Home Ahead of print Instructions
About us Current issue Subscribe
Editorial board Archives Contact us
Search Submit article Login 
Print this page Email this page

 Table of Contents  
Year : 2017  |  Volume : 14  |  Issue : 2  |  Page : 121-126

Association of hypertension and activity of angiotensin converting enzyme in malaria patients attending Sheik Muhammad Jidda General Hospital, Kano State, Nigeria

1 Center for Biotechnology Research, Bayero University, Kano, Nigeria
2 Department of Biochemistry, Faculty of Basic Medical Sciences, College of Health Sciences, Bayero University, Kano, Nigeria

Date of Web Publication5-Oct-2017

Correspondence Address:
B Kurfi
Department of Biochemistry, Faculty of Basic Medical Sciences, College of Health Sciences, Bayero University, Kano
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njbcs.njbcs_6_17

Rights and Permissions

Background: Peptides of the renin angiotensin aldosterone system (RAAS) have been implicated in the pathogenesis of malaria infection; however, available data are limited. Thus, this study was aimed at determining the association between hypertension and activity of angiotensin converting enzyme (ACE) in malaria patients attending Sheikh Muhammad Jiddah General Hospital, Kano State, Nigeria. Materials and Methods: Four hundred and fifty consenting adults (300 malaria positive and 150 control participants) were evaluated. Data on sociodemographic characteristics were obtained using a questionnaire. ACE level was determined as described by Cushman and Cheung (1971) and blood pressure (BP) was evaluated using standard methods. Statistical Analysis: ACE activity and BP were expressed as mean ± SEM. Comparison between groups was carried out using one-way analysis of variance. Pearson's Chi-square (χ2) test was employed to establish association between Plasmodium infection, hypertension, sex, age, educational, and occupational status. P <0.05 was regarded as statistically significant. Results: A total of 300 (66.6%) patients tested positive for malaria, of which 60 (20%) were hypertensive. The prevalence differed significantly by gender, age group, and occupational status. The serum ACE activity was significantly lower in male (1.54 ± 1.04 μmol/min/ml) and female (2.01 ± 1.29 μmol/min/ml) patients with malaria compared to controls (7.09 ± 2.42 and 7.48 ± 2.42 μmol/min/ml, for males and females, respectively); and this further decreased with severity of infection. Moreover, the ACE activity of malaria patients with hypertension (11.67 ± 0.5 and 10.60 ± 0.40 μmol/min/ml) was significantly higher than nonhypertensive (3.20 ± 1.31 and 3.16 ± 0.74 μmol/min/ml) male and female patients, respectively. Conclusions: There was a significant association between the activity of ACE and hypertension in malaria infection, showing that ACE might play a significant role in the outcome of malaria.

Keywords: Angiotensin converting enzyme, hypertension, malaria, prevalence

How to cite this article:
Abdulazeez A M, Ya'u M, Kurfi B. Association of hypertension and activity of angiotensin converting enzyme in malaria patients attending Sheik Muhammad Jidda General Hospital, Kano State, Nigeria. Niger J Basic Clin Sci 2017;14:121-6

How to cite this URL:
Abdulazeez A M, Ya'u M, Kurfi B. Association of hypertension and activity of angiotensin converting enzyme in malaria patients attending Sheik Muhammad Jidda General Hospital, Kano State, Nigeria. Niger J Basic Clin Sci [serial online] 2017 [cited 2022 Oct 6];14:121-6. Available from: https://www.njbcs.net/text.asp?2017/14/2/121/216057

  Introduction Top

Malaria is one of the most important global health problem, with approximately 189–327 million clinical cases reported worldwide and nearly a million deaths annually. Malaria infection caused by Plasmodium falciparum alone is associated with approximately 230 million cases and is responsible for most of the severe cases of the disease.[1] Hypertension on the other hand is one of the most common clinical conditions which still remains one of the most important public health problem in the world.[2] It is defined as systolic blood pressure ≥140 mmHg and diastolic blood pressure ≥90 mmHg.[1] There are some indications that the burden of noncommunicable diseases including hypertension is increasing in epidemic proportions in Africa,[1] and it is projected that up to three quarters of the world's hypertensive population will be in economically developing countries by the year 2025.[3] In Nigeria, malaria accounts for an estimated 100 million cases and over 300,000 deaths per year, whereas hypertension affects 11.2% Nigerians (i.e., about 4.33 million).[4] With increased prevalence of hypertension and endemicity of malaria in Nigeria, the resultant greater economic and health burden will no doubt be felt due to its population size.[4]

Studies have demonstrated that standardized mean blood pressures (BPs) are higher in many parts of Asia and sub-Saharan Africa than those in high-income countries, resulting in a rise of cardiovascular disease in low- and middle-income countries (LMIC) against the background of continuing high burden of infectious diseases, one of which is malaria.[5] Although malaria and hypertension do not have an obviously direct cross influence, both diseases have been shown to have physiopathologic similarities such as endothelial dysfunction, ischemia, and production of proinflammatory cytokines. Furthermore, recent studies have suggested that peptides of the renin angiotensin aldosterone system (RAAS) play a significant role in the pathogenesis of malaria and may influence its severity.[6] The impairment of endothelial function, a key phenomenon of severe P. falciparum malaria, has been shown to occur due to homeostatic imbalance and the antagonistic interaction of nitric oxide (NO) and angiotensin II (Ang II) in several vascular diseases. However, the biologic mechanisms are still poorly understood in malaria.[7]

Ang II is the main active product of RAAS that acts on the adrenal cortex, causing aldosterone release that stimulates reabsorption of sodium and water, which increases blood pressure. Ang II is produced by the action of angiotensin converting enzyme (ACE), a zinc metallopeptidase, on angiotensin I, an inactive decapeptide. ACE also plays important roles in the kinin-kallikrein cascade, where it metabolizes bradykinin, a strong vasodilator, forming the inactive metabolite bradykinin. In contrast, recent studies have shown that the actions of Ang II via the type 2 receptor are counter regulatory to those mediated via the AT1 receptor because Ang II acts via AT2 receptor to produce a vasodilator effect through bradykinin-dependent activation of endothelial nitric oxide synthase. Several studies have demonstrated the protective effect of Ang II on malaria.[6],[7] Other reports have shown that angiotensin peptides can cause impairment of the erythrocyte cycle of plasmodium, reducing the parasite growth in vitro,[8],[9] though the biologic mechanisms have not been established. This has prompted research regarding the prevalence of hypertension in malaria infection in different parts of the world to pave the way for better understanding of whether malaria could have a possible driving evolutionary force for hypertension. This study was therefore aimed at determining the prevalence and risk factors of hypertension and to evaluate the activity of ACE in severe and non-severe malaria patients attending Sheik Muhammad Jidda Specialist Hospital, Kano State, Nigeria.

  Materials and Methods Top

This was a cross-sectional study involving 450 male and female patients who were referred (between July to September, 2015) to the Haematology Department of Sheikh Muhammad Jiddah General Hospital, Kano State, Nigeria. Three hundred patients tested positive for malaria infection, whereas 150 tested negative (controls). The patients were chosen via simple random sampling. Approval was sought from the Hospital Management Board, Kano State, with an ethical clearance number HMB/GEN/488/VOL. 1. Individuals who consented and were between the ages of 18 and 80 years were included in the study, whereas those below 18 years and pregnant women were excluded. Those who refused to give their consent were also excluded. A standard questionnaire was made available. Sociodemographic data collected included gender, age, socioeconomic and educational status, as well as awareness about hypertension.

Determination of blood pressure

BP of individual patients was determined using a digital BP monitor (Boots Upper Arm Blood Pressure Monitor, Omron HEM-742-UK). Hypertension was defined as systolic BP greater than or equal to 140 mmHg and diastolic BP as greater than or equal to 90 mmHg.[2]

Laboratory methods

Determination of parasitemia

Venous blood (5 cm 3) was aseptically collected from the patients and parasitemia determined as described by Cheesbrough.[10] Patients were considered having severe P. falciparum malaria if they met the predefined, modified WHO criteria for severe malaria (hyperparasitemia >10% parasitemia).

Determination of ACE activity

The assay for ACE activity was determined using the Cushman and Cheung method,[11] with some modifications. Briefly, blood was collected by venipuncture and serum separated by centrifuging at 2000 xg and 4°C for 10 minutes. About 50 μl of serum was added to 50 μl deionized water and the reaction was started by adding 0.2 ml of 5 mmol/L hippuric-histidyl-leucine (HHL). This was incubated at 37°C for 15 minutes. The reaction was terminated by adding 0.25 ml of 1.0 N hydrochloric acid and then 2.0 ml ethyl acetate to extract the hippuric acid formed by the action of ACE. This was centrifuged at 3600 xg for 2 min, and 1 ml of upper layer was transferred into a microcentrifuge tube and heated by dry bath at 100°C for 15 minutes to remove ethyl acetate by evaporation. The resulting hippuric acid was dissolved in 3.0 ml distilled water, and the absorbance was read at 228 nm. Serum enzyme activity was expressed in units, which corresponded to 1 μmol of hippuric acid released by hydrolysis of HHL per minute per milliliter serum.

Statistical analysis

ACE activity and BP were expressed as mean ± SEM. Comparison between groups was computed using one-way analysis of variance (ANOVA). Least significant difference (LSD) post-hoc test was applied for multiple comparisons between the groups. Pearson's Chi-square (χ2) test was employed to establish association between Plasmodium infection, hypertension, sex, age, and educational and occupational status. P < 0.05 was regarded as statistically significant.

Data analysis was carried out using Student Package for the Social Sciences version 20.0 (IBM Corporation).

  Results Top

Out of 450 participants, 265 (58.9%) were males and 185 (41.1%) were females [Table 1]. The overall prevalence of malaria infection was 66.6%. There was a significant (P < 0.05) difference between males and females (47.4 vs 94.6%; χ2 = 110.4, P = 0.0001), age groups (χ2 = 35.6, P = 0.001), and occupational status (χ2 = 14.2, P = 0.01). The highest prevalence based on age (83.9%) was found in patients between the ages of 18 and 29, whereas those above 70 years had the least prevalence (36.8%). With respect to occupation, the highest prevalence was among the unemployed (79.3%) whereas retirees had the least prevalence (53.3%) [Table 2].
Table 1: General characteristics of the participants (n=450)

Click here to view
Table 2: Prevalence and distribution of malaria among the participants according to age, gender, and educational and occupational status (n=450)

Click here to view

[Table 3] shows the prevalence of hypertension in malaria-positive patients according to age and gender. Out of the 300 malaria-positive patients, 60 (20%) were hypertensive. The gender-related prevalence was significantly (P < 0.05) different (χ2 = 4.20, P = 0.04), with the highest prevalence evident in females above 70 years compared to males (57.1 vs 14.3%), followed by those between the ages of 60 and 69 (44.0%).
Table 3: Prevalence of hypertension among the malaria positive patients according to age and gender (n=300)

Click here to view

Regarding age group, the prevalence differed significantly (χ2 = 101.4, P = 0.0001), with those above 60 years having the highest prevalence (72%). None of those aged 18–29 years had hypertension while those between 30 and 39 years had a prevalence of 11.4% [Table 3].

The occupation-related prevalence of hypertension in malaria-positive patients is presented in [Table 4]. The prevalence in retirees (50%) was significantly (χ2 = 40.1, P = 0.0001) higher than that recorded for employed (8.7%) and unemployed (28.4%) patients.
Table 4: Prevalence of hypertension among the malaria positive patients according to occupational status (n=300)

Click here to view

The activity of ACE decreased significantly (P < 0.05) in male and female patients with malaria compared to malaria-negative patients. Furthermore, there was a significant (P < 0.05) difference in ACE levels of male (1.54 ± 1.04 μmol/min/ml) and female (2.01 ± 1.29 μmol/min/ml) patients with malaria, as well as those in the control group [Table 5]. Based on severity, ACE activity was significantly (P < 0.05) lower in both male and female patients with severe malaria than those with mild or moderate malaria [Table 6].
Table 5: Serum angiotensin converting enzyme (ACE) activity of malaria.positive and negative patients (n=450)

Click here to view
Table 6: Serum angiotensin converting enzyme (ACE) activity based on severity of malaria in malaria positive participants (n=300)

Click here to view

The ACE activity of malaria-positive patients with hypertension was significantly (P < 0.05) higher than that of nonhypertensive patients. However, no statistical differences (P > 0.05) were observed between male and female hypertensive and nonhypertensive malaria-positive patients. The systolic and diastolic BP was significantly (P < 0.001) higher in hypertensive patients than nonhypertensive patients [Table 7].
Table 7: Blood pressure and serum angiotensin converting enzyme (ACE) activity in hypertensive and non-hypertensive malaria positive patients (n=300)

Click here to view

  Discussion Top

The prevalence of malaria infection in the study population was 66.6%, which falls within the recent estimated risk map of less than 20% to over 70% in some areas in Nigeria.[12] According to Health reporters,[13] there were over 22,000 deaths from malaria infection in Kano State in 2015. Several studies also reported very high prevalence of 62.5%, 51.7%, and 61.35%, respectively, within Kano metropolis.[14],[15],[16] These findings show that malaria continues to be a leading cause of morbidity and mortality in Kano State, northwestern Nigeria. In conformity with the findings of this study, were high prevalence rates of 64.0%, 59.6%, and 58.0% reported in Kebbi,[17] Awka,[18] and Abuja,[19] respectively. However, a higher prevalence was reported in Aba (86.4%) and Umuahia (74.4%),[20] whereas an extraordinary population-based prevalence rate (99.2%) was reported among pregnant women in Enugu State.[21] However, other studies have reported lower prevalence of malaria – 35.7% in patients attending the General Hospital, Makarfi, Kaduna State;[22] 39.2% of 360 patients who visit primary healthcare facilities in Kano State;[23] 36.6% in Plateau;[24] and 27.29% in Sokoto.[25] This variation can be attributed to different climatic conditions, less rainfall, and surface water that serve as mosquito breeding sites, along with the socioeconomic pattern of the population.

This study demonstrated that gender, age, and occupational status were significant risk factors associated with malaria infection among patients of this study area. The higher prevalence rate among female than that in male patients observed in this study agrees with previous findings reported by Azfar et al.[26] who demonstrated a higher prevalence of malaria infection in females (56%) than males (44%). In addition, Gobir [27] reported a higher prevalence rate (61%) in females than males (38%) within Kano metropolis. However, the present finding contradicts the studies by Akanbi et al.[28] and Abdullahi et al.[29] who reported higher prevalence in males than females. Although there is no established scientific fact regarding the positive correlation between gender and susceptibility to malaria infection,[29] some studies have demonstrated that the vague understandings of the methods of malaria transmission due to illiteracy [30] and lifestyle such as involvement in outdoor household responsibilities like cooking and washing,[31] inability to access healthcare when needed, as well as the rate of unemployment among female gender in the region [32] may play significant roles.

This study also revealed that malaria prevalence significantly (P < 0.05) decreased as age group increased. This increment was higher among those aged 18–29 years (83.9%), followed by 30–39 years (66.0%) and the lowest prevalence among those >70 years (36.8) [Table 2]. This was in line with a previous report by Kanu et al.[20] that, in Aba and Umuahia, there was a progressive decline in the prevalence of malaria infection from younger ages to those above 60 years of age. The high infection rate in this age group could be due to inadequate protection against mosquito bites or insufficient knowledge about malaria transmission. Moreover, the age group is made up of youths who are vulnerable to incessant bites of malaria vectors by exposing their bodies, especially when the weather is hot as they are least likely to use insecticide-treated nets.[29],[30],[31]

The high malaria prevalence among unemployed (79.3%) patients is consistent with previous reports from other African countries demonstrating that malaria is more common among people of lower socioeconomic status who often live in poor housing conditions that increase their exposure to infection.[33],[34],[35],[36]

Sixty out of the 300 malaria positive patients were hypertensive, giving a prevalence rate of 20%. This was within the prevalence rate of hypertension of 8.0–46.0% and 14.0–20.0%[37] recorded from different parts of Nigeria. It also agrees with the prevalence rate of 20.2% reported in Benin City, south-south Nigeria [38] and overall prevalence among adults in Nigeria.[39] The significant (P < 0.05) difference observed in male and female patients (χ2 = 4.20, P = 0.04), the different age groups (χ2 = 101.4, P = 0.0001), and occupational status (χ2 = 40.06, P = 0.0001) of these patients shows that gender, age, and occupational status are important risk factors associated with hypertension in malaria-positive patients. Although there is paucity of information on the prevalence of hypertension in malaria, previous studies have indicated that malaria contributes to the burden of hypertension in highly endemic areas, particularly in LMIC.[40] This has been attributed to the following – malaria in pregnancy leads to low birth weight in children and increases the incidence of hypertension later in life;[41] malaria is associated with stunting and malnutrition in childhood, which predisposes to the development of hypertension in later life;[42] and malaria also results in chronic inflammation, which predisposes to cardiovascular diseases.[43]

Genetic and functional studies suggest that high levels of Ang II may confer protection against cerebral malaria by strengthening the integrity of the endothelial brain barrier. A genetic association study carried out in Orissa, India to search for a possible influence of polymorphisms in ACE 1 and ACE2 on the outcome of malaria showed that the D allele of ACE I/D polymorphism, which increases Ang II production, is associated with mild malaria.[7] This same polymorphism has also been associated with hypertension.[44] In fact, studies by Gallego-Delgado and Rodriguez [6] provided evidence that these polymorphisms and increased plasma levels of Ang II in people with African genetic background confer protection from severe malaria in childhood, but are also responsible for the deleterious effects of hypertension in adulthood. The association of this polymorphism with malaria and hypertension can be explained by the fact that D/D genotype is associated with high ACE levels, which converts Ang I to Ang II. This was consistent with the results of the present study, where the levels of ACE were significantly (P < 0.05) higher in patients with mild malaria compared to those with moderate and severe malaria. In addition, significantly (P < 0.05) high ACE levels were observed in malaria-positive patients with high blood pressure. Ang II causes hypertension due to its vasoconstriction property, but the molecular mechanism of its protective action on severe malaria has not been established, although it is believed to confer protection by strengthening the integrity of the endothelial brain barrier.[45]

  Conclusion Top

The high ACE activity in blood of hypertensive malaria patients and those with mild malaria suggests that ACE activity may probably play a significant role in the pathology of malaria infection.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

World Health Organization (WHO). WHO World Malaria Report. Geneva; 2008. WHO/HTM/GMP/2008.1.  Back to cited text no. 1
Rahimmanesh I, Marzieh S, Rashidi B. High blood pressure and endothelial dysfunction: Effects of high blood pressure medication on endothelial dysfunction and new treatments. J Res Med Sci 2012;2:298-311.  Back to cited text no. 2
Kearney PM, Whelton M, Reynolds K, Whelton PK, He J. Worldwide prevalence of hypertension: A systematic review. J Hypertens 2004;22:11-9.  Back to cited text no. 3
Ekwunife CA, Ozumba NA, Eneanya CI, Nwaorgu OC. Malaria infection among Blood Donors in Onitsha Urban, Southeast Nigeria. Sierra Leone. J Biomed Res 2011;3:21-6.  Back to cited text no. 4
Danaei G, Finucane MM, Lin JK, Singh GM, Paciorek CJ, Cowan MJ, et al. Global Burden of Metabolic Risk Factors of Chronic Diseases Collaborating Group (Blood Pressure). National, regional, and global trends in systolic blood pressure since 1980: Systematic analysis of health examination surveys and epidemiological studies with 786 country-years and 5.4 million participants. Lancet 2011;377:568-77.  Back to cited text no. 5
Gallego-Delgado J, Rodriguez A. Malaria and hypertension: Another co-evolutionary adaptation. Front Cell Infect Microbiol 2014;4:1-4.  Back to cited text no. 6
Dhangadamajhi G, Mohapatra BN, Kar SK, Ranjit M. Gene polymorphisms in angiotensin I converting enzyme (ACE I/D) and angiotensin II converting enzyme (ACE2C–>T) protect against cerebral malaria in Indian adults. Infect Genet Evol 2010;10:337-41.  Back to cited text no. 7
Maciel C, de Oliveira Junior VX, Fazio MA, Nacif-Pimenta R, Miranda A, Pimenta PF. Anti-plasmodium activity of angiotensin II and related synthetic peptides. PLoS One 2008;3:e3296.  Back to cited text no. 8
Saraiva VB, de Souza SL, Ferreira-DaSilva CT, da Silva-Filho JL, Teixeira-Ferreira A, Perales J, et al. Impairment of the Plasmodium falciparum erythrocytic cycle induced by angiotensin peptides. PLoS One 2011;6:e17174.  Back to cited text no. 9
Cheesbrough M. District Laboratory Practice in Tropical Countries, Part 1. University Press: Cambridge; 2006. pp. 239-58.  Back to cited text no. 10
Cushman DW, Cheung HS. Spectrophotometric assay and properties of angiotensin converting enzyme from rabbit lungs. Biochem Pharmacol 1971;20:1637-48.  Back to cited text no. 11
Onyiri N. Estimating malaria burden in Nigeria: A geostatistical modelling approach. Geospat Health 2015;10:306.  Back to cited text no. 12
Health reporters, Africa's online health newspaper. 2016. Available from: http://www. healthreporters.info/2016/04/27/kano-records-22000-malaria-deaths- in-2015. [Last accessed on 8 June 2016].  Back to cited text no. 13
Oyeyi TI, Hamidu MR, Dakata MA. Slide positivity rate of malaria among patients attending two hospitals in Kano Metropolis. Bayero J Pure Appl Sci. 2009;2:194-6.  Back to cited text no. 14
Taura DW, Oyeyi TI. Prevalence of malarial parasites in pregnant women attending Sir Muhammad Sunusi Specialist Hospital, Kano, Nigeria. Bayero J Pure Appl Sci 2009;2:186-8.  Back to cited text no. 15
Isah MA, Darma AI, Sani I. Prevalence of malarial parasites in pregnant women attending Aminu Kano Teaching Hospital, Kano, Nigeria. Asian J Adv Basic Sci 2014;3:117-21.  Back to cited text no. 16
Singh R, Godson II, Singh S, Singh RB, Isyaku NT, Ebere UV. High prevalence of asymptomatic malaria in apparently healthy schoolchildren in Aliero, Kebbi state, Nigeria. J Vector Borne Dis 2014;51:128-32.  Back to cited text no. 17
[PUBMED]  [Full text]  
Mbanugo JI, Ejims DO. Plasmodium infections in children aged 0–5 years in Awka Metropolis, Anambra State, Nigeria. Niger J Parasitol 2000;21:55-9.  Back to cited text no. 18
Nmadu PM, Peter E, Alexander P, Koggie AZ, Maikenti JI. The prevalence of malaria in children between the ages 2-15 visiting Gwarinpa General Hospital life-camp, Abuja, Nigeria. J Health Sci 2015;5:47-51.  Back to cited text no. 19
Kalu MK, Nwogo AO, Nduka FO, Otuchristian G. A Comparative Study of the Prevalence of Malaria in Aba and Umuahia Urban Areas of Abia State, Nigeria. Res J Parasitol 2012;7:17-24.  Back to cited text no. 20
Gunn JK, Ehiri JE, Jacobs ET, Ernst KC, Pettygrove S, Kohler LN, et al. Population-based prevalence of malaria among pregnant women in Enugu State, Nigeria: The healthy beginning initiative. Malar J 2015;14:438.  Back to cited text no. 21
Umaru ML, Uyaiabasi GN. Prevalence of Malaria in Patients Attending the General Hospital Makarfi, Makarfi Kaduna-State, North-Western Nigeria. Am J Infect Dis Microbiol 2015;3:1-5.  Back to cited text no. 22
Gajida AU, Iliyasu Z, Zoakah AI. Malaria among antenatal clients attending primary health care facilities in Kano state, Nigeria. Ann Afr Med 2010;9:188-93.  Back to cited text no. 23
[PUBMED]  [Full text]  
Fana SA, Bunza MD, Anka SA, Imam AU, Nataala SU. Prevalence and risk factors associated with malaria infection among pregnant women in a semi-urban community of north-western Nigeria. Infect Dis Poverty 2015;4:24.  Back to cited text no. 24
Abdullahi K, Abubakar U, Adamu T, Daneji AI, Aliyu RU, Jiya N, et al. Malaria in Sokoto, North Western Nigeria. Afr J Biotech 2009;8:7101-5.  Back to cited text no. 25
Azfar FA, Qayyum AH, Ghaffar A. Haematological abnormalities in malaria. Biomedica 2009;25:52-5.  Back to cited text no. 26
Gobir Z. Prevalence of malaria parasitemia using rapid diagnostic test among apparently healthy children in Kano, Nigeria. J Med Trop 2014;16:21-4.  Back to cited text no. 27
Akanbi OM, Badaki JA, Adeniran OY, Olotu OO. Effect of blood group and demographic characteristics on malaria infection, oxidative stress and haemoglobin levels in South Western Nigeria. Afr J Microbiol Res 2010;4:877-80.  Back to cited text no. 28
Gilles HM, Warell DA. Bruce-Chwatt's Essential Malariology. London: Edward Arnold; 1993. p. 19-124.  Back to cited text no. 29
Rugemalila JB, Wanga CL, Kilama WL. Sixth Africa Malaria day in 2006: How far have we come after the Abuja declaration? Malar J 2006;5:102.  Back to cited text no. 30
Tolhurst R, Nyonator FK. Looking within the household: Gender roles and responses to malaria in Ghana. Trans R Soc Trop Med Hyg 2006;100:321-6.  Back to cited text no. 31
Tanner M, Vlassoff C. Treatment-Seeking Behavior for Malaria: A Typology based on endemicity and gender. Soc Sci Med 1998;46:523-32.  Back to cited text no. 32
Noor AM, Gething PW, Alegana VA, Patil AP, Hay SI, Muchiri E, et al. The risks of malaria infection in Kenya in 2009. BMC Infect Dis 2009;9:180.  Back to cited text no. 33
Pullan RL, Bukirwa H, Staedke SG, Snow RW, Brooker S. Plasmodium infection and its risk factors in eastern Uganda. Malar J 2010;9:2.  Back to cited text no. 34
Loha E, Lindtjørn B. Predictors of Plasmodium falciparum malaria incidence in Chano Mille, South Ethiopia: A longitudinal study. Am J Trop Med Hyg 2012;87:450-9.  Back to cited text no. 35
Kepha S, Nikolay B, Nuwaha F, Mwandawiro CS, Nankabirwa J, Ndibazza J, et al. Plasmodium falciparum parasitaemia and clinical malaria among school children living in a high transmission setting in western Kenya. Malar J 2016;15:157.  Back to cited text no. 36
Ogah OS, Madukwe OO, Chukwuonye II, Onyeonoro UU, Ukaegbu AU, Akhimien MO, et al. Prevalence and determinants of hypertension in Abia State Nigeria: Results from the Abia State non-communicable diseases and cardiovascular risk factors survey. Ethn Dis 2013;23:161-7.  Back to cited text no. 37
Ukoh VA. Admission of hypertensive patients at the University of Benin Teaching Hospital, Nigeria. East Afr Med J 2007;84:329-35.  Back to cited text no. 38
Akinlua JT, Meakin R, Umar AM, Freemantle N. Current prevalence pattern of hypertension in Nigeria: A systematic review. PLoS One 2015;10:e0140021.  Back to cited text no. 39
Etyang AO, Liam SJ, Kennedy CJ, Anthony GS. The Malaria-High Blood Pressure Hypothesis. Circ Res 2016;119:36-40.  Back to cited text no. 40
Bertagnolli M, Luu TM, Lewandowski AJ, Leeson P, Nuyt AM. Preterm birth and hypertension: Is there a link? Curr Hypertens Rep 2016;18:28.  Back to cited text no. 41
Cruickshank JK, Mzayek F, Liu L, Kieltyka L, Sherwin R, Webber LS, et al. Origins of the “black/white” difference in blood pressure: Roles of birth weight, postnatal growth, early blood pressure, and adolescent body size: The Bogalusa heart study. Circulation 2005;111:1932-7.  Back to cited text no. 42
Hotamisligil GS. Inflammation and metabolic disorders. Nature 2006;444:860-7.  Back to cited text no. 43
Choudhury I, Jothimalar R, Patra AK. Angiotensin converting enzyme gene polymorphism and its association with hypertension in south Indian population. Ind J Clin Biochem 2012;27:265-9.  Back to cited text no. 44
Gallegho-Delgado J, Thomas W, Rodriguez, A. The High Blood Pressure-Malaria Protection Hypothesis. Circ Res 2016;119:1071-5.  Back to cited text no. 45


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]

This article has been cited by
1 Malaria link of hypertension: a hidden syndicate of angiotensin II, bradykinin and sphingosine 1-phosphate
Gunanidhi Dhangadamajhi,Shailja Singh
Human Cell. 2021;
[Pubmed] | [DOI]
2 Evolutionary trilogy of malaria, angiotensin II and hypertension: deeper insights and the way forward
Auley De,Aparna Tiwari,Veena Pande,Abhinav Sinha
Journal of Human Hypertension. 2021;
[Pubmed] | [DOI]
3 Age and genotype dependent erythropoietin protection in COVID-19
Konstantinos I Papadopoulos, Warachaya Sutheesophon, Somjate Manipalviratn, Tar-Choon Aw
World Journal of Stem Cells. 2021; 13(10): 1513
[Pubmed] | [DOI]
4 Human Angiotensin-Converting Enzyme may be under malaria selection pressure: a need to explore
Aparna Tiwari,Auley De,Veena Pande,Abhinav Sinha
Human Cell. 2020;
[Pubmed] | [DOI]
5 The Malaria-High Blood Pressure Hypothesis: Revisited
Chukwuemeka R Nwokocha,Enitome E Bafor,Olutayo I Ajayi,Anthony B Ebeigbe
American Journal of Hypertension. 2020;
[Pubmed] | [DOI]
6 Epidemiological links between malaria parasitaemia and hypertension
Ikenna C. Eze,Fidèle K. Bassa,Clémence Essé,Siaka Koné,Félix Acka,Véronique Laubhouet-Koffi,Dinard Kouassi,Jürg Utzinger,Bassirou Bonfoh,Eliézer K. N’Goran,Nicole Probst-Hensch
Journal of Hypertension. 2019; 37(7): 1384
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Materials and Me...
Article Tables

 Article Access Statistics
    PDF Downloaded264    
    Comments [Add]    
    Cited by others 6    

Recommend this journal