title: Idiopathic osteonecrosis, hypofibrinolysis, high plasminogen activator inhibitor, high lipoprotein(a), and therapy with Stanozolol.
abstract: In five patients with idiopathic osteonecrosis (ON) of the hip, four having hypofibrinolysis mediated by high plasminogen activator inhibitor (PAI-Fx), and one with high Lp(a), our specific aim was to determine whether therapy (Rx) with the anabolic-androgenic steroid, Stanozolol (6 mg/day), would normalize PAI-Fx and Lp(a) and thus potentially ameliorate ON. Prior to Rx, none of the four patients with high PAI-Fx could normally elevate tissue plasminogen activator (tPA-Fx) after 10 min venous occlusion at 100 mm Hg. After 12-18 weeks on Rx, PAI-Fx and stimulated tPA-Fx normalized in all four patients. Prior to Rx, mean (SD) stimulated tPA-Fx was low, 0.4 +/- 0.3 IU/ml (lower limit of normal 2.28 IU/ml). On Rx, stimulated tPA-Fx normalized, rising to 2.83 +/- 1.9 IU/ml, P = .004. Prior to Rx, mean (SD) basal PAI-Fx was high, 99 +/- 68 (upper limit of normal 26.9 U/ml), and fell on Rx to 22.5 +/- 22, P = .004. In two of the five patients normalization of hypofibrinolysis or high Lp(a) was accompanied by major symptomatic improvement. Prior to Rx, and 2 years after onset of unilateral hip pain, one of the four patients with high PAI-Fx and low stimulated tPA-Fx could walk only one block painfully. After 8 weeks on Stanozolol Rx, and continuing through 54 weeks on Rx, he walked 2 miles per day without pain, despite radiographic progression of ON. In three of the four patients with high PAI and with osteonecrosis present 0.3, 2, and 6 years prior to Stanozolol Rx, there was no clinical improvement after 14-156 weeks of Rx despite normalization of stimulated tPA-Fx and PAI-Fx. The fifth patient, 1 month after onset of disabling hip pain, had normal PAI-Fx but high Lp(a) (27 mg/dl), and MRI evidence of bone marrow edema ("transient osteoporosis").(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Cholesterol Center Jewish Hospital, Cincinnati, OH 45229, USA.
authors.forename: C J
authors.initials: CJ
authors.lastname: Glueck
authors.forename: R
authors.initials: R
authors.lastname: Freiberg
authors.forename: H I
authors.initials: HI
authors.lastname: Glueck
authors.forename: T
authors.initials: T
authors.lastname: Tracy
authors.forename: D
authors.initials: D
authors.lastname: Stroop
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000328:Adult; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D005500:Follow-Up Studies; D006615:Hip / Q000473:pathology; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010020:Osteonecrosis / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D015849:Plasminogen Inactivators / Q000097:blood*; D013197:Stanozolol / Q000627:therapeutic use*
chemical_list: D017270:Lipoprotein(a); D015849:Plasminogen Inactivators; D013197:Stanozolol