Platelet Function Defects in Adolescents with Menorrhagia

Platelet function defects (PFDs) are reported to occur frequently in adult women with menorrhagia. There is limited information and lack of uniform testing for platelet dysfunction in the adolescent population, with the few available studies reporting varying incidence from 2 to 44%, depending on the testing methodology employed. We sought to look at our experience in detecting and managing platelet dysfunction in the adolescent menorrhagia population seen in the Texas Children's Hematology Center (TCHC) and Gynecology sub-specialty clinics at Texas Children's Hospital, Houston, Texas.

Adolescents with menorrhagia aged </= 18 years seen at the TCHC undergo a comprehensive bleeding disorders work-up by both hematology and gynecology providers. Menorrhagia was defined as menses lasting longer than 7 days, pictorial blood assessment chart score of > 100 points, using more than 8–10 pads and/or tampons per day, and/or passing clots greater than 1 inch in diameter. Whole blood platelet aggregometry with low/high dose ADP, arachidonic acid, collagen, ristocetin and thrombin agonists are performed as a second tier test in these patients after ruling out thrombocytopenia, coagulation factor deficiencies, and von Willebrand disease. We retrospectively reviewed the medical records of adolescents with menorrhagia seen at the TCHC between June 2009 and November 2010, as approved by the Institutional Review Board. Patient demographics, laboratory results including results of whole blood platelet aggregometry, platelet count, von Willebrand antigen and ristocetin cofactor activity levels were analyzed; menorrhagia therapy details, patient outcome, and follow-up information were obtained.

During the study period, 114 female patients with menorrhagia were evaluated for a bleeding disorder at the TCHC. The median age was 14 years with a range of 9–19 years. Of these, 68 patients (59%) had platelet aggregation studies performed. Patients were instructed to avoid non-steroidal anti-inflammatory medications for at least 1 week prior to testing. All patients tested had a platelet count of 150,000 or above. Twenty-eight percent (n=19) of the patients had decreased aggregation and/or secretion results for 1 or more agonist/s. Of these, 6 had defects in aggregation only, 6 had defects in secretion only and 7 had both aggregation and secretion defects. Eleven patients (16%) had 2 or more aggregation and/or secretion defects. Of these, 3 had decreased secretion only, 1 had decreased aggregation only, and 7 patients had combined aggregation and secretion defects.

Five of 19 patients with defects in the platelet aggregation studies also had von Willebrand ristocetin cofactor activity < 50%. Of these, 2 had abnormal platelet aggregation to ristocetin only, and 3 had decreased aggregation to ristocetin and ADP. Seventy-nine percent (n=15/19) of patients with platelet dysfunction were managed with hormonal therapy, 42% (n=8/19) received anti-fibrinolytic agents and 16% (n=3/19) received intra-nasal DDAVP for menorrhagia. Of these, 84% (n=16) had improved outcome, with a median follow-up of 15.6 months with a range of 1–66 months.

We conclude that platelet aggregation abnormalities are present in up to one-third of adolescents with menorrhagia. This percentage may be higher as only 59% of our patients were tested for PFDs. Prospective studies to evaluate for PFDs in adolescents with menorrhagia are needed to identify their true prevalence in this population, which will enable accurate diagnosis of PFDs and appropriate management of menorrhagia.

Dietrich:CSL Behring: Consultancy, Research Funding; Duramed: Consultancy, Research Funding. Shah:CSL Behring: Research Funding.