Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus

Zizic, Thomas M.; Marcoux, C.; Ds, Hungerford; Dansereau, Jerome; Stevens, Mary Betty

doi:10.1016/0002-9343(85)90057-9

Cited by 276 publications

(161 citation statements)

References 23 publications

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“…The results are in accordance with previous clinical observations that occurrence of the ONFH associates with maximal daily dose of corticosteroid rather than total dose over the course of treatment, 3,22 indicating exposure of bone to high level of corticosteroids might be a possible risk factor for developing ONFH. Therefore, ONFH, as well as steroid-induced osteonecrosis in other parts of the skeleton, might be caused by excessive or toxic effects of exogenous corticosteroid.…”

Section: Discussionsupporting

confidence: 92%

“…Most of the ONFH patients require surgical treatment such as core decompression, osteotomy or total hip arthroplasty depending on stages of the progression of destruction of the hip joints. Despite the widely spread use of corticosteroids for treating various diseases [2][3][4] and a known association between prevalence of ONFH and daily dose of corticosteroids, pathomechanism for the development of ONFH has not been identified.…”

Section: Introductionmentioning

confidence: 99%

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Increased hepatic cytochrome P4503A activity decreases the risk of developing steroid‐induced osteonecrosis in a rabbit model

Masada

Iwakiri

Oda

et al. 2007

Journal Orthopaedic Research

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Low hepatic cytochrome P4503A (CYP3A) activities might play an important role for inducing osteonecrosis of the femoral head (ONFH) by corticosteroids. However, the relationship between hepatic CYP3A activity and steroid-induced ONFH is unknown. We have examined the relationship between hepatic CYP3A activity and the inducibility of ONFH in a rabbit model. Sixty rabbits were divided into three groups. Hepatic CYP3A inducer (phenobarbital, group P; n ¼ 15), inhibitor (itraconazole, group I; n ¼ 15), or saline (group C, n ¼ 30) was administrated for 3 weeks before intramuscular methylprednisolone. In groups P and I, hepatic CYP3A levels were measured by midazolam clearance before treatment (baseline) and before methylprednisolone injection. All animals were sacrificed 3 weeks after methylprednisolone injection and both femurs were harvested and examined histologically for osteonecrosis. Midazolam clearance was significantly increased and decreased, compared with baseline in groups P and I respectively (p < 0.0005, p < 0.002). The incidence of osteonecrosis in group P (33%) was significantly lower than in group I (100%) and group C (83%; p < 0.001 for both). The percentage necrotic area to whole bone marrow area on cross sections in group P (8.2 AE 5.9%) was significantly lower than in group I (69.8 AE 20.8%) and group C (51.5 AE 30.7%; p < 0.005 for both). Hepatic CYP3A activity inversely correlated with the incidence of osteonecrosis and extent of the necrotic area caused by the same dose of corticosteroids, suggesting possible prevention of the steroid-induced osteonecrosis by reducing steroid dose in poor corticosteroid metabolizers. ß

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Increased hepatic cytochrome P4503A activity decreases the risk of developing steroid‐induced osteonecrosis in a rabbit model

Masada

Iwakiri

Oda

et al. 2007

Journal Orthopaedic Research

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“…Osteonecrosis of the hip occurs more frequently in patients who receive high-dose corticosteroid therapy for the treatment of diseases including systemic lupus erythematosus and inflammatory bowel disease, and also for immunosuppression after renal transplants (Spencer and Maisey 1985, Zizic et al 1985, Vakil and Sparberg 1989). When osteonecrosis involves a large volume of the femoral head, it collapses in many cases with a need for arthroplasty.…”

Section: Introductionmentioning

confidence: 99%

Vitamin E prevents steroid-induced osteonecrosis in rabbits

et al. 2010

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Background and purposePrevention of osteonecrosis after corticosteroid administration would be important. We examined the potential of vitamin E (α-tocopherol) to reduce the incidence of corticosteroid-induced osteonecrosis in an animal model.MethodsJapanese white rabbits were divided into 2 groups; the control group was fed a normal diet and the experimental group was fed α-tocopherol-supplemented diet in which α-tocopherol (600 mg/kg diet) was added to the normal diet. To induce osteonecrosis, high-dose methylprednisolone acetate (MPSL) (20 mg/kg body weight) was injected once into the right gluteus medius muscle of all rabbits. 4 weeks after the injection of MPSL, the presence or absence of osteonecrosis of bilateral femurs was examined histopathologically. The tocopherol/cholesterol ratios were calculated. The plasma levels of thiobarbituric acid-reactive substances (TBARS) were measured.ResultsAlpha-tocopherol-supplemented diet reduced the incidence of osteonecrosis, which developed in 14 of 20 rabbits in the control group and 5 of 21 rabbits in the experimental group (p = 0.004). The tocopherol/cholesterol ratio was higher in the experimental group than in the control group after the α-tocopherol administration. The plasma TBARS level was lower in the experimental group than in the control group at 4 weeks after the MPSL administration.InterpretationOur findings may offer a new approach for the prevention of corticosteroid-induced osteonecrosis.

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“…The occurrence of AVN after steroid use appears to be dose-related. But it appears in the majority of the studies that patients are at increased risk of AVN who receive > 20 mg/day of prednisone (which is equivalent of 80 mg of hydrocortisone) which is much higher than the dose of our patient [6]. However, another study done by Dimant et al [10] failed to find a correlation between peak dose, duration or cumulative dose of steroid and osteonecrosis.…”

Section: Discussionmentioning

confidence: 73%

“…Patients who are receiving prolonged high doses of glucocorticoids are at significant risk of developing AVN. However, this risk appeared to be low in patients receiving doses of prednisone less than 15 -20 mg/day [6]. The case we presented here is an example of such case who developed AVN while on very low dose of steroid and relatively shorter period of time.…”

Section: Introductionmentioning

confidence: 71%

Unilateral Femoral Head Osteonecrosis Caused by Low-Dose Oral Corticosteroid Used for Secondary Adrenal Insufficiency From Idiopathic Hypopituitarism

et al. 2017

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Osteonecrosis, commonly known as avascular necrosis (AVN) of bone, is one of the universally recognized side effects of high-dose steroid and commonly involves femur head leading to significant morbidity. But AVN of femur head due to low-dose oral corticosteroid and relatively shorter span of time is a rare occurrence. We report a case of a 41-year-old woman with hypopituitarism who developed right-sided AVN while on a little physiological replacement dose of oral hydrocortisone used only for 7 months for secondary adrenal insufficiency from idiopathic hypopituitarism. Patient was diagnosed with MRI at early stage and managed with lowest possible physiological preparation of hydrocortisone and alendronate and eventually prevented from hip collapse. There should be a high clinical index for patients with any dose of steroid to recognize early, and prevent fracture and ultimately replacement.

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Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus

Cited by 276 publications

References 23 publications

Increased hepatic cytochrome P4503A activity decreases the risk of developing steroid‐induced osteonecrosis in a rabbit model

Increased hepatic cytochrome P4503A activity decreases the risk of developing steroid‐induced osteonecrosis in a rabbit model

Vitamin E prevents steroid-induced osteonecrosis in rabbits

Unilateral Femoral Head Osteonecrosis Caused by Low-Dose Oral Corticosteroid Used for Secondary Adrenal Insufficiency From Idiopathic Hypopituitarism

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