It has been documented that pregnancy is associated with an increase in plasma volume in healthy pregnancy and to a less extent in pregnant sickle cell subjects. This Plasma volume expansion is due to vasodilatation among other mechanisms. Many factors are responsible for the vasodilatation among which is Prostacyclin believed to be secreted in larger amounts in pregnant subjects. In this study urinary prostacyclin (UP) levels, were determined in Pregnant Hb AA and Hb SS subjects, using non-pregnant Hb AA and non-pregnant Hb SS as controls. The urinary Prostacyclin was determined using competitive immunoassay, ELISA Urinary Prostacyclin kit. (Assay Deigns, Inc, 800 Technology drive Ann Arbor, MI 48108 USA). Prostacyclin has a half-life of 60 mins in plasma, and it is typically monitored by the measurement of 6-keto prostaglandin F2, which is produced by non enzymatic hydration of PGI2. All subjects were bled into EDTA specimen bottles, for full blood count determination including red cell indices using Sysmex 21N auto analyzer. A total of 63 subjects consisting of 34 HB AA subjects ( of which 15 were pregnant) and 29 HB SS subjects of which 10 were pregnant. The age range of all the subjects was 19-38, the median for AA and Subjects were 26 and 27years respectively. The mean UP of non-pregnant AA subjects (427.73 ± 425pg/ml) was significantly lower than the mean UP of pregnant AA subjects (1759 ±1023pg/ml) P = 0.0000436). In AA patients, pregnancy induces higher urinary prostacyclin levels. Likewise the mean UP for non pregnant HB SS subjects (518±708 pg/ml) was lower than that for pregnant HB SS subjects (682±876 pg/ml) but this is far from reaching a significant level. P = 0.613. In SS subjects pregnancy did not induce higher UP levels. The UP of non-pregnant HB SS subjects is higher than that of non-pregnant HB AA subjects but the difference is not statistically significant. P = 0.636. In non-pregnant situation SS did not induce higher UP. As expected the mean PCV (32. 94±3.46) and HB (10.6±0.96g/dl) concentration in pregnant AA subjects is significantly lower than that of non-pregnant AA subjects, PCV(36.03% ± 3.29 )Hb (11.63 ± 1.05g/dl) ,p = 0.0121 and 0.0.000613 respectively. Pregnancy reduces PCV and Hb in AA subjects. As expected too, the PCV (21.7% ±2.49) and HB (7.1g/dl±0.6) of pregnant SS subjects was significantly lower than that of non pregnant SS subjects. (25.16% ±1.58 and 8.44g/dl ± 0.5 for PCV and HB respectively) p = 0.000452 and 1.88 X 10-7 respectively. Pregnancy reduces PCV and Hb in SS subjects. A significant difference was also noted in the total White blood Cell Count (WBC) of pregnant (6.93±2.49 x 109/L) and non-pregnant (4.10±1.26 X 109/L) AA subjects. P = 0.000336. However total WBC of pregnant SS subjects (7.76±0.47 x 109/L) is significantly lower than that of non-pregnant (10.5 ± 2.7 x 109/L) SS subjects. P = 0.0002. Pregnancy induces higher WBC in AA but lower in SS subjects. Whereas there are no significant changes in platelet count of pregnant (197.07±74.27 x109/L) and non-pregnant (188.62±48.8 x109/L) AA subjects (P =.70), the platelet count was found to be significantly lower in the pregnant SS subjects (217±96.3 x109/L) compared with non-pregnant SS subjects (364±167 x 109/L). P = 0.0058. Pregnancy may reduce platelet count in SS subjects. Correlation statistics showed significant relationships between UP (in non-pregnant HB AA subjects) and WBC and platelet count. r = 0.6 (p=0.001) and –0.49 (p=0.014) respectively. In pregnant AA subjects, UP positively correlated with HB, PCV and WBC. r = 0.535, 0.508 and 0.58: p = 0.032, 0.04 and 0.018 respectively. In non pregnant SS subjects, positive significant correlation existed between UP and HB and PCV. R= 0.535, 0.508 p =0.032 and 0.04 respectively. There as a near perfect negative relationship between UP and HB and PCV in Pregnant HB SS subjects r =-0.90, -0.84: p ==0.00026 and 0.0019 respectively. This study has demonstrated that the expected rise in plasma prostacyclin levels (measured as urinary product of PGI2) during pregnancy as observed in HB AA study arm does not occur in pregnant SS subjects. This finding may partly explain the previous reports in literature that there is impairment of plasma volume expansion in pregnant SS subjects since one of the major effects PGI2 is generalized vasodilatations resulting in vascular volume expansion.