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
Main Authors: OTIENO, Richard O, OUMA, Collins, ONG'ECHA, John M, KELLER, Christopher C, WERE, Tom, WAINDI, Eliud N, MICHAELS, Marian G, DAY, Richard D, VULULE, John M, PERKINS, Douglas J
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Language:English
Published: 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.
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
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  fullname: OUMA, Collins
  organization: University of Pittsburgh/KEMRI Laboratories of Parasitic and Viral Diseases, Centre for Vector Biology and Control Research, Kisumu, Kenya
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  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
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  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
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  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
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  surname: WAINDI
  fullname: WAINDI, Eliud N
  organization: Department of Zoology, Maseno University, Kisumu, Kenya
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  givenname: Marian G
  surname: MICHAELS
  fullname: MICHAELS, Marian G
  organization: Department of Pediatrics, University of Pittsburgh Children Hospital, Pittsburgh, Pennsylvania, United States
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  givenname: Richard D
  surname: DAY
  fullname: DAY, Richard D
  organization: Department of Biostatistics, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
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  givenname: John M
  surname: VULULE
  fullname: VULULE, John M
  organization: Kenya Medical Research Institute, Centre for Vector Biology and Control Research, Kisumu, Kenya
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  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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Issue 2
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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References Nguyen-Dinh (R1-17-20210130) 1987; 65
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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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StartPage 275
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
URI https://www.ncbi.nlm.nih.gov/pubmed/16511422
https://search.proquest.com/docview/19289692
https://search.proquest.com/docview/67706253
Volume 20
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