Increased severe anemia in HIV-1-exposed and HIV-1-positive infants and children during acute malaria
Since the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote life-threatening severe malarial anemia (SMA). The primary objective of the study was to determine if HIV-1 exposure [HIV-1(exp)] and/or HIV-1 infection [HIV-1(+)...
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Published in: | AIDS (London) Vol. 20; no. 2; pp. 275 - 280 |
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Hagerstown, MD
Lippincott Williams & Wilkins
09-01-2006
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Abstract | Since the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote life-threatening severe malarial anemia (SMA). The primary objective of the study was to determine if HIV-1 exposure [HIV-1(exp)] and/or HIV-1 infection [HIV-1(+)] increased the prevalence of SMA in children with acute malaria.
The effect of HIV-1 exposure and HIV-1 infection on the prevalence of SMA (hemoglobin < 6.0 g/dl), parasitemia (parasites/microl), and high-density parasitemia (HDP, >or= 10 000 parasites/mul) was investigated in children <or= 2 years of age presenting at hospital with acute Plasmodium falciparum malaria in a rural holoendemic malaria transmission area of western Kenya.
Upon enrollment, a complete hematological and clinical evaluation was performed on all children. Malaria parasitemia was determined and children with acute P. falciparum malaria were evaluated for HIV-1 exposure and infection by two rapid serological antibody tests and HIV-1 DNA PCR, respectively.
Relative to HIV-1(-) group (n = 194), the HIV-1(exp) (n = 100) and HIV-1(+) (n = 23) groups had lower hemoglobin concentrations (P < 0.001 and P < 0.001, respectively), while parasitemia and HDP were equivalent between the three groups. Multivariate analyses demonstrated that the risk of SMA was elevated in HIV-1(exp) children (odds ratio, 2.17; 95% confidence interval, 1.25-3.78; P < 0.01) and HIV-1(+) children (odds ratio, 8.71; 95% confidence interval, 3.37-22.51; P < 0.0001). The multivariate model further revealed that HIV-1 exposure or infection were not significantly associated with HDP.
Results presented here demonstrate that both HIV-1 exposure and HIV-1 infection are associated with increased prevalence of SMA during acute P. falciparum infection, independent of parasite density. |
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AbstractList | Since the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote life-threatening severe malarial anemia (SMA). The primary objective of the study was to determine if HIV-1 exposure [HIV-1(exp)] and/or HIV-1 infection [HIV-1(+)] increased the prevalence of SMA in children with acute malaria.
The effect of HIV-1 exposure and HIV-1 infection on the prevalence of SMA (hemoglobin < 6.0 g/dl), parasitemia (parasites/microl), and high-density parasitemia (HDP, >or= 10 000 parasites/mul) was investigated in children <or= 2 years of age presenting at hospital with acute Plasmodium falciparum malaria in a rural holoendemic malaria transmission area of western Kenya.
Upon enrollment, a complete hematological and clinical evaluation was performed on all children. Malaria parasitemia was determined and children with acute P. falciparum malaria were evaluated for HIV-1 exposure and infection by two rapid serological antibody tests and HIV-1 DNA PCR, respectively.
Relative to HIV-1(-) group (n = 194), the HIV-1(exp) (n = 100) and HIV-1(+) (n = 23) groups had lower hemoglobin concentrations (P < 0.001 and P < 0.001, respectively), while parasitemia and HDP were equivalent between the three groups. Multivariate analyses demonstrated that the risk of SMA was elevated in HIV-1(exp) children (odds ratio, 2.17; 95% confidence interval, 1.25-3.78; P < 0.01) and HIV-1(+) children (odds ratio, 8.71; 95% confidence interval, 3.37-22.51; P < 0.0001). The multivariate model further revealed that HIV-1 exposure or infection were not significantly associated with HDP.
Results presented here demonstrate that both HIV-1 exposure and HIV-1 infection are associated with increased prevalence of SMA during acute P. falciparum infection, independent of parasite density. Objective: Since the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote life-threatening severe malarial anemia (SMA). The primary objective of the study was to determine if HIV-1 exposure [HIV-1(exp)J and/or HIV-1 infection [HIV-1 (+)] increased the prevalence of SMA in children with acute malaria. Design: The effect of HIV-1 exposure and HIV-1 infection on the prevalence of SMA (hemoglobin < 6.0 g/dl), parasitemia (parasites/[mu]l), and high-density parasitemia (HDP, >= 10 000 parasites/[mu]l) was investigated in children <= 2 years of age presenting at hospital with acute Plasmodium falciparum malaria in a rural holoendemic malaria transmission area of western Kenya. Methods: Upon enrollment, a complete hematological and clinical evaluation was performed on all children. Malaria parasitemia was determined and children with acute P. falciparum malaria were evaluated for HIV-1 exposure and infection by two rapid serological antibody tests and HIV-1 DNA PCR, respectively. Results: Relative to HIV-1 (-) group (n = 194), the HIV-1 (exp) (n = 100) and HIV-1 (+) (n = 23) groups had lower hemoglobin concentrations (P < 0.001 and P < 0.001, respectively), while parasitemia and HDP were equivalent between the three groups. Multivariate analyses demonstrated that the risk of SMA was elevated in HIV-1(exp) children (odds ratio, 2.17; 95% confidence interval, 1.25-3.78; P < 0.01) and HIV-1(+) children (odds ratio, 8.71; 95% confidence interval, 3.37-22.51; P < 0.0001). The multivariate model further revealed that HIV-1 exposure or infection were not significantly associated with HDP. Conclusions: Results presented here demonstrate that both HIV-1 exposure and HIV-1 infection are associated with increased prevalence of SMA during acute P. falciparum infection, independent of parasite density. OBJECTIVESince the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote life-threatening severe malarial anemia (SMA). The primary objective of the study was to determine if HIV-1 exposure [HIV-1(exp)] and/or HIV-1 infection [HIV-1(+)] increased the prevalence of SMA in children with acute malaria.DESIGNThe effect of HIV-1 exposure and HIV-1 infection on the prevalence of SMA (hemoglobin < 6.0 g/dl), parasitemia (parasites/microl), and high-density parasitemia (HDP, >or= 10 000 parasites/mul) was investigated in children <or= 2 years of age presenting at hospital with acute Plasmodium falciparum malaria in a rural holoendemic malaria transmission area of western Kenya.METHODSUpon enrollment, a complete hematological and clinical evaluation was performed on all children. Malaria parasitemia was determined and children with acute P. falciparum malaria were evaluated for HIV-1 exposure and infection by two rapid serological antibody tests and HIV-1 DNA PCR, respectively.RESULTSRelative to HIV-1(-) group (n = 194), the HIV-1(exp) (n = 100) and HIV-1(+) (n = 23) groups had lower hemoglobin concentrations (P < 0.001 and P < 0.001, respectively), while parasitemia and HDP were equivalent between the three groups. Multivariate analyses demonstrated that the risk of SMA was elevated in HIV-1(exp) children (odds ratio, 2.17; 95% confidence interval, 1.25-3.78; P < 0.01) and HIV-1(+) children (odds ratio, 8.71; 95% confidence interval, 3.37-22.51; P < 0.0001). The multivariate model further revealed that HIV-1 exposure or infection were not significantly associated with HDP.CONCLUSIONSResults presented here demonstrate that both HIV-1 exposure and HIV-1 infection are associated with increased prevalence of SMA during acute P. falciparum infection, independent of parasite density. |
Author | VULULE, John M WERE, Tom MICHAELS, Marian G OUMA, Collins WAINDI, Eliud N DAY, Richard D ONG'ECHA, John M PERKINS, Douglas J KELLER, Christopher C OTIENO, Richard O |
Author_xml | – sequence: 1 givenname: Richard O surname: OTIENO fullname: OTIENO, Richard O organization: Department of Zoology, Maseno University, Kisumu, Kenya – sequence: 2 givenname: Collins surname: OUMA fullname: OUMA, Collins organization: University of Pittsburgh/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Vector Biology and Control Research, Kisumu, Kenya – sequence: 3 givenname: John M surname: ONG'ECHA fullname: ONG'ECHA, John M organization: University of Pittsburgh/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Vector Biology and Control Research, Kisumu, Kenya – sequence: 4 givenname: Christopher C surname: KELLER fullname: KELLER, Christopher C organization: Department of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, United States – sequence: 5 givenname: Tom surname: WERE fullname: WERE, Tom organization: University of Pittsburgh/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Vector Biology and Control Research, Kisumu, Kenya – sequence: 6 givenname: Eliud N surname: WAINDI fullname: WAINDI, Eliud N organization: Department of Zoology, Maseno University, Kisumu, Kenya – sequence: 7 givenname: Marian G surname: MICHAELS fullname: MICHAELS, Marian G organization: Department of Pediatrics, University of Pittsburgh Children Hospital, Pittsburgh, Pennsylvania, United States – sequence: 8 givenname: Richard D surname: DAY fullname: DAY, Richard D organization: Department of Biostatistics, University of Pittsburgh, Pittsburgh, Pennsylvania, United States – sequence: 9 givenname: John M surname: VULULE fullname: VULULE, John M organization: Kenya Medical Research Institute, Centre for Vector Biology and Control Research, Kisumu, Kenya – sequence: 10 givenname: Douglas J surname: PERKINS fullname: PERKINS, Douglas J organization: University of Pittsburgh/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Vector Biology and Control Research, Kisumu, Kenya |
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Keywords | Human HIV-1 Immunopathology Pediatrics Protozoal disease hematological complications Malaria HIV-1 virus Anemia Acute Retroviridae AIDS Hemopathy Parasitosis Immune deficiency Lentivirus Infection Virus Viral disease Complication severe malarial anemia Human immunodeficiency virus Child pediatric HIV |
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Snippet | Since the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote life-threatening... Objective: Since the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote... OBJECTIVESince the primary hematological complication in both pediatric HIV-1 and malaria is anemia, co-infection with these pathogens may promote... |
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SubjectTerms | Acute Disease AIDS/HIV Anemia - blood Anemia - parasitology Anemia - virology Anemias. Hemoglobinopathies Biological and medical sciences Child, Preschool Developing Countries Diseases of red blood cells Female Hematocrit Hematologic and hematopoietic diseases Hemoglobins - analysis HIV Infections - complications HIV-1 - isolation & purification Human immunodeficiency virus 1 Human protozoal diseases Human viral diseases Humans Infant Infectious diseases Kenya Malaria Malaria, Falciparum - complications Male Medical sciences Parasitemia - complications Parasitic diseases Plasmodium falciparum Protozoal diseases Rural Health - statistics & numerical data Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids |
Title | Increased severe anemia in HIV-1-exposed and HIV-1-positive infants and children during acute malaria |
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