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Potential aetiological factors concerning the development of osteonecrosis of the femoral head
C Zalavras1, Z Dailiana, M Elisaf
1University of Ioannina, Ioannina; University of Athens, Athens; University Hospital of Ioannina, Ioannina; University of Thessalia, Larissa, Greece.
Background:
The aetiology and pathogenesis of non-traumatic osteonecrosis (ON) of the femoral head have not been fully elucidated. The present study was conducted to evaluate the possible correlation of relevant haematological and biochemical factors with the development of ON.
Patients And Methods:
Our investigation consisted of measurement of haematological indices and assessment of the biochemical and lipid profile of a study population of 68 patients with non-traumatic ON of the femoral head and 36 healthy controls. The disease was considered idiopathic in 17 and secondary in 51 patients.
Results:
There were no statistically significant differences in the parameters measured among the idiopathic ON, secondary ON and control groups, except for globulins alpha1, alpha2 and beta, which were significantly increased in both patient groups, and apolipoprotein B (Apo B), which was increased in patients with idiopathic disease compared with the control group. Both patient groups presented increased von Willebrand factor (VWF) and lipoprotein (a) [Lp(a)] levels and decreased protein C and S concentrations, but without statistical significance. However, both patient groups exhibited a greater proportion of abnormal values of any of these parameters, in 58.9% of the idiopathic and in 62.7% of the secondary ON patients, compared with 8.3% of the controls.
Conclusion:
Our study underlines the potential association of abnormal values of protein C, protein S, VWF and Lp(a) with ON. To our knowledge this is the first reported association of VWF with the disease. The majority of both idiopathic and secondary ON patients in our series exhibits a thrombotic potential that adds further support to the postulation that intravascular coagulation is a major pathogenetic mechanism leading to the disease.
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