title: Very early development of steroid-associated osteonecrosis of femoral head in systemic lupus erythematosus: prospective study by MRI.
abstract: The objective of this study was to define prospectively the early development of corticosteroid-induced osteonecrosis of femoral head (ONF) in patients with systemic lupus erythematosus (SLE) and to identify the association of initial steroid treatment with the development of early (silent) ONE Forty-five patients who were newly diagnosed as having SLE and required 40 mg/day or more prednisolone were enrolled. To detect silent ONF, examinations using magnetic resonance imaging (MRI) were done three months after starting steroid therapy, followed by every year's MRI and plain radiography for over five years. Clinical and laboratory data were compared between silent ONF and non-ONF groups. Of 45 patients, 15 (33%) developed silent ONF and five (11%) symptomatic ONE It was of interest that MRI detected silent ONF very early (by three months) in 14 patients (93%). It should be noted that pulse therapy with 1000 mg/day methylprednisolone was found to be done very frequently (13 of 15, 87%) in the silent ONF group compared to non-ONF group (11 of 30, 37%) (P < 0.01) although other clinical features were not significantly different between both groups. High dose corticosteroids caused elevation of serum levels of total cholesterol, albumin, and leukocyte count in most of patients. The degree of elevation of those parameters at one or three months was more prominent in the silent ONF group. In particular, the change ratio of total cholesterol at one month was outstanding in the silent ONF group compared to non-ONF group (0.551 versus 0.374, P < 0.05). In conclusion, pathological ONF develops very early in one-third of SLE patients who received high dose corticosteroids and steroid pulse therapy could be a significant risk factor. An abrupt elevation of serum total cholesterol and/or sensitivity to steroids seem to be associated with the pathogenesis of ONF.
authors.affiliation: Department of Internal Medicine, Saga Medical School, Saga, Japan. nagasak@post.saga-med.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Nagasawa
authors.forename: Y
authors.initials: Y
authors.lastname: Tada
authors.forename: S
authors.initials: S
authors.lastname: Koarada
authors.forename: T
authors.initials: T
authors.lastname: Horiuchi
authors.forename: H
authors.initials: H
authors.lastname: Tsukamoto
authors.forename: K
authors.initials: K
authors.lastname: Murai
authors.forename: A
authors.initials: A
authors.lastname: Ueda
authors.forename: S
authors.initials: S
authors.lastname: Yoshizawa
authors.forename: A
authors.initials: A
authors.lastname: Ohta
mesh_terms: D000293:Adolescent; D000328:Adult; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D005260:Female; D005270:Femur Head / Q000473:pathology; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D007958:Leukocyte Count; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000188:drug therapy*; D008279:Magnetic Resonance Imaging; D008297:Male; D008775:Methylprednisolone / Q000008:administration & dosage / Q000009:adverse effects* / Q000627:therapeutic use; D008875:Middle Aged; D010020:Osteonecrosis / Q000139:chemically induced* / Q000175:diagnosis; D011239:Prednisolone / Q000009:adverse effects* / Q000627:therapeutic use; D011446:Prospective Studies; D020551:Pulse Therapy, Drug; D012709:Serum Albumin / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D012709:Serum Albumin; D002784:Cholesterol; D011239:Prednisolone; D008775:Methylprednisolone