title: Sustained hemostatic abnormality in patients with steroid-induced osteonecrosis in the early period after high-dose corticosteroid therapy.
abstract: To determine whether the development of steroid-induced osteonecrosis in collagen disease patients was related to hemostatic abnormality after corticosteroid administration, we examined levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha2-plasmin inhibitor complex (PIC) in 32 patients who were treated with high-dose corticosteroid. All were prospectively followed for osteonecrosis, with serial magnetic resonance imaging (MRI), for at least 12 months from the beginning of corticosteroid therapy. MRI was performed on bilateral hips and knees. Of the 32 patients, 17 (53.1%) had osteonecrosis in the hip or knee. Osteonecrosis was detected on MRI at an average 3.1 months after the start of high-dose corticosteroid therapy. PIC levels were significantly higher in the group of 17 patients with osteonecrosis (ON group) than in the group of 15 patients without osteonecrosis (non-ON group) (P < 0.0001). The difference in PIC levels was most prominent 20 days after the start of the high-dose corticosteroid therapy. Moreover, the number of osteonecrotic joints was significantly correlated with PIC levels (P < 0.0001). The sustained hemostatic abnormality after corticosteroid therapy in the ON group suggests that microvascular coagulation participates in the development of osteonecrosis.
authors.affiliation: Department of Orthopedic Surgery, Chiba University School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Oinuma
authors.forename: Y
authors.initials: Y
authors.lastname: Harada
authors.forename: Y
authors.initials: Y
authors.lastname: Nawata
authors.forename: K
authors.initials: K
authors.lastname: Takabayashi
authors.forename: I
authors.initials: I
authors.lastname: Abe
authors.forename: K
authors.initials: K
authors.lastname: Kamikawa
authors.forename: H
authors.initials: H
authors.lastname: Moriya
mesh_terms: D000293:Adolescent; D000305:Adrenal Cortex Hormones / Q000009:adverse effects* / Q000627:therapeutic use; D000328:Adult; D000368:Aged; D000818:Animals; D000933:Antifibrinolytic Agents / Q000378:metabolism; D000990:Antithrombin III / Q000378:metabolism; D001327:Autoimmune Diseases / Q000188:drug therapy*; D003095:Collagen Diseases / Q000188:drug therapy*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005271:Femur Head Necrosis / Q000097:blood / Q000139:chemically induced*; D005341:Fibrinolysin / Q000378:metabolism; D006487:Hemostasis / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000378:metabolism; D012016:Reference Values; D019851:Thrombophilia / Q000097:blood / Q000139:chemically induced*; D000979:alpha-2-Antiplasmin
chemical_list: D000305:Adrenal Cortex Hormones; D000933:Antifibrinolytic Agents; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin