A STUDY OF URINARY PROSTACYCLIN LEVELS IN PREGNANT HAEMOGLOBIN SS AND AA WOMEN IN LAGOS, NIGERIA

Abstract

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
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(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.
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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.