Objective: Human immunodeficiency virus (HIV)-infected patients, especially those on antiretrovirals are at risk of cardiovascular disease (CVD). The haemorheologic and fibrinolgtic activity of treatment naïve Nigerian HIV-infected patients were investigated.
Methods: Blood was collected from 50 newly diagnosed treatment naïve HIV-infected patients and 50 apparently healthy HIV seronegative individuals that served as controls. Haematocrit values, plasma and serum viscosity, plasma fibrinogen concentration and
euglobin lysis time were determined. Result: The mean ± standard deviation of haematocrit value of HIV infected patients (31.70 ± 6.33%) was significantly lower (

Adeghe, JE

Ekeh, CC

Ogefere, HO

Omokaro, EU

Omoregie, R

English

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African Health Sciences Vol 8 No 4 December 2008 217Haemorheologic and fibrinolytic activity in Nigerian HIV infectedpatients.Richard Omoregie1,2*, Judith E. Adeghe2, Helen O. Ogefere1, Evelyn U. Omokaro2 And Chinedu C.Ekeh2.1 Department Of Medical Microbiology, School of Medical Laboratory Science, University of Benin Teaching Hospital P.M.B.1111, Benin City, Edo State, Nigeria.2 Department of Haematology and Blood Transfusion Science, School Of Medical Laboratory Science, University Of BeninTeaching Hospital, P.M.B. 1111, Benin City, Edo State, Nigeria.AbstractObjective: Human immunodeficiency virus (HIV)-infected patients, especially those on antiretrovirals are at risk of cardiovasculardisease (CVD). The haemorheologic and fibrinolgtic activity of treatment naïve Nigerian HIV-infected patients were investigated.Methods: Blood was collected from 50 newly diagnosed treatment naïve HIV-infected patients and 50 apparently healthy HIVseronegative individuals that served as controls. Haematocrit values, plasma and serum viscosity, plasma fibrinogen concentration andeuglobin lysis time were determined.Result: The mean ± standard deviation of haematocrit  value of HIV infected patients (31.70 ± 6.33%) was significantly lower(p<0.0001) than those of controls (39.50 ± 2.43%). The plasma serum viscosity, plasma fibrinogen concentration and euglobin lysistime of HIV-infected patients were significantly higher compared with those of controls (p<0.0001).Conclusion: Treatment naive Nigerian HIV-infected patients have a defective blood flow and fibrinolytic system, which maypredispose them to CVD.Key words: Haemorheology, Fibrinolytic activity, HIV, Cardiovascular disease, HIV Treatment naïve, Nigerian.African Health Sciences 2008; 8(4): 217-219Corresponding AuthorRichard OmoregieDepartment Of Medical Microbiology,School of Medical Laboratory Science,University of Benin Teaching Hospital P.M.B. 1111, Benin City, Edo State, Nigeria.Telephone - +2348029582386Email: richyomos@yahoo.comIntrdouctionHuman immunodeficiency virus (HIV)-infected patientshave been reported to be at risk of cardiovascular diseases(CVD), mostly due to the use of antiretroviral agents 1,2.Protease inhibitors have been mostly implicated3. Allthese are also connected to fat redistributiondyslipidaemia and insulin resistance observed in HIVpatients 4,5.Plasminogen activator inhibitor-1 (PAI-1) andtissue type plasminogen activator (tPA) antigens,markers of inpaired fibrinolysis and increased CVD risk,are increased in association with hyperinsulinaemia inpatients with HIV and fat redistribution1. This indicatesthat the CVD observed among HIV patients is connectedto fibrinolytic activity. Also, it has been reported thatHIV-infected patient have a defective blood flow system6, thus predisposing them to CVD.Being of African origin has been reported as arisk factor for anaemia among HIV-infected patients7,thus in this study, we report on the haemorheologic andfibrinolytic activity of treatment naive Nigerian HIV-infected patients.Materials and methodsStudy Population:A total of 100 subjects consisting of 50 newly diagnosedtreatment navie HIV positive patients and 50 apparentlyhealthy HIV sero-negative individuals that served ascontrols were used in this study. The HIV patients wereattending the heart-to-heart clinic in Central HospitalBenin City. Verbal informed consent was obtained fromall subjects (HIV positive and controls). The controlswere matched with the HIV patients for age and gender.The protocol for this study was approved by the EthicalCommittee of Central Hospital Benin City, Nigeria.Ten milliliter of blood was obtained from eachsubject and 4.5ml was dispensed into a 0.5ml 3.8%sodium citrate container. The remaining blood samplewas dispensed into a plain container, allowed to clot andthe serum used for serum viscosity test.Determination of Haematocrit Values andPlasma Fibrinogen Concentration.Haematocrit values were estimated manually while theplasma fibrinogen concentration was estimated using themethod of Millar et al (8). Briefly, two microhaematocritAfrican Health Sciences Vol 8 No 4 December 2008218tubes were about three-quarters of their length filledwith citrated blood and sealed on one end followingcentrifugation for 5mins at 12,000g (Hawksley,haematocrit centrifuge; Hawksley, England), thehaematocrit values is read with a Hawksley haematocritreader. The capillary tubes were then placed inside a waterbath at 56% for 3mins and re-centrifuaged for 3mins at12,000g. The thickness of the precipitated fibrinogenwas measured under a binocular lens microscope fittedwith a calibrated eyepiece micrometer. The fibrinogenconcentration (g/L) was estimated as the ratio offibrinogen precipitate to the total height of plasma plusfibrinogen and multiplied by 100. The mean of the 2tubes was taken.Determination of Plasma and Serum Viscosities.A modification of the method of Reid and Ugwu (9)was used. A 1ml syringe with a hypodermic needle (21.6x 0.8 x 4mm) was used. Briefly, plasma or serum wasdrawn into the syringe, avoiding or bubbles, till the 1.0mlmark. The plunger was carefully, removed and the timetaken for the entire plasma or serum to drain was noted.This was done twice for each sample and the averagetaken for that sample. The entire process was repeatedusing distilled water. The plasma or serum viscosity isthe ratio of the flow rate of plasma or serum to that ofwater.Determination of Euglobin Lysis Time.The method described by Omoigberale et al.  (10) wasused Briefly, to 9.5ml of 1% acetic acid in a test tube,0.5ml of citrated plasma was added and the tube kept at40C for 30mins to precipitate the euglobin fraction. Thetube is then centrifuged at 2000rpm for 10mins. Thesupernatant is discarded and the tube inverted to removeall acetic acid. The deposit was reconstituted with 0.5mlborate buffer (sodium borate, 1g, sodium chloride, 9gand distilled water, 1000ml). The tube was pre-warmedat 370C alongside calcium chloride (0,025M) for 2mins,and 0.5ml of the calcium chloride was added to thetube containing the deposit and borate buffer. A stopwatch was started immediately a clot was observed andthe time taken for the euglobin fraction to lysecompletely was recorded in minutes.Statistical AnalysisThe data were analyzed using unpaired student t-test.ResultThe range, mean ± standard deviation of haematocritvalues of HIV-infected patients and controls were 16-45%, 31.70 ± 6.33% and 35-46%, 39.50 ± 2.43%respectively. This differences was statistically significant(p<0.0001). The plasma viscosity serum viscosity,plasma fibrinogen concentration and euglobin lysis timewere significantly higher than those of controls(p<0.0001) (Table 1).Haematocrit (%)                     16-45         1.70 ± 6.33 (30.31, 33.01)35-46        39.50 ± 2.43 (38.17, 40.87) P < 0.0001Plasma Viscosity                      1.21-3.59  1.98 ± 0.34 (1.91,2.05) 1.06-1.35 1.22 ± 0.08 (1.16, 1.29) P < 0.0001Serum Viscosity                       0.98-4.02  1.94 ± 0.55 (1.83, 2.05) 1.06-1.48 1.24 ± 0.09 (1.13, 1.36) P < 0.0001Plasma Fibrinogen Concen.     1.33-9.67 5.13 ± 1.90 (4.74, 5.52)      2.00-4.00 2.90 ± 0.52 (2.51, 3.29) P < 0.0001(g/L)Euglobinlysis Time (mins)        243-1440  544 ± 401 (462.50, 624.90)115-274    189 ± 37.70 (105.70, 273.20) P < 0.0001x   = Mean, S.D = Standard deviation, CI = Confidence interval.Table 1: Comparison of haematologic parameters in HIV infected subjects and controlsHIV+ve sujects (n=50) Controls (n=50)Parameters Range   x   ±S.D (95%CI) Range  x   ±S.D (95%)                         p-valueDiscussionIn this study HIV-infected treatment naivepatients had a significantly lower haematocrit value thancontrols (p<0.0001). This observation is in line withearlier reports7,11. The haematocrit value affects theenythrocyte sedimentation rate which in turn affectsenythrocyte aggregation and ultimately blood flow6.Thus, HIV patients may be at risk of CVD. Haematocritvalues of HIV patients are usually used to check diseaseprogression and quality of life7. The introduction of thehighly active antiretroviral therapy (HAART) hasseriously improved haematocrit values and quality oflife of HIV patients11. Thus, the placement of thesepatients on HAART may improve their haematocritvalues. The increase in plasma viscosity observed amongHIV patients in this study correlates with the observedincrease in plasma fibrinogen concentration. Fibrinogenconcentration significantly affects plasma viscosity. TheseAfrican Health Sciences Vol 8 No 4 December 2008 219findings agree with earlier reports6,12. It has beenreported that increase in fibrinogen concentration (andby extension plasma viscosity) is a risk factor for CVD13. Increase in serum viscosity has similar effect. Bothplasma and serum viscosity are useful indicators of acuteinflammation. Increase in inflammatory proteins suchas haptoglobin, c-reactive proteins and immunoglobulinsproduced against the HIV virus or any otheropportunistic infection associated with HIV, cause anincrease in serum viscosity.Impaired fibrinolysis is a risk factor for CVD.Fibrinolytic activity can be measured either bydetermining the euglobin lysis time (ELT) or theconcentrations of PAI-1 and tPA, etc. In this study, theELT was measured and found to be significantly higher(p<0.0001) in HIV patients than controls. This means alower or defective fibrinolytic activity in HIV patients.Increase in both PAI-1 and tPA have been reported inHIV patients1. In the ELT method used in this study, theeuglobin consist of tPA, plasminogen and fibrinogen. 10tPA antigen assays measure both free tPA and inactivetPA complexed with PAI-1(1). If follows therefore, thatthe defective fibrinolytic system in HIV patients is dueto very low levels of free tPA.These findings suggest a likely problem inmanagement of HIV patients, as some antiretrovirals,though improving haematocrit value, predispose toCVD. Those in the management of these patients shouldbear in mind the associated risk of CVD.In conclusion, this study reveals that treatmentnaïve Nigerian HIV patients have a defective blood flowand fibrinolytic system, which are important risk factorsfor CVD.AcknowledgementWe acknowledge with thanks the management and Staffof Central Hospital Benin City for their permission tocarry out this study.References1. Hadigan, C., Meigs, J.B., Rabe, J., D., et al.  Increased PAI-1 and tPA antigen levels, are reduced, with metformintherapy in HIV-infected patients with fat redistribution andinsulin resistance.  J. Clin. Endocrinol. Metab. 2001; 86:939-943.2. Andrade, A.C.O., Cotter, B.R. Endothelial Function andVascular diseases in HIV infected patient. Braz. J. Infect.Dis. 2006; 10 (2): 139-145.3. Barbaro, G. HIV infection, highly active antiretroviraltherapy and the cadiovascular system, Cardiovasc. Res. 2003;111 (3): 389-397.4. Carr, A., Samaras, K., Thorisdottir, A., Kauffman, G.R.,Chisolm, D.J., Cooper, D.A. Diagnosis, prediction andnatural course of HIV-1 protease-inhibitor associatedlipodystrophy, hyperlipidemia, and diabetes mellitus; acohort study. Lancet. 1999; 353: 2093-2099.5. Hadigan, C., Miller, K., Corcoran, C., Anderson, E., Basgoz,N., Grinspoon, S., Fasting hyperinsulinemia and changes inregional body composition in HIV-infected women. J. Clin.Endocrinol. Metab. 1999; 84: 1932-1937.6. Kim, A., Dadgostar, H., Holland, G.N.., et al.Hemorheologic abnormalities associated with HIV infection:altered erythrocyte aggregation and deformability. Invest.Opthalmol. Vis. Sci. 2006; 47: 3927-3932.7. Moyle, G. Anaemia in persons with HIV infection;prognostic marker and contributor to morbidity. AIDS Rev.2002; 4:  13-18.8. Millar, H.R., Simpson, J.G., Stalker, A.L. An evaluation ofthe heat precipitation method for plasma fibrinogenestimation. J. Clin. Path. 1971; 24: 827-830.9. Reid, H., Ugwu, A.C.A Simple technique of rapiddetermination of plasma and whole blood Viscosity. Nig. J.Physiol. Sci. 1987; 3: 45-48.10. Omoigberale, A.I., Abiodun, P.O., Famodu, A.A.Fibrinolytic activity in children with Plasmodium falciparummalaria. East Afr. Med. J. 2005; 82 (2): 104-106.11. Odunukwe, N., Idigbe, O., Kanki, P.., et al Haematologicaland biochemical response to treatment of HIV-1 infectionwith a combination of nevirapine + stavudine + Lamivudinein Lagos Nigeria. Turk. J. Haematol. 2005; 22 (3): 125-131.12. Wilkins, E.G., Fraser, I.,Barnes, A., Khoo, S., Hamour, A.Plasma viscosity in HIV infection. Int. Conf. AIDs. 1992; 8:143 (Abstract No. PUB 7587).13. Dintenfass, L., Kammer, S. Re-evaluation of heatprecipitation method for plasma fibrinogen estimation: effectof abnormal proteins and plasma viscosity. J. Clin. Path.1976; 29: 130-134.

Haemorheologic and fibrinolytic activity in Nigerian HIV infected

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Haemorheologic and fibrinolytic activity in Nigerian HIV infected

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