ristocetin and Menorrhagia

Topics: Antibody Specificity; Blood Coagulation Tests; Blood Platelets; Capillary Fragility; Factor VIII; Female; Hemophilia A; Hemorrhage; Humans; Male; Menorrhagia; Plasma; Platelet Adhesiveness; Ristocetin; von Willebrand Diseases

This study was performed to evaluate the effect of iron therapy on platelet function among women with unexplained menorrhagia in order to better understand possible interactions between iron deficiency anemia and platelet behavior and menorrhagia. Platelet aggregation and adenosine triphosphate (ATP) release induced by 5.0 mM adenosine diphosphate (ADP), 0.5 mM arachidonic acid (AA), 1.0 mg/ml ristocetin and 2 microg/ml collagen were studied by whole-blood platelet lumi-aggregometer in 50 menorrhagic women before and after oral iron therapy and in 22 women of the control group. There was a significant increase in AA- induced platelet aggregation (p < 0.05) and a decrease in ristocetin-induced platelet aggregation (p < 0.01) after treatment. Pre- and posttreatment platelet aggregation responses to ADP and collagen were not significantly different (p > 0.05). Pre- and posttreatment platelet secretion responses to all agonists disclosed no significant difference (p > 0.05). There was no significant difference between the study group after treatment and the control group in respect to platelet aggregation and ATP secretion values induced by all agonists (p > 0.05). We conclude that iron deficiency anemia in women causes AA-induced platelet dysfunction, which may give rise to increased menstrual blood loss and can be reversed by iron repletion.

Topics: Adenosine Diphosphate; Adenosine Triphosphate; Anemia, Iron-Deficiency; Arachidonic Acid; Collagen; Female; Humans; Iron; Menorrhagia; Platelet Aggregation; Platelet Function Tests; Ristocetin

Menorrhagia is a common clinical problem and is unexplained in more than 50% of women. Although studies suggest that von Willebrand's Disease (VWD) is found in a substantial number of women with unexplained menorrhagia, the prevalence of platelet defects in women with menorrhagia is unknown. To determine the prevalence of platelet and other hemostatic defects, we evaluated women ages 17-55 diagnosed with unexplained menorrhagia. Seventy-four women (52 white, 16 black, six other) were studied. Bleeding time was prolonged in 23 women (31.5%). Maximal percent platelet aggregation was decreased with one or more agonists in 35 (47.3%) women. The most commonly found platelet function defects were reduced aggregation responses to ristocetin in 22 women and to epinephrine in 16 women. Sixteen of 22 women with reduced ristocetin aggregation had von Willebrand ristocetin cofactor (VWF:RCo) and von Willebrand factor antigen (VWF:Ag) > 60%. Platelet ATP release was decreased with one or more agonists in 43 (58.1%) women. Of the black women studied, 11/16 (69%) had abnormal platelet aggregation studies compared with 20/52 white women (39%) (P = 0.06). Black women with menorrhagia had a higher prevalence of decreased platelet aggregation in response to ristocetin and epinephrine than did white women (P = 0.0075, P = 0.02). Ten women (13.5%) had VWF:RCo and/or VWF:Ag < 60%. Using race and blood group specific ranges, 5 (6.8%) women had decreased VWF:RCo, VWF:Ag and/or collagen binding (VWF:CB). Mild factor XI deficiency was found in two women and one woman with mild factor V deficiency and one hemophilia A carrier were identified. We conclude that the prevalence of platelet function defects and other inherited bleeding disorders is substantial in a multiracial US population of women with unexplained menorrhagia.

Topics: Adolescent; Adult; Blood Coagulation Factors; Blood Coagulation Tests; Blood Platelet Disorders; Epinephrine; Female; Humans; Menorrhagia; Middle Aged; Platelet Aggregation; Platelet Function Tests; Prevalence; Racial Groups; Ristocetin; von Willebrand Diseases

Diagnosis of von Willebrand disease (vWD) is based on a panel of laboratory tests that measure the amount and function of von Willebrand factor (vWF). In population studies, vWF is higher in African Americans than Caucasians. Bleeding time, factor VIII activity (FVIII), vWF antigen (vWF:Ag), "vWF activity" ELISA (vWF:Act), ristocetin cofactor (vWF:RCof), and ristocetin-induced platelet aggregation (RIPA) were measured on 123 women with menorrhagia and 123 randomly selected control women; 70 cases and 76 controls were African American. Among controls, African Americans had significantly higher levels of vWF:Ag (mean 120 vs. 102 U/dl, P = 0.017). Among all subjects, African Americans had higher levels of vWF:Ag (mean 123 vs. 103, P = 0.001), vWF:Act (mean 101 vs. 89, P = 0.006), and FVIII (mean 118 vs. 104, P = 0.008). VWF:RCof did not differ between races (93 vs. 94 U/dl). RIPA was reduced in African Americans (P < 0.0001). In both races, women with type O blood differed significantly from those with other ABO types in vWF:Ag, vWF:Act, FVIII, and vWF:RCof. Based on criteria of two or more tests below race- and ABO-specific reference ranges, 6.5% of menorrhagia cases and 0.8% of controls were classified as having vWD, or its phenocopy. Among Caucasians, no controls and 7 cases (15.6%) were classified as affected, and in African Americans, 1 control (1.3%) and 1 case (1.4%) were so classified. Racial differences in vWF further complicate the issues surrounding diagnosis of vWD. The finding of increased vWF:Ag not accompanied by increased vWF:RCof has implications for understanding the structure-function relationships of vWF. Published 2001 Wiley-Liss, Inc.

Topics: ABO Blood-Group System; Black People; Case-Control Studies; Factor VIII; Female; Humans; Menorrhagia; Platelet Aggregation; Ristocetin; von Willebrand Diseases; von Willebrand Factor; White People