Abstract 1628


Evidence suggests a disparity in the incidence of venous thromboembolic events (VTE) amongst racial groups, with blacks purported to have a higher occurrence of VTE than whites. In contrast, Hispanics and Asians have been observed to have a lower occurrence of VTE. Sickle cell anemia is a known prothrombotic state and recent studies contend that sickle cell trait (SCT) may also predispose to VTE. We hypothesized that SCT might play a role in the increased VTE risk for blacks. To this end, we conducted a study to investigate whether pregnant/postpartum women with SCT have a higher VTE incidence than controls without SCT.


Patient information was obtained using our hospital database spanning the eleven years 1998–2008. All pregnant women seen in our large urban medical center had hemoglobin (Hb) electrophoresis screening on their first clinic visit; demographic data was obtained from the patient at registration. Using prospectively-collected data, three patient cohorts were identified. Group A included women with SCT as identified by %HbS of 30–45% on Hb electrophoresis. To ensure exclusion of patients with sickle cell disease who were post-transfusion, subjects who at any time in their medical record had %HbS >45% were excluded from analysis. HbAA black (Group B) and white (Group C) cohorts were included if %HbA was ≥95.5%. Women who self-identified themselves as Hispanic, multiracial, “declined”, “not available” or “not applicable” were also excluded. VTE cases were identified using ICD-9 codes from hospital, ER or outpatient visit discharges during the pregnancy or postpartum period (294 days before delivery or 56 days after delivery). All charts of VTE indexed cases were reviewed (by SP) to ensure accuracy of reporting.


The prevalence of SCT was found to be high (11.1%) in our Group A population as compared to 8.3% in the general pregnant/postpartum non-white population that included Hispanics, multiracial and unavailable individuals. We identified 679 black subjects with SCT, 5465 black subjects with HbAA and 1162 white subjects with HbAA. VTE incidence was 0.44% in Group A (SCT), in 0.49% in Group B (Black AA) and in 0.26% in Group C (White AA). The rate of VTE did not significantly differ between these groups. When patients were included who had been thromboprophylaxed secondary to previous VTEs, the incidence of VTE in Black AA was 0.6%, still not significantly different from the white AA group (p=0.13). Age was a more important factor: patients with VTE were significantly older than non-VTE pregnant patients (mean 32.2 vs. 27.6 years, p=0.0002). As expected, the majority of VTE occurred in the postpartum period (61%).


Our results suggest that there is a nonsignificant trend toward a higher incidence of VTE in black HbAA (Group B) as compared to white women with HbAA (Group C) in the pregnant/postpartum period. We could not detect a difference in VTE incidence between black SCT (Group A) and black HbAA (Group B). The role of sickle cell trait as an inherited prothrombotic mutation remains unclear. Even a mild increase in age appears to constitute a prothrombotic risk. However, as VTE remains one of the major causes of maternal mortality, further studies will be needed to better identify risk factors of VTE in pregnancy. Prospective studies identifying such patients may help characterize the true impact of sickle cell trait on venous thromboembolism in pregnancy and postpartum.


No relevant conflicts of interest to declare.

Author notes


Asterisk with author names denotes non-ASH members.