Prevention of steroid-induced osteonecrosis of femoral head in systemic lupus                 erythematosus by anti-coagulant

Nagasawa, Kohei; Tada, Yutaka; Koarada, Syuichi; Tsukamoto, Hiroshi; Horiuchi, Takahiko; Yoshizawa, S.; Murai, Koichi; Ueda, Akira; Haruta, Yoshio; Ohta, Akio

doi:10.1191/0961203306lu2311oa

Cited by 56 publications

(44 citation statements)

References 14 publications

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“…Several researchers have shown steroid-induced ON can be prevented by medications [6,17,18], and a study that used the same rabbit model as ours reported a reduction in ON frequency to 30% to 40% [16]. Our study showed similar suppressive effects, and no rabbits developed tissue damage due to electromagnetism.…”

Section: Groupsupporting

confidence: 69%

Electromagnetic Fields

Ishida

Fujioka

Takahashi

et al. 2008

Clinical Orthopaedics &Amp; Related Research

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Establishing a means to prevent osteonecrosis after corticosteroid administration is an important theme. We asked whether pulsed electromagnetic field stimulation, a noninvasive treatment, could prevent osteonecrosis. Ninety rabbits were divided into four treatment groups: (1) exposure of 10 hours per day to electromagnetic stimulation for 1 week, followed by injection of methylprednisolone (20 mg/kg), and exposure of 10 hours per day to electromagnetism for a further 4 weeks (n = 40); (2) methylprednisolone injection only (n = 40); (3) no treatment (n = 5); and (4) exposure of 10 hours per day to electromagnetism for 5 weeks (n = 5). After 5 weeks, we harvested and histologically examined femurs bilaterally. The frequency of osteonecrosis was lower in the steroidelectromagnetism group (15/40) than in the steroid-only group (26/40). No necrotic lesions were found in the two control groups. We observed no clear effects of electromagnetism on the number, location, extent, and repair of necrotic lesions and intramedullary fat cell size in affected rabbits. Pulsed electromagnetic field stimulation reportedly augments angiogenesis factors and dilates blood vessels; these effects may lower the frequency of osteonecrosis. Exposure to pulsed electromagnetic field stimulation before corticosteroid administration could be an effective means to reduce the risk of osteonecrosis.

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Section: Groupsupporting

confidence: 69%

Electromagnetic Fields

Ishida

Fujioka

Takahashi

et al. 2008

Clinical Orthopaedics &Amp; Related Research

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“…These reactions might be important factor in onset of osteonecrosis of femoral head. Several studies reported that a combination of anticoagulant and lipid-lowering agent showed a significant decrease in the onset of osteonecrosis compared with an anticoagulant or a lipidlowing agent alone in human and animal models (14,15,20). Another report suggested that a high serum PAI-1 level may be a risk factor for the development of osteonecrosis of the femoral head by studying thrombophilis and hypofibrolysis patients (4, 6).…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone-induced plasminogen activator inhibitor-1 expression in human primary bone marrow adipocytes

et al. 2010

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Several studies have demonstrated the association of plasminogen activator inhibitor-1 (PAI-1) with osteonecrosis, but the underlying mechanism of osteonecrosis and its relationship with local PAI-1 is not clear. The objective of this study was to evaluate PAI-1 production by primary human bone marrow adipocytes and the effects of glucocorticoid administration. Bone marrow was obtained from 25 individuals during prosthetic insertion. Mature adipocytes were cultured for 24 h with or without dexamethasone. PAI-1, adiponectin, tumor necrosing factor-α (TNFα) expression were measured by latex photometric immunoassay or RT-PCR. Adiponectin, TNFα and PAI-1 were detected in all culture media. PAI-1 expression was significantly increased by treatment with 10 −6 mol/L dexamethasone up to 24 h in protein and mRNA levels, while the levels of other adipokines did not change by dexamethasone. These results suggest that bone marrow adipocytes may play important roles for the development of glucocorticoid-induced osteonecrotic diseases by enhancing PAI-1 expression.

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“…Accordingly, anticoagulation therapy has been tried for prevention of ION in SLE patients, and warfarin has been modestly beneicial in this respect. One study of 60 SLE patients receiving prednisolone at more than 40 mg/day found that treatment with warfarin signiicantly reduced the onset of ION [31]. Among various physical modalities, extracorporeal shockwave therapy, hyperbaric oxygen, and pulsed electromagnetic therapy have yielded encouraging results, but further large prospective studies will be necessary to conirm these efects.…”

Section: Treatment Of Ionmentioning

confidence: 99%

“…The widespread use of MRI now makes it possible to detect osteonecrotic change in SLE patients soon after administration of glucocorticoid, thus facilitating early diagnosis. Nagasawa et al reported that 33% of patients developed ION within 3 months after the start of glucocorticoid treatment and that symptomatic ION became apparent at 2 years and beyond [31]. Radiographically, a subchondral radiolucency known as the crescent sign appeared at a late stage in ION, indicating subchondral fracture.…”

Section: Timing Of Osteonecrosis-related Ischemia In Patients With Slementioning

confidence: 99%

“…Nagasawa et al [31] investigated the rate of increase in serum total cholesterol (TC) levels 1 month after glucocorticoid administration in patients with new-onset SLE, and found that they were signiicantly high in the ION group. It was also found that lipid levels, and the rates of increase in almost all the TC and triglyceride (TG) parameters, were higher in the group that developed ION.…”

Section: Lipid Levels Statins and Ionmentioning

confidence: 99%

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Idiopathic Osteonecrosis and Atypical Femoral Fracture in Systemic Lupus Erythematosus

Kuroda¹,

Sato²

2017

Lupus

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Osteonecrosis and osteoporosis are frequent adverse efects of glucocorticoid therapy of systemic lupus erythematosus (SLE). Idiopathic osteonecrosis (ION) of the femoral head occurs in 3-40% of patients receiving glucocorticoid, and can also develop in other bones. Higher doses of glucocorticoid and steroid pulse therapy are considered to be risk factors for ION of the femoral head. To analyze these risk factors, it seems important to detect early changes in the femoral head by magnetic resonance imaging and to monitor early clinical events atributable to steroid therapy. Prophylaxis with statins and warfarin remains debatable. The use of glucocorticoid is increase the risk of bone fractures. Bisphosphonate (BP) is used for its prevention and treatment of osteoporosis. Atypical femoral fracture (AFF) has been recently recognized as a complication associated with BP use. AFF is considered to be a form of stress fracture; localized periosteal thickening of the lateral cortex is often present at the fracture site. The thickening has been recently recognized as a complication associated with the use of antiresorptive agents such as BP and denosumab. As long-term BP/glucocorticoid use is a risk factor for beaking in patients with SLE , temporary withdrawal of BP administration should be considered.

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Prevention of steroid-induced osteonecrosis of femoral head in systemic lupus erythematosus by anti-coagulant

Cited by 56 publications

References 14 publications

Electromagnetic Fields

Electromagnetic Fields

Dexamethasone-induced plasminogen activator inhibitor-1 expression in human primary bone marrow adipocytes

Idiopathic Osteonecrosis and Atypical Femoral Fracture in Systemic Lupus Erythematosus

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