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ORIGINAL ARTICLE |
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Year : 2019 | Volume
: 8
| Issue : 14 | Page : 68-74 |
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Relationship between ABO blood group phenotypes and hypertensive disorders of pregnancy: A hospital-based cross-sectional study in Kano, North-West Nigeria
Isyaku Gwarzo Mukhtar1, Aisha A Yakubu1, Bashir Wada Yakasai1, Salisu Ibrahim Ahmed1, Shamsuddeen Mansur2
1 Department of Human Physiology, Bayero University, Kano, Nigeria 2 Department of Anatomy, Bayero University, Kano, Nigeria
Date of Submission | 01-May-2019 |
Date of Acceptance | 01-Jul-2019 |
Date of Web Publication | 04-Oct-2019 |
Correspondence Address: Dr. Isyaku Gwarzo Mukhtar Department of Human Physiology, Bayero University, Kano Nigeria
Source of Support: None, Conflict of Interest: None | Check |
DOI: 10.4103/nnjcr.nnjcr_28_19
Background: Hypertensive disorders of pregnancy (HDP) complicate an estimated 5%–10% of pregnancies globally. Studies have linked non-O blood group with the development of HDP, especially preeclampsia (PE). However, these reports have not been consistent. This study aimed to determine the relationship between ABO blood group and HDP among pregnant women attending antenatal clinic at Murtala Muhammad Specialist Hospital, Kano, Nigeria. Materials and Methods: Two hundred and ten pregnant women with clinically diagnosed HDP and an equal number of age-matched normotensive controls were recruited for the study. Blood pressure was measured using a mercury sphygmomanometer and a Littman's stethoscope which was positioned on the medial aspect of the right arm at sitting position. Urinalysis was performed using a urine dipstick (Medi-Test Combi 9®). ABO blood groups were determined by tile agglutination method using potent monoclonal anti-A, anti-B, and anti-D reagents (Plasmatec Lab., Bridport, UK). Data were analyzed using Statistical Package for Social Sciences version 23.0. Chi-square test of association, Student's t-test, and logistic regression were used as statistical tools, and results were presented as frequencies, percentages, mean ± standard, odds ratio (OR), and confidence interval (CI); P ≤ 0.05 was considered statistically significant. Results: The mean age of the cases and controls was 26.20 ± 6.96 and 25.90 ± 6.37, P = 0.65, respectively. The mean gestational age of the cases and controls was 32.30 ± 4.15 and 29.06 ± 4.25, P = 0.01, respectively. The mean systolic and diastolic blood pressure of the cases and controls in mmHg were 176.62 ± 32.62 and 123.08 ± 6.40, P = 0.01, and 114.20 ± 20.08 and 76.43 ± 5.07, P = 0.01, respectively. Of the 210 individuals in the HDP group (cases), 90 (42.86%) had gestational hypertension (GH), 50 (23.81%) had PE, and 70 (33.33%) had eclampsia. Type O blood group was the most common group in both cases (93 [44.3%]) and controls (98 [46.7%]). This was followed by groups A (40 [19.0%] and 45 [21.45]), B (58 [27.6%] and 53 [25.2%]), and AB (19 [9.0%] and 14 [6.7%]) for cases and controls, respectively. There was no statistically significant difference in the frequencies of ABO blood group between the cases and controls (χ2 = 1.41, P = 0.70, df = 3). Compared to type O blood group individuals, non-O blood group individuals had 1.106 times odd of developing HDP than the controls (OR: 1.106, 95% CI: 0.753–1.625, P = 0.61). Similarly, types A, B, and AB blood group individuals had 1.292, 1.492, and 1.882 times odds of developing GH compared to blood Group O and controls (OR: 1.292, 95% CI: 0.670–2.490, P = 0.45; OR: 1.492, 95% CI: 0.813–2.740, P = 0.20; and OR: 1.882, 95% CI: 0.746–4.748, P = 0.18), respectively. Equally, types A, B, and AB blood group individuals had 1.243, 0.990, and 1.699 times odds of developing PE compared to blood group O individuals and controls (OR: 1.243, 95% CI: 0.561–2.754, P = 0.59; OR; 0.990, 95% CI: 0.442–2.217, P = 0.98; and OR: 1.699, 95% CI: 0.546–5.281, P = 0.36), respectively. Compared to type O blood group individuals, types A, B, and AB blood group individuals had 0.463, 0.690, and 0.901 times odds of developing eclampsia compared to controls (OR: 0.463, 95% CI: 0.199–1.079, P = 0.74; OR: 0.960, 95% CI: 0.505–1.825, P = 0.90; and OR; 0.901, 95% CI: 0.301–2.695, P = 0.85), respectively. Primiparity (OR: 2.320, 95% CI: 1.451 – 3.711, P = 0.01, for HDP) and gestational age (OR: 1.078, 95% CI: 1.013 – 1.148, P = 0.02 – gestational hypertension; OR: 1.328, 95% CI: 1.212 – 1.456, P = 0.01 – preeclampsia; OR: 1.467, 95% CI: 1.333 – 1.614, P = 0.01 – eclampsia) were identified as pregnancy related risk factors for HDP. Conclusion: The frequencies of ABO phenotypes in women with HDP are similar to that of normotensive pregnant women. There is no relationship between ABO phenotypes and HDP as observed in this study. However, nulliparity and gestational age were identified as risk factors for HDP. Similar hospital-based and population-based studies should be conducted to further evaluate this phenomenon in this environment.
Keywords: ABO, eclampsia, gestational hypertension, Kano, preeclampsia
How to cite this article: Mukhtar IG, Yakubu AA, Yakasai BW, Ahmed SI, Mansur S. Relationship between ABO blood group phenotypes and hypertensive disorders of pregnancy: A hospital-based cross-sectional study in Kano, North-West Nigeria. N Niger J Clin Res 2019;8:68-74 |
How to cite this URL: Mukhtar IG, Yakubu AA, Yakasai BW, Ahmed SI, Mansur S. Relationship between ABO blood group phenotypes and hypertensive disorders of pregnancy: A hospital-based cross-sectional study in Kano, North-West Nigeria. N Niger J Clin Res [serial online] 2019 [cited 2024 Mar 29];8:68-74. Available from: https://www.mdcan-uath.org/text.asp?2019/8/14/68/268531 |
Introduction | | |
Hypertensive disorders of pregnancy (HDP) are a combination of pregnancy-related disorders that together constitute one of the leading causes of maternal death worldwide. Globally, they complicate an estimated 5%–10% of pregnancies.[1] Elevated blood pressure is common in pregnancy; it is reported to complicate 1 in 10 pregnancies and affect an estimated 240,000 women annually in the United States.[2] The prevalence varies from one region to another and from one country to another. The variations in the reported prevalence are largely due to differences in operational definition of the disorders and study design. While most population-based studies reported lower prevalence, hospital-based studies tend to overestimate the magnitude of the problem. In a multicentered study involving over 300,000 women in 357 facilities across Africa, Asia, and Latin America, the World Health Organization reported an overall prevalence of 2.7%.[3] The figures range from as low as 1.8% in the Middle East and 4.5% in the Americas.
In sub-Saharan Africa, HDP are a leading cause of maternal mortality, second only to obstetric hemorrhages and in some countries overtaking it.[4] HDP are responsible for about 16% of maternal mortality in sub-Saharan Africa.[5]
The prevalence of HDP in Nigeria varies from one region to another. While reports from the southern parts of the country indicate a relatively lower prevalence, those from the northern parts are relatively higher. For example, while Singh et al.[6] reported a high prevalence of 17% among pregnant women in Sokoto, North-west Nigeria, Satunsa et al.[7] reported a prevalence of 10.3% from Ogun state, South-west Nigeria. Like in many other African countries, HDP continue to be one of the leading causes of maternal mortality in Nigeria.[8]
Apart from its traditional role in transfusion and tissue graft medicine, ABO blood group system is increasingly been linked to a number of diseases.[9],[10] Specifically, non-O blood group and, in particular, type AB blood group have been linked to an increased risk of preeclampsia (PE).[11],[12],[13] However, there have been reported inconsistencies in the reported relationship between ABO blood group phenotypes and HDP.[13] In addition, there is paucity of information on the relationship between ABO blood group phenotypes and HDP in Africa, in Nigeria, and in this environment.
This study aimed to determine the relationship between ABO blood group phenotypes and HDP (gestational hypertension [GH], PE, and eclampsia) so as to develop better strategies for risk stratification and management.
Materials and Methods | | |
Study area and population
The study was conducted at the Obstetrics and Gynaecology Department of Murtala Muhammad Specialist Hospital, Kano, Nigeria, between June and October, 2018.
Two hundred and ten pregnant women with HDP (GH, PE, and eclampsia) were recruited as cases from the high-risk clinic and eclamptic ward. An equal number of normotensive pregnant women were recruited from the antenatal clinic as controls.
Ethical consideration
Ethical approval was obtained from Kano State Ministry of Health. A clearance was also received from the management of the hospital, and all participants were requested to sign an informed consent form before commencing the study. All procedures and protocols were in accordance with the revised version of Helsinki declaration of 1975.
Sample size determination
Sample size was determined using the formula for minimum sample size by Lwanga and Lemeshow[14] as follows:
N = Z2P (1 − P)/d2, where
N = Minimum sample size
Z = Standard normal deviation corresponding to 95% confidence interval (CI) (1.96)
P = Prevalence from previous study which is 17% (Singh et al.)[6]
d = Degree of precision at 5% (0.05).
Therefore,
N = (3.8416) × (0.17) × (0.83)/(0.0025) = 217.
Study design and sampling technique
The study was of a descriptive cross-sectional design. Systematic sampling technique was used to recruit the participants.
Inclusion criteria
- All pregnant women diagnosed with GH, PE, or eclampsia
- All pregnant women with a gestational age of 20 weeks and above
- All pregnant women who fulfilled the above two criteria and signed informed consent form
- Age-matched normotensive pregnant women from the antenatal clinic of the same hospital were recruited as controls.
Exclusion criteria
- Gestational age <20 weeks
- Previous history of hypertension
- Those who declined consent.
Data collection
A semi-structured interviewer-administered questionnaire was used to obtain the sociodemographic information and clinical characteristics of the participants.
Blood pressure was measured using a mercury sphygmomanometer and a Littman's stethoscope which was positioned on the medial aspect of the right arms with the participants resting in sitting position. The appearance of first Korotkoff's sound was used as systolic blood pressure (SBP), whereas its disappearance was used as diastolic blood pressure (DBP).
The operational definitions of GH, PE, and eclampsia were adopted from the report of National High Blood Pressure Education Program Working Group Report on High Blood Pressure in Pregnancy of 2000.[2]
- GH was defined as SBP of ≥140 mmHg or DBP of ≥90 mmHg in a previously normotensive pregnant woman after 20 weeks of gestation in the absence of proteinuria
- PE was defined as GH in the presence of proteinuria
- Eclampsia was defined as PE with convulsion.
Urinalysis was performed using urine test strips (Medi-Test Combi 9® by Macherey-Nagel GmbH Co. KG, Düren, Germany). The test was performed according to manufacturer's guidelines.
ABO blood group was determined manually using potent monoclonal anti-A, anti-B, and anti-D reagents (Plasmatec Lab. Ltd., Bridport, UK). The traditional tile agglutination method was used as described by Rawley and Milkins.[15]
Statistical analysis
Data were analyzed using Statistical Package for Social Sciences version 23.0 (International Business Machines Corporation, IBM SPSS Statistics for Windows, Version 23.0, Armonk, NY, IBM Corp., 2015).[16] The results were expressed as mean ± standard deviation, frequencies, percentages, odds ratio (OR), and 95% CI, and P ≤ 0.05 was considered statistically significant. Chi-square test was used to determine the association between categorical variables, whereas Student's t-test was used to determine the association between continuous variables. Logistic regression was used to calculate ORs and 95% CI for the risk of developing HDP among non-O (A, B, and AB) blood groups compared to type O.
Results | | |
Sociodemographic and clinical characteristics of the subjects
A total of 210 pregnant women clinically diagnosed with HDP (GH, PE, and eclampsia) were recruited as cases, whereas an equal number of normotensive pregnant women were recruited as controls. The mean age in years of the cases and controls was 26.20 ± 6.96 and 25.90 ± 6.37, respectively. There was no statistically significant difference in the mean age of women (P = 0.65), implying that the two groups were matched for age. Similarly, the mean gestational age in weeks of the cases and controls was 32.30 ± 4.15 and 29.06 ± 4.25, respectively. There was a statistically significant difference in the mean gestational age of the women (P = 0.01).
Majority of the women in both case (99.0%) and control (99.0%) groups were of Hausa-Fulani origin. Furthermore, a larger proportion of the women in both groups had at least primary education. A considerable number of women in both groups were full-time homemakers and were carrying singleton pregnancies.
The mean SBP and DBP of the cases and controls in mmHg were 176.62 ± 32.62 and 123.08 ± 6.40, P = 0.01, and 114.20 ± 20.08 and 76.43 ± 5.07, P = 0.01, respectively. This implies that the cases were hypertensive, whereas the controls were normotensive.
Of the 210 women in the HDP group (cases), 90 (42.86%) had GH, 50 (23.81%) had PE, and 70 (33.33%) had eclampsia.
Information on the sociodemographic and clinical characteristics of the women is presented in [Table 1]a and [Table 1]b.
Frequencies of ABO and Rh (D) blood groups among the subjects
Type O blood group was the most common group in both cases (93 [44.3%]) and controls (98 [46.7%]). This was followed by types A (40 [19.0%] and 45 [21.45]), B (58 [27.6%] and 53 [25.2%]), and AB (19 [9.0%] and 14 [6.7%]) for cases and controls, respectively. Thus, the distribution of ABO blood group among the women was in the order of O > B > A > AB. There was no statistically significant difference in the frequencies of ABO blood group between the cases and controls (χ2 = 1.41, P = 0.70, df = 3).
Most of the women in both case (207 [98.6%]) and control (202 [96.2%]) groups were Rh D positive, whereas 3 (1.4%) and 8 (3.8%) were Rh D negative, respectively. There was no statistically significant difference in the pattern and distribution of Rh D blood group between the cases and controls (χ2 = 2.33, P = 0.13, df = 1) [Table 2].
Relationship between ABO blood group phenotypes and hypertensive disorders of pregnancy
Compared to type O blood group women, non-O blood group women had 1.106 times odds of developing HDP than the controls (OR: 1.106, 95% CI: 0.753–1.625, P = 0.61). This implies that there is no statistically significant difference in the odds of developing HDP between type O blood group women and non-O blood group women. When age was considered as an independent factor, a unit increase in age in years was associated with only 0.993 odds of developing HDP (OR: 0.993, 95% CI: 0.965–1.022, P = 0.63).
Compared to type O blood group women, types A, B, and AB blood group women had 1.292, 1.492, and 1.882 times odds of developing GH compared to controls (OR: 1.292, 95% CI: 0.670–2.490, P = 0.45; OR: 1.492, 95% CI: 0.813–2.740, P = 0.20; and OR: 1.882, 95% CI: 0.746–4.748, P = 0.18), respectively. Similarly, a unit increase in age in years was associated with 1.016 times odds of developing GH (OR: 1.016, 95% CI: 0.979–1.054, P = 0.41). This implies that neither type A, B, and AB blood groups nor age had a significant influence on the development of GH in the cases compared to type O blood group. Even though type AB blood group had the greatest influence on the development of GH, the influence was weak and statistically insignificant.
Compared to type O blood group women, types A, B, and AB blood group women had 1.243, 0.990, and 1.699 times odds of developing PE compared to controls (OR: 1.243, 95% CI: 0.561–2.754, P = 0.59; OR; 0.990, 95% CI: 0.442–2.217, P = 0.98; and OR: 1.699, 95% CI: 0.546–5.281, P = 0.36), respectively. Similarly, a unit increase in age in years was associated with 1.061 times odds of developing PE (OR: 1.061, 95% CI: 1.016–1.108, P = 0.01). This implies that neither types A and B nor type AB blood group had a significant influence on the development of PE. Although type AB had the greatest influence, the influence was weak and not statistically significant. However, advancing age increases the odds of developing PE.
Compared with type O blood group women, types A, B, and AB blood group women had 0.463, 0.960, and 0.901 times odds of developing eclampsia compared to the controls (OR: 0.463, 95% CI: 0.199–1.079, P = 0.74; OR: 0.960, 95% CI: 0.505–1.825, P = 0.90; and OR; 0.901, 95% CI: 0.301–2.695, P = 0.85), respectively. Similarly, a unit increase in age in years was associated with 0.946 odds of developing eclampsia (OR: 0.946, 95% CI: 0.901–0.993, P = 0.03). The results of the relationship between ABO blood group and HDP are presented in [Table 3]. | Table 3: Relationship between ABO blood group and hypertensive disorders of pregnancy
Click here to view |
Relationship between other pregnancy-related factors and hypertensive disorders of pregnancy
Primiparity was associated with 2.320 times odds of developing HDP compared to multiparity (OR: 2.320, 95% CI: 1.451–3.711, P = 0.01). Similarly, advanced gestational age was associated with 1.078 times odds of developing GH (OR: 1.078, 95% CI: 1.013–1.148, P = 0.02); 1.328 times odds of developing PE (OR: 1.328, 95% CI: 1.212–1.456, P = 0.01); and 1.467 times odds of developing eclampsia (OR: 1.467, 95% CI: 1.333–1.614, P = 0.01). However, singleton gestation had no statistically significant influence on HDP (OR: 2.050, 95% CI: 0.689–6.104, P = 0.20). The results of the relationship between some pregnancy-related factors and HDP are presented in [Table 4]. | Table 4: Relationship between pregnancy-related factors and hypertensive disorders of pregnancy
Click here to view |
Discussion | | |
This study has demonstrated that the most common ABO blood group among pregnant women in this environment is O followed by B, A, and AB, in that order. Similarly, the pattern of the distribution in both cases and controls is O > B > A > AB. Human ABO blood groups are determined by the presence or absence of antigenic materials made up of complex carbohydrates located on the surfaces of red blood cells and in some instances bodily fluids and tissues.[17],[18] These antigenic materials are inherited in a Mendelian fashion and passed from one generation to another. Various evolutionary factors have over the years played a significant role in the distribution of these antigens in human population. Even though there are over thirty different human blood group antigens, ABH antigens are the most clinically important. ABO blood group system is made up of three antigens, namely, antigen A, antigen B, and antigen H.[19] Type O blood group individuals possess antigen H, type A blood group individuals possess antigen A, type B blood group individuals possess antigen B, and type AB blood group individuals possess both antigens A and B. Diversity in the expression of these antigens and their role in disease causation could be responsible for the wide ethnic and regional variations in the distribution of ABO and Rh D blood groups.
Type O blood group has been reported to protect against severe form of malarial infection by Plasmodium falciparum, whereas type AB is said to be the least protective against the infection.[20] This could explain the predominance of type O blood group and the lower frequency of type AB in tropical countries where malarial infection is endemic. Type O blood group individuals have also been reported to be susceptible to infection by some strains of Vibrio cholerae.[21] Perhaps that may be the reason for the higher frequency of type O blood group in areas prone to frequent cholera outbreaks.
The findings of this study on the frequencies and distribution of ABO and Rh D blood group phenotypes are similar to what was reported by a number of researchers from North-west Nigeria.[22],[23] However, there is a slight difference in the frequencies of types A and B blood group between this study and indeed studies from North-west Nigeria to what was reported from the southern parts of the country.[24] While type B blood group is the second most common type after O in this study and other parts of North-West Nigeria, type A is the second most common in South-South, South-East, South-West, North-Central, and some parts of North-East Nigeria.[24] The ethnic compositions of these regions may be the reason for this slight difference in the frequencies of types A and B blood groups.
This study has demonstrated no significant difference in the frequencies and distribution of ABO and Rh (D) blood groups between pregnant women with HDP and their age-matched controls. On multivariate logistic regression analysis using type O as a reference group, none of the non-O blood group types (A, B, and AB) had a significant influence on the development of GH, PE, or eclampsia. Although type AB blood group had the greatest influence among the three groups, the influence was weak and statistically insignificant. This finding is similar to what was reported by Hentschke et al.[11] They reported no significant association between ABO blood group phenotypes and development of PE among over 10,000 pregnant women in Brazil. Salman[25] also reported no significant association between ABO blood group and HDP among pregnant women in Baquba-Diyala province of Iraq. In their meta-analysis of 17 case–control studies on this topic, Clark and Wu[26] demonstrated no consistent relationship between ABO blood group and PE. However, in a recent systematic literature analysis spanning 50 years (1965–2015), Franchini et al.[27] reported types AB and A to be associated with HDP. Similarly, Hiltunen et al.[28] reported type AB blood group as a risk factor for PE among Finnish population.
PE is a multisystem disorder consisting of development of hypertension and proteinuria after 20 weeks of gestation. Despite numerous years of research, the exact mechanisms mediating the observed clinical features of PE still remain unknown. However, considerable progress has been made to allow for a number of theories to be considered. At the center of the pathogenesis of PE is the failure of trophoblastic invasion by maternal uterine spiral arteries leading to uteroplacental insufficiency.[29] This is followed by systemic reactive vascular response leading to the various manifestations of the disease. The exact pathophysiological mechanisms mediating these systemic vascular responses are not known with certainty. One possible explanation is hypercoagulability state with thrombus formation and deposition of fibrin in the placental microcirculation and other vascular beds. Indeed, pregnancy, even though a normal physiological state, is associated with elevated plasma levels of von Willebrand factor (VWF) and coagulation factor VIII (FVIII).[30]
ABO blood group is generally determined by the presence or absence of antigenic material on the surfaces of red blood cells. These antigenic materials are however not only limited to the surfaces of red cells but also to other bodily fluids and tissues. The ABH antigens, the antigens that determine ABO blood group, originate from a common precursor molecule called H determinant.[30] While antigens A and B (expressed by types A, B, and AB blood group individuals – non-O) encode different transferases that add different side chains to the precursor H determinant, antigen H (expressed by type O blood group individuals) does not encode any functional enzyme and therefore has the unaltered copy of the H determinant as its antigen.[28],[30] Therefore, the ABH antigens are structurally and functionally different, and this serves as the basis for variation in the susceptibility of ABO genotypes to diseases.
One molecule that expresses ABH antigens is the VWF, a molecule that plays a critical role in coagulation. Apart from carrying coagulation FVIII in the plasma thereby protecting it from destruction, VWF also enhances platelet attachment to injured subendothelial surfaces, platelet–platelet interactions, and platelet aggression. VWF together with coagulation FVIII is thus a prothrombotic molecule.[31] A number of studies have reported increased plasma levels of both VWF and coagulation FVIII in non-O individuals compared to type O individuals.[30],[32] Indeed, Mannucci et al.[33] reported a 35% lower plasma levels of VWF and coagulation FVIII in type O blood group individuals compared to non-O individuals. The lower plasma levels of VWF in type O blood group individuals are believed to be due to the presence of a metalloprotease responsible for cleaving VWF called ADAMTS-13.[33] Thus, non-O blood group individuals have elevated plasma levels of prothrombotic factors, VWF and FVIII, and lower plasma level of the VWF cleaving protease, ADAMTS-13, and hence are predisposed to an increased risk of arterial and venous thrombosis.
Therefore, pregnancy with its hypercoagulability state and non-O blood group with elevated plasma levels of VWF and FVIII and lower ADAMTS-13 serve as synergistic and potent risk factors for the widespread fibrin deposition on vascular beds and in particular uteroplacental bed, causing insufficiency and hence PE. However, despite numerous evidences to this relationship, Alpoim et al.[30] did not find any relationship between elevated plasma levels of VWF and FVIII and lower plasma level of ADAMTS-13 on the one hand and ABO blood group on the other hand among preeclamptic patients. They argued that the heightened plasma levels of VWF and FVIII in preeclamptic patients could not be accounted on the basis of ABO blood group alone. In their analysis of data on pregnant women who survived PE, pregnancy-related hypertension, or intrauterine growth retardation 10 weeks postpartum, Witsenburg et al.[34] reported no significant difference in the serum levels of coagulation FVIII between these women and normal controls. They concluded that if the mechanism linking PE to ABO blood group is solely via alteration in the plasma level of coagulation FVIII, then there is no relationship between non-O blood group and PE.
The apparent inconsistencies in the reports linking ABO blood group to the development of PE could be due to the wide ethnic and regional variations in the frequencies and distribution of ABO phenotypes.
This study also found nulliparity, advanced maternal age, and gestational age as risk factors for HDP. This is similar to what was reported by Anorlu et al.[35] that nulliparity is an important risk factor for PE among pregnant women in Lagos, Nigeria. However, while multiple gestations have been reported to be an important risk factor for HDP, we found no statistically significant influence of multiple gestations on HDP.
Conclusion | | |
This study found no statistically significant association in the frequency and distribution of ABO blood group between pregnant women with HDP and their age-matched normotensive controls. Similarly, non-O blood group was not associated with increased risk of HDP. Similar hospital-based and population-based studies should be conducted to further evaluate this phenomenon in this environment.
Acknowledgment
We wish to thank Kano state ministry of health, management and staff of Murtala Muhammad Specialist Hospital Kano, and the study participants for their cooperation and support throughout the period of the study.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4]
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