-year-old man with familial acroosteolysis involving 9 fingers. Bone biopsy of an affected digit showed osteolysis with no tetracycline deposition, rare osteoclasts, increased vascularity, and numerous mast cells. In contrast, the iliac crest bone showed active ,bone remodeling and normal doubletetracycline labeling. We believe mast cells deserve further study as possible factors in this form of localized osteolysis.Idiopathic acroosteolysis is an uncommon disorder which involves painful osteolysis of the distal phalanges. When it occurs in a familial form, with a characteristic facies, generalized osteoporosis, and early loss of teeth (l), the condition is termed HajduChencey syndrome. We describe a patient and his mother: the fifth family reported to have this disorder. for the first time in this syndrome. The non-decalcified iliac crest bone biopsy specimen showed active bone remodeling features.Case report. The patient was a 27-year-old white man with a 7-year history of gradually progressive deformity in 9 fingers and loss of distal phalangeal mass. He had continuous pain in the tips of all involved fingers. He denied having Raynaud's phenomenon, frostbite, or burns, or having been exposed to ergot, vinyl chloride, or trauma. He had no history of acute or chronic arthritis, myalgias, skin rash, tight skin, or symptoms in his feet. Graves' disease had been diagnosed 2 years after the onset of his hand symptoms. This had been treated successfully with 1311, 2 years previously; however hypothyroidism had evolved and was being controlled with levothyroxine sodium, 0.1 mg daily. In addition, he was taking diazepam, 5 mg 3 times daily. He also had impotence, noted approximately since the diagnosis of thyroid disease.The patient's mother had similar "shrinking fingers," which first appeared approximately at age 50, progressed for 2 years, then became asymptomatic and have remained stable for the past 15 years. His father had normal hands, and had died at age 64 of lung cancer. The patient has 2 sisters, ages 37 and 38, who are in good health without musculoskeletal problems.The patient was short, with a broad face and prominent eyebrows (Figure 1). His temperature was 98"F, pulse rate 68/minute, blood pressure 110/70, respirations 16/minute, weight 162 lbs, and height 66 inches. He had slight proptosis, but extraocular muscle and funduscopic examination results were normal. He had numerous caries, but all his teeth were

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“…[8][9][10][11] LMWHs are routinely used in HD in European clinical settings. 23 Bernieh et al 24 reported that enoxaparin had been routinely used for 7 years.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6][7] Other advantages include low incidence rates of heparin-induced bleeding, 8 osteoporosis, 9 thrombocytopenia, 10 and lipid abnormalities. 11 degree of anticoagulation of LMWHs.…”

Section: Introductionmentioning

confidence: 99%

Clinical Safety and Anticoagulation Efficacy of Low-Molecular-Weight Heparins in Chronic Hemodialysis Patients: A Single Medical Center Experience

et al. 2011

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Background: In many countries low-molecular-weight heparins (LMWHs) are increasingly used for hemodialysis (HD). Low-range activated clotting time (ACT-LR) values and anti-Xa activity had been used to monitor the degree of anticoagulation caused by LMWH. However, the facilities are not easily available at most hospitals. Such data are limited in Taiwan. Methods: A total of 76 patients receiving maintenance HD were prospectively enrolled. The HD patients were randomized to receive either nadroparin or enoxaparin and checked the ACT-LR values and anti-Xa activity. We aimed to analyze ACT-LR values and anti-Xa activity along with the clotting of the dialyzer or bleeding events associated with two LMWHs after they were administered. We also aimed to determine the dose necessary to reach maximum safety and efficacy. Results: We found no significant differences in LMWH dosage, ACT-LR values, and anti-Xa activity between the two groups. There were no significant differences in bleeding/adverse events and extracorporeal circuit thrombosis between the two groups. Most of the bleeding and adverse events were subcutaneous minor bleeding. No major bleeding or mortality was found. We found significant differences in mean dosage, cost, bleeding/adverse effect, and extracorporeal circuit thrombosis between excessive and reduced nadroparin dosage groups. Conclusion: LMWH is not still routinely used due to its high cost in Taiwan. In our clinical experience, nadroparin and enoxaparin exhibited high levels of safety and efficacy in chronic HD patients. Reduced LMWHs dosage could promote patient's safety and decreased HD cost in HD patients with excessive dosage of LMWHs.

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Heparin Osteoporosis

Cited by 41 publications

References 0 publications

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

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

Idiopathic familial acroosteolysis: Histomorphometric study of bone and literature review of the Hajdu‐Cheney syndrome

Clinical Safety and Anticoagulation Efficacy of Low-Molecular-Weight Heparins in Chronic Hemodialysis Patients: A Single Medical Center Experience

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