American Journal of Microbiological Research
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American Journal of Microbiological Research. 2018, 6(2), 47-56
DOI: 10.12691/ajmr-6-2-3
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Immuno-hematological Profile Trends of HIV/AIDs Patients on HAART in the South West Region of Cameroon: Retrospective Medical Report Review for Possible Stratified follow-up Pattern in Low Income Settings

Simon Eyongabane Ako1, 2, , Longdoh Anna Njunda1, Eric Achidi Akum3, Pokam Thumamo Benjamin1, 4, Julius Clement Assob1, Jude Eteneneng Enoh1, 5, Wabo Bernard1 and Njiomegnie Gaitan Fabrice1

1Department of Medical Laboratory Sciences, Faculty of Health Science .University of Buea, P.O.Box 63, Buea, Cameroon

2Biaka University Institute of Buea, School of Health Science

3Faculty of Science, University of Buea, P.O. Box 63, Buea, Cameroon

4Noguchi Memorial Institute for Medical Research, University of Ghana, Legon- Accra, Ghana

5Laboratory of Endocrinology and Radio-element (LER), Medical Research Center (CRM), Institute of Medical Research and Medicinal Plants studies (IMPM)

Pub. Date: March 24, 2018

Cite this paper:
Simon Eyongabane Ako, Longdoh Anna Njunda, Eric Achidi Akum, Pokam Thumamo Benjamin, Julius Clement Assob, Jude Eteneneng Enoh, Wabo Bernard and Njiomegnie Gaitan Fabrice. Immuno-hematological Profile Trends of HIV/AIDs Patients on HAART in the South West Region of Cameroon: Retrospective Medical Report Review for Possible Stratified follow-up Pattern in Low Income Settings. American Journal of Microbiological Research. 2018; 6(2):47-56. doi: 10.12691/ajmr-6-2-3


Background: If found with people infected with human immunodeficiency virus (HIV), Immuno-hematological abnormalities can increase the risk of disease progression and death. Inorder to understand the pattern of the immune and hematology cells during Antiretroviral (ARV) therapy, we reviewed and analyse the immune-hematological profiles of HIV patients to determine the possible parameters and patterns that could be used to follow up patients in low income setting where the access of viral load testing is still not affordable. Methodology: A descriptive hospital based cross-sectional study of 285 HIV-1/AIDS adult patients on highly active antiretroviral therapy (HAART) was carried out from January to May, 2015. Review of participants records was also done to obtain baseline and other progressive data. A total of Four groups were created based on the patients duration on HAART. The composition was as follows: Group I (6months - 1year), group II (>1year - 3years), group III (>3years - 5years) and group IV (>5years). After the achieve data was obtain, venous blood was collected, and the number of CD4+ and CD8+ T cells count measured using a flow cytometer. The level of Hemoglobin, number of Platelets, total and differential White Blood Cells were enumerated with automated hematology analyzer. Analyses was carried out to determine changes in various parameters with respect to established baseline values. Results : The pattern for CD4+ T cell at stratified baseline count between < 99 - 499 cells/μl , showed a significant progressive increase from group I to group IV; while CD4+ T cell at stratified baseline count >500 cells/μl had a reversing turn, decreasing gradually among groups II, III and IV, and drastically in group I. The pattern for CD8+ T cell at stratified baseline count between <500 - 999 cells/μl, increased progressively from group I to IV, remaining at the normal range; while at stratified baseline count between >1000 cells/μl, the pattern decreased gradually from group I to IV, with group II showing a significant decrease. Also hemoglobin baseline level between <7 - 12g/dl, showed a pattern with significant increase among all groups to normal hemoglobin level. With platelets baseline between <150 - 399cells/μl, the pattern of all the groups increased and stayed within normal range, but platelets baseline at >400cells/μl showed a reversing turn, with significant decreases to normal level. Furthermore eosinophil baseline at <3%, showed a pattern of constant increase to abnormal levels in groups I,II and III; while group IV had a reversing decreasing pattern to normal levels meanwhile eosinophil baseline at > 3%, had a significant decreasing pattern from group I to IV. Leukocytes stratified baseline count at < 4000 cells/ μl had an irregular increasing pattern from group II to IV, then group I and finally group III, while leukocytes stratified baseline count at > 4000 cells/ μl had a similar pattern but reversed in group III and group I. in addition neutrophil at baseline count <40% had a significant progressive increasing pattern from group I to IV, but neutrophil baseline count >40% had an irregular increasing pattern from group II to group III, followed by group I and finally group IV. Conclusion: Group I profile can be used to detect early complications in patients using CD4+ T cell, hemoglobin, platelets, WBC, and neutrophils counts; while CD4+ T cell, hemoglobin, platelets, WBC, neutrophils count and CD8+ T cell baseline of >1000cells/ μL count can be used to monitor the patients’ successful treatment outcome on HAART in group II,III and IV. Starting ARV treatment with a CD4+ T cell of > 500 cells might not be advisable, we equally observed that eosinophils variation is associated with treatment duration. Further studies with larger sample sizes are recommended to make affirmative conclusions.

HIV AIDs HAART immunohematology parameters Treatment follow-up South West

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[1]  Tripathathi AK., Pramila K., Misra R., Kumar A., Neetu G. Study of bone marrow abnormalities in patients with HIV Disease. JAPI 2005; 53: 105-110.
[2]  Bain BJ. The haematological features of HIV infection. Br Journal Haematology, 1997; 99: 1-8.
[3]  Coyle TE. Management of the HIV infected patients. Part II. Med Clin North America 1997; 81: 449-470.
[4]  Saag MS., Holodniy M., Kuritzkes DR.. HIV viral load markers in clinical practice. Nature Medicine 1996; 2: 625.
[5]  WHO: HIV/AIDS Programme. Antiretroviral therapy for HIV infection in adults and adolescents: recommendations for public health approach. 2006 revision
[6]  Mathews SE., Srivastava D., Bala YR., Sharma A. Association of hematological profile of human immunodeficiency virus-positive patients with clinicoimmunologic stages of the disease. Journal of Laboratory Physicians, 2013; 5: 34-7.
[7]  Clinical and Laboratory Monitoring of Antiretroviral Therapy in Resource Limited and Unlimited Settings.WHO HIV/AIDS, Antiretroviral Newsletter. 2000; issue No 4.
[8]  Gifford R.J., De-Oliveira T., Rambaut A. UK collaborative Group on HIV Drug Resistance: Phylogenetic surveillance of viral genetic diversity and the evolving molecular epidemiology of human immunodeficiency virus type 1. Journal of Virology. 2007; 81 (23): 13050-56
[9]  Chu H., Gange S J., Yamashita T E., Hoover D R., Joan S. Chmiel J S., Margolick J B., and Jacobson L P. Individual Variation in CD4 Cell Count Trajectory among Human Immunodeficiency Virus-infected Men and Women on Long-term Highly Active Antiretroviral Therapy: An Application using a Bayesian Random Change-Point Model. American Journal of Epidemiology 2005; 162: 787-797.
[10]  Decks SG. Barbour JD., Grant RM., Martin JN., Duration and predictors of CD4 T cell gains in patients who continue combination therapy despite detectable plasma Viraemia. AIDS 2002; 16: 201-207.
[11]  Kamga HL., Assob JC., Njunda AL., Nde FP., Nsagha DS., Atanga MB., Weledji P., et al. The kidney function trends in human immunodeficiency virus/acquired immune deficiency syndrome (HIV/AIDS) patients at the Nylon District Hospital, Douala, Cameroon .Journal of AIDS and HIV Research, 2011; 3(2): 30-37.
[12]  Christian L., Charles K., Laurence V. Antiretroviral Drug Resistance and Routine Therapy, Cameroon. Emerging Infectious Diseases, 2006; 12(6): 1001-1004.
[13]  Fokam J., Salpini R., Santoro MM., et al. Drug resistance among drug-naive and first-line antiretroviral treatment-failing children in Cameroon. Pediatric Infectious Disease Journal 2011: 30(12); 1062-8.
[14]  Moh R, Danel C, Messou E, Ouassa T, Gabillard D, Anzain A, et al. Determinants of motality and morbidity following early antiretroviral therapy initiation in HIV- infected adults in West Africa. AIDS, 2007; 27: 2483-2491.
[15]  Henry DM., Kukwah AT., Mbunkah HA., Bernard AN., Pascal NA et al, Immunohaematologic and virologic responses and predictors of virologic failure in HIV-1 infected adults on firstline antiretroviral therapy in Cameroon. Infectious Diseases of Poverty 2014; 3: 5.
[16]  Christian LC., Gabriele LB., Aghokeng A., Jules B. Monitoring of HIV viral loads, CD4 counts and Clinical assessments versus clinical monitoring alone for antiretroviral therapy in rural district hospitals in Cameroon (Stratall ANRS 12110/ESTHER): a randomized non inferiority trial. 2011.
[17]  Moore D R., and Keruly C J. CD4+ Cell Count 6 Years after Commencement of Highly Active Antiretroviral Therapy in Persons with Sustained Virologic Suppression. Clinical Infectious Diseases 2007; 44: 441-6.
[18]  Michael CG, Kirk O, Mathiesen L, Nielsen SD. The naı¨ve CD4 count in HIV-1-infected patients at time of initiation of highly active anti-retroviral therapy is strongly associated with the level of immunological recovery. Scand J Infect Dis 2002; 34: 45-9.
[19]  kaufmann G R., Furrer H., Ledergerber B., Perrin L., Opravil M., Vernazza P., Cavassini M., Bernasconi E., Rickenbach M., Hirschel B., Battegay M. The Swiss HIV cohort study. Characteristics, determinants, and clinical relevance of CD4 T cell recovery to < 500 cells/μl in HIV type 1-infected individuals receiving potent antiretroviral therapy. Clinical Infectious Diseases 2005; 41: 361-372.
[20]  Autran B.,Carcelain G., Li TS.,Blanc C., Mathez D., Tubiana R., Katlama C., Debre P., Leibowitch. Positive effects of combined antiretroviral therapy on CD4+ Tcell homeostasis and function in advanced HIV disease. Science 1997; 277: 112-116.
[21]  Negredo E., Cruz L., Paredes R., Ruiz L., Fumaz CR., Bonjoch A., Gel S., Tuldra A., Montserrat Balague M., Johnston S., Arno A., Jou A., Tural C., Sirera G., Joan Romeu J., and Clotet B. Virological, Immunological, and Clinical Impact of Switching from Protease Inhibitors to Nevirapine or to Efavirenz in Patients with Human Immunodeficiency Virus Infection and Long-Lasting Viral Suppression. Clinical Infectious Diseases 2002; 34: 504-10.
[22]  Evans TG, Bonnez W, Soucier HR, et al. Highly active antiretroviral therapy results in a decrease in CD8+ T cell activation and preferential reconstitution of the peripheral CD4+ T cell population with memory rather than naive cells. Anviral Res 1998; 39: 163-73.
[23]  Brookmeyer R, Gail MH 1994. AIDS Epidemiology: A Quantitative Approach. New York, Oxford, 354 pp.
[24]  Hess C, Altfeld M, Thomas SY, Addo MM, Rosenberg ES, et al. (2004) HIV-1 specific CD8+T cells with an effector phenotype and control of viral replication. Lancet 363: 863-866.
[25]  van Baarle D, Kostense S, van Oers MH, Hamann D, Miedema F. Failing immune control as a result of impaired CD8+ T-cell maturation: CD27 might provide a clue. Trends Immunol 23 (12): 586-591, 2002.
[26]  Mocroft A, Kirk O, Barton SE, EuroSIDA Study Group (1999) Anemia is an independent predictive marker for clinical prognosis in HIV infected patients across Europe. AIDS 13: 943-950.
[27]  Huang SS, Barbour JD, Deeks SG, Huang SJ, Grant RM et al (2000) Reversal of human immunodeficiency Virus type 1-Associated hematosuppression by effective antiretroviral therapy. Clin Infect Dis 30: 504-510.
[28]  Ellaurie M, Bernstein LJ, Shah K et al (1986) Thrombocytopenia in Paediatrics AIDS. Blood 68:124a.
[29]  Landrø L, Ueland T, Otterdal K, Frøland SS, Aukrust P. Persistently raised plasma levels of platelet-derived inflammatory mediators in HIV-infected patients during highly active antiretroviral therapy. J Thromb Haemost. 2011 May; 9 (5): 1075-7.
[30]  Gleissner CA, von Hundelshausen, Ley K. Platelet chemokines in vascular disease. Arterioscler Thromb Vasc Biol 2008; 28: 1920-7.
[31]  Weyrich AS, Zimmerman GA. Platelets: signaling cells in the immune continuum. Trends Immunol 2004; 25: 489-95.
[32]  Berger EA, Murphy PM, Farber JM. Chemokine receptors as HIV-1 coreceptors: roles in viral entry, tropism, and disease. Annu Rev Immunol 1999; 17: 657-700.
[33]  Claudio M., Miriam L., Fabio M., Claudia D., Gabriele F., Gabriella D, Paola S and Vincenzo V. Improvement in neutrophil and monocyte function during highly active antiretroviral treatment of HIV-1-infected patients. AIDS 1999, 13: 883-890.
[34]  Elizabeth GK., Ruth N, Dalton W and Nyambura K. Impact of highly active antiretroviral therapy on hematological indices among HIV‑ 1 infected children at Kenyatta National Hospital‑ Kenya: retrospective study. AIDS Res Ther (2015) 12: 26.
[35]  Al Mohajer M, Villarreal-Williams E, Andrade RA, Giordano TP, Serpa JA. Eosinophilia and associated factors in a large cohort of patients infected with human immunodeficiency virus. South Med J. 2014 Sep; 107(9): 554-8.
[36]  Sivaram M, White A, Radcliffe KW. Eosinophilia: clinical significance in HIV-infected individuals. Int J STD AIDS. 2012 Sep; 23(9): 635-8.
[37]  Tietz A, Sponagel L, Erb P, Bucher H, Battegay M, Zimmerli W. Eosinophilia in patients infected with the human immunodeficiency virus. Eur J Clin Microbiol Infect Dis. 1997 Sep; 16(9): 675-7.