Background Various conditions are considered as classical etiologies of nontraumatic avascular necrosis (AVN), such as endogenous or exogenous hypercorticism, alcoholism, barotraumatisms, systemic lupus, diabetes mellitus and hyperlipidemia. However, in many cases, none of these conditions are identified and AVN is considered to be idiopathic.
Objectives To seek thrombophilic disorders in a cohort of patients with AVN.
Methods All patients with AVN hospitalised in our departments during a couple of years were enrolled in this prospective study. Diagnosis of AVN was performed on X-rays and/or MRI when necessary and possible. Biological investigations included: glycemia, cortisolemia, ferritinemia, cholesterolemia, lipoproteinemia, haemoglobin electrophoresis, ANA, antiphospholipid antibodies, anti-B2GP1 antibodies, lupus anticoagulant, antiprothrombin antibodies, antithrombin, protein C, protein S, factor VIII, IX, XI, activated protein C resistance, prothrombin gene mutation, homocysteinemia and methionin load test.
Results 17 patients were enrolled, 9 men and 8 women, aged 34 to 76, with various stages of AVN (from stage 1 to 4). Antithrombin III deficiency was diagnosed in a woman. Resistance to activated protein C was found in another woman. Hyperhomocysteinemia was identified in 6 patients: two women (associated with antiphospholipid antibodies in one case), and 4 men. A lupus anticoagulant was found in one man and one woman. Two other patients were found to be homozygous to methyl-tetra-hydrofolate reductase (MTHFR) mutation, condition which leads to a susceptibility to hyperhomocysteinemia.
Conclusion 59% of our patients with AVN were found to have a thrombophilic disorder. We suggest that such a disorder may precipitate thrombosis when added to other risk factors. Among these thrombophilic disorders, hyperhomocysteinemia seemed to be the most frequent factor associated with AVN. If hyperhomocysteinemia is confirmed to be involved in AVN, these results should be of special interest in prevention of recurrences, as hyperhomocysteinemia can be corrected by folic acid, B6 and B12 supplementation.
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