Lim SK, Ferraro B, Moore K, Halliwell B, 2001. Role of haptoglobin in free hemoglobin metabolism. Redox Report. Commun Free Rad Res 6 :219–227.
Kristiansen M, Graversen JH, Jacobsen C, Sonne O, Hoffman HJ, Law SK, Moestrup SK, 2001. Identification of the haemoglobin scavenger receptor. Nature 409 :198–201.
Dobryszycka W, 1997. Biological functions of haptoglobin—new pieces to an old puzzle. Eur J Clin Chem Clin Biochem 35 :647–654.
Delanghe JR, Langlois MR, 2002. Haptoglobin polymorphism and body iron stores. Clin Chem Lab Med 40 :212–216.
Okazaki T, Nagai T, 1997. Difference in hemoglobin-binding ability of polymers among haptoglobin phenotypes. Clin Chem 43 :2012–2013.
Langlois M, Delanghe J, DeBuyzere M, 1996. Relation between serum IgA concentration and haptoglobin type. Clin Chem 42 :1722–1723.
McGuire W, D’Alessandro U, Olaleye BO, Thomson MC, Langerock P, Greenwood BM, Kwiatkowski D, 1996. C-reactive protein and haptoglobin in the evaluation of a community-based malaria control programme. Trans R Soc Trop Med Hyg 90 :10–14.
Trape JF, Fribourgblanc A, Bosseno MF, Lallemant M, Engler R, Mouchet J, 1985. Malaria, cause of ahaptoglobinemia in Africans. Trans R Soc Trop Med Hyg 79 :430–434.
Trape JF, Fribourgblanc A, 1988. Ahaptoglobinemia in African Populations and Its Relation to Malaria Endemicity. Am JEpidemiol 127 :1282–1288.
Elagib AA, Kider AO, Akerstrom B, Elbashir MI, 1998. Association of the haptoglobin phenotype (1-1) with falciparum malaria in Sudan. Trans R Soc Trop Med Hyg 92 :309–311.
Quaye IKE, Ekuban FA, Goka BQ, Adabayeri V, Kurtzhals JAL, Gyan B, Ankrah NA, Hviid L, Akanmori BD, 2000.Haptoglobin 1-1 is associated with susceptibility to severe Plasmodium falciparum malaria. Trans R Soc Trop Med Hyg 94 :216–219.
Bienzle U, Eggelte TA, Adjei LA, Dietz E, Ehrhardt S, Cramer JP, Otchwemah RN, Mockenhaupt FP, 2005. Short Communication: Limited influence of haptoglobin genotypes on severe malaria in Ghanaian children. Trop Med Int Health 10 :668–671.
Aucan C, Walley AJ, Greenwood BM, Hill AV, 2002. Haptoglobin genotypes are not associated with resistance to severe malaria in The Gambia. Trans R Soc Trop Med Hyg 96 :327–328.
Imrie H, Carter M, Hadjuk S, Day KP, 2004. Killing of Plasmodium falciparum by human serum haptoglobin. Mol Biochem Parasitol 133 :93–98.
Hunt NH, Driussi C, Sai-Kiang L, 2001. Haptoglobin and malaria. Redox Rep 6 :389–392.
Eaton JW, Brandt P, Mahoney JR, Lee JT Jr, 1982. Haptoglobin: a natural bacteriostat. Science 215 :691–693.
Delanghe J, Langlois M, Jin OY, Claeys G, DeBuyzere M, Wuyts B, 1998. Effect of haptoglobin phenotypes on growth of Streptococcus pyogenes. Clin Chem Lab Med 36 :691–696.
Weatherall DJ, Clegg JB, 2001. The Thalassaemia Syndromes. Oxford, UK: Blackwell Science.
Higgs D, Bowden DK, 2001. Clinical and laboratory features of the alpha-thalassemia syndromes. Steinburg M, Forget B, Higgs D, Nagel RL, eds. Disorders of Hemoglobin: Genetics, Pathophysiology, and Clinical Management. Cambridge, UK: Cambridge University Press, 431–469.
Poyart C, Wajcman H, 1996. Hemolytic anemias due to hemoglobinopathies. Mol Aspects Med 17 :129–142.
Weatherall DJ, 1998. Pathophysiology of thalassaemia. Baillieres Clin Haematol 11 :127–146.
Allen SJ, O’Donnell A, Alexander ND, Alpers MP, Peto TEA, Clegg JB, Weatherall DJ, 1997. alpha+-Thalassemia protects children against disease caused by other infections as well as malaria. Proc Natl Acad Sci USA 94 :14736–14741.
Sisay F, Byass P, Snow RW, Greenwood BM, Perrin LH, Yerly S, 1992. Measurement of serum haptoglobin as an indicator of the efficacy of malaria intervention trials. Trans R Soc Trop Med Hyg 86 :14–16.
Hill AVS, Whitehouse DB, Bowden DK, Hopkinson DA, Draper CC, Peto TEA, Clegg JB, Weatherall DJ, 1987. Ahaptoglobinemia in melanesia—DNA and malarial antibody studies. Trans R Soc Trop Med Hyg 81 :573–577.
Cattani JA, Tulloch JL, Vrbova H, Jolley D, Gibson FD, Moir JS, Heywood PF, Alpers MP, Stevenson A, Clancy R, 1986. The epidemiology of malaria in a population surrounding Madang, Papua New Guinea. Am J Trop Med Hyg 35 :3–15.
Burkot TR, Graves PM, Cattan JA, Wirtz RA, Gibson FD, 1987. The efficiency of sporozoite transmission in the human malarias, Plasmodium falciparum and P. vivax. Bull World Health Organ 65 :375–380.
Engwerda CR, Beattie L, Amante FH, 2005. The importance of the spleen in malaria. Trends Parasitol 21 :75–80.
Cox MJ, Kum DE, Tavul L, Narara A, Raiko A, Baisor M, Alpers MP, Medley GF, Day KP, 1994. Dynamics of malaria parasitaemia associated with febrile illness in children from a rural area of Madang, Papua New Guinea. Trans R Soc Trop Med Hyg 88 :191–197.
Bruce MC, Donnelly CA, Alpers MP, Galinski MR, Barnwell JW, Walliker D, Day KP, 2000. Cross-species interactions between malaria parasites in humans. Science 287 :845–848.
Flint J, Hill AV, Bowden DK, Oppenheimer SJ, Sill PR, Serjeantson SW, Bana-Koiri J, Bhatia K, Alpers MP, Boyce AJ, Weatherall DJ, Clegg JB, 1986. High frequencies of alpha-thalassaemia are the result of natural selection by malaria. Nature 321 :744–750.
Flint J, Harding RM, Boyce AJ, Clegg JB, 1993. The population genetics of the haemoglobinopathies. Baillieres Clin Haematol 6 :215–262.
O’Donnell A, Allen SJ, Mgone CS, Martinson JJ, Clegg JB, Weatherall DJ, 1998. Red cell morphology and malaria anaemia in children with Southeast-Asian ovalocytosis band 3 in Papua New Guinea. Br J Haematol 101 :407–412.
Brabin L, Brabin BJ, 1990. Malaria and glucose 6-phosphate de-hydrogenase deficiency in populations with high and low spleen rates in Madang, Papua New Guinea. Hum Hered 40 :15–21.
Hill AVS, Bowden DK, Flint J, Whitehouse DB, Hopkinson DA, Oppenheimer SJ, Serjeantson SW, Clegg JB, 1986. A population genetic survey of the haptoglobin polymorphism in melanesians by DNA analysis. Am J Hum Genet 38 :382–389.
Mastana SS, Bernal JE, Onyemelukwe GC, Papiha SS, 1994. Haptoglobin subtypes among 4 different populations. Hum Hered 44 :10–13.
Harvey PW, Heywood PF, Nesheim MC, Galme K, Zegans M, Habicht JP, Stephenson LS, Radimer KL, Brabin B, Forsyth K, Alpers M, 1989. The effect of iron therapy on malarial infection in Papua New Guinean schoolchildren. Am J Trop Med Hyg 40 :12–18.
Chong SS, Boehm CD, Higgs DR, Cutting GR, 2000. Single-tube multiplex-PCR screen for common deletional determinants of alpha-thalassemia. Blood 95 :360–362.
Jarolim P, Palek J, Amato D, Hassan K, Sapak P, Nurse GT, Rubin HL, Zhai S, Sahr KE, Liu SC, 1991. Deletion in erythrocyte band 3 gene in malaria-resistant Southeast Asian ovalocytosis. Proc Natl Acad Sci U S A 88 :11022–11026.
Fowkes FJ, Imrie H, Migot-Nabias F, Michon P, Justice A, Deloron P, Luty AJ, Day KP, 2006. Association of haptoglobin levels with age, parasite density, and haptoglobin genotype in a malaria-endemic area of Gabon. Am J Trop Med Hyg 74 :26–30.
Venables WN, Ripley BD, 2002. Modern Applied Statistics with S. New York: Springer-Verlag.
Development R Core Team, 2005. R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing.
Yenchitsomanus PT, Summers KM, Bhatia KK, Cattani J, Board PG, 1985. Extremely high frequencies of alpha-globin gene deletion in Madang and on Kar Kar Island, Papua New Guinea. Am J Hum Genet 37 :778–784.
Allen SJ, O’Donnell A, Alexander ND, Mgone CS, Peto TE, Clegg JB, Alpers MP, Weatherall DJ, 1999. Prevention of cerebral malaria in children in Papua New Guinea by southeast Asian ovalocytosis band 3. Am J Trop Med Hyg 60 :1056–1060.
Serjeantson SW, Board PG, Bhatia K, 1992. Population genetics in Papua New Guinea: a perspective on human evolution. Attenborough R, Alpers MP, eds. Human Biology in Papua New Guinea. Oxford, UK: Clarendon Press, 198–233.
Schneweis S, Maier WA, Seitz HM, 1991. Haemolysis of infected erythrocytes–a trigger for formation of Plasmodium falciparum gametocytes? Parasitol Res 77 :458–460.
Ritchie RF, Palomaki GE, Neveux LM, Navolotskaia O, Ledue TB, Craig WY, 2000. Reference distributions for the positive acute phase serum proteins, alpha1-acid glycoprotein (orosomucoid), alpha1-antitrypsin, and haptoglobin: a practical, simple, and clinically relevant approach in a large cohort. J Clin Lab Anal 14 :284–292.
Curtain CC, Gajdusek DC, Kidson C, Gorman JG, Champness L, Rodrigue R, 1965. Haptoglobins and transferrins in Melanesia: relation to hemoglobin, serum haptoglobin and serum iron levels in population groups in Papua New Guinea. Am J Phys Anthropol 23 :363–379.
Rosales FJ, Topping JD, Smith JE, Shankar AH, Ross AC, 2000. Relation of serum retinol to acute phase proteins and malarial morbidity in Papua New Guinea children. Am J Clin Nutr 71 :1582–1588.
Marinkovic S, Baumann H, 1990. Structure, hormonal-regulation, and identification of the interleukin-6-responsive and dexa-methasoneresponsive element of the rat haptoglobin gene. Mol Cell Biol 10 :1573–1583.
McFaul SJ, Bowman PD, Villa VM, 2000. Hemoglobin stimulates the release of proinflammatory cytokines from leukocytes in whole blood. J Lab Clin Med 135 :263–269.
Liu X, Spolarics Z, 2003. Methemoglobin is a potent activator of endothelial cells by stimulating IL-6 and IL-8 production and E-selectin membrane expression. Am J Physiol Cell Physiol 285 :C1036–C1046.
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Haptoglobin (Hp) is an acute phase protein that removes free hemoglobin (Hb) released during hemolysis. Hp has also been shown to be toxic for malaria parasites. α+-Thalassemia is a hemoglobinopathy that results in subclinical hemolytic anemia. α+-Thassemia homozygosity confers protection against severe malarial disease by an as yet unidentified mechanism. Hp levels were measured in a serial cross-sectional survey of children in Madang Province, Papua New Guinea (PNG). Hp levels were related to age, Hp genotype, Hb levels, parasitemia, splenomegaly, and α+-thalassemia genotype. Surprisingly, children who were homozygous for α+ -thalassemia had significantly higher levels of Hp than did heterozygotes, after controlling for relevant confounders. We suggest that this is the result of either reduced mean cell Hb associated with α+ -thalassemia homozygosity or an elevated IL-6–dependent acute phase response.