Evaluation of inherited and acquired platelet function disorders in iron deficient women with menorrhagia by whole blood lumi-aggregometer.

The commonest cause of iron deficiency anemia (IDA) in premenopausal women is often menstrual blood loss. However, no organic pathology is identified in more than 50% of menorrhagic women. We therefore investigated inherited and acquired bleeding disorders among women with unexplained menorrhagia who developed IDA. In vitro whole blood platelet aggregation (PA) with ADP, arachidonic acid (AA), ristocetin and collagen was studied in addition to full blood count, serum iron levels, serum iron binding capacity, transferrin saturation, ferritin, prothrombin and activated partial thromboplastin time, fibrinogen, D-Dimer, Factor VIII, Factor IX, Factor XI, ristocetin cofactor activity, blood type and bleeding time in 67 women before and after therapy. Before therapy; decreased agonist induced PA was observed in 20% of women by ADP, in 12% by AA, in 2% by ristocetin and in 6% by collagen. After oral iron therapy, decreased platelet aggregation was shown in 8% of women with ADP and 2% of women with AA while initial abnormal ristocetin and collagen induced platelet aggregation responses became normal. Also there was a statistically significant increase of ristocetin cofactor activities and FXI levels after iron repletion. We conclude that; rather than von Willebrand disease, platelet function abnormalities and FXI deficiency are the most common hemostatic disorders in women with unexplained menorrhagia and significant portion of these disorders can be reversed by iron therapy.