SECONDHAND SMOKE, HYPOFIBRINOLYSIS, AND LEGG-PERTHES-DISEASE

In 39 children with Legg-Perthes disease who were nonsmokers, the spec ific aim was to assess relationships among parental cigarette smoking during pregnancy, household smoking before diagnosis of Legg-Perthes d isease, hypofibrinolysis, and thrombophilia, Fifteen (38%) children ha d no secondhand smoke exposure; 24 (62%) had secondhand smoke exposure before their diagnosis. Seventeen (71%) of these 24 children were exp osed while in utero to smoking by a parent or live in relative and als o had exposure to household smoke during childhood; seven (29%) had on ly household smoke exposure in childhood. In the full cohort of 39 chi ldren, secondhand smoke exposure correlated inversely with the major s timulator of fibrinolysis, stimulated tissue plasminogen activator act ivity. Of the children exposed to smoking, 48% had low stimulated tiss ue plasminogen activator activity (<2.9 IU/ml) compared with 7% of the children without secondhand smoke exposure and 14% of 22 healthy cont rol children. Secondhand smoke exposure had no significant effects on other measures of coagulation. Secondhand smoke exposure while in uter o and during childhood appears to lower stimulated tissue plasminogen activator activity and additionally may depress heritable low stimulat ed tissue plasminogen activator activity, leading to hypofibrinolysis, Hypofibrinolysis may facilitate thrombotic venous occlusion in the he ad of the femur, leading to venous hypertension and hypoxic bone death , Legg-Perthes disease.