title: Haptoglobin phenotypes and malaria infection in pregnant women at delivery in western Cameroon.
abstract: Plasmodium falciparum-infected erythrocytes have been reported to sequester in the placenta by adhering to chondroitin 4-sulfate during pregnancy. Earlier studies have highlighted higher susceptibility of primigravidae to P. falciparum compared to multigravidae living within the same endemic areas. The haptoglobin phenotype (Hp1-1) has been associated with susceptibility to severe P. falciparum malaria and the presence of Hp in human endometrium has been reported. The possible role of different Hp phenotypes in susceptibility to or protection from placental infection by P. falciparum in both primigravid and multigravid women at delivery in western Cameroon was investigated in this study. Only the three major haptoglobin phenotypes; Hp1-1, Hp2-1 and Hp2-2, were found in the study population with the Hp1-1 phenotype being the predominant (53%). There was no significant difference in the distribution of the three Hp phenotypes between the two gravidity groups. Women carrying the Hp1-1 phenotype had higher parasite prevalences in both peripheral blood (21.6% against 9.1%) and placentas (42% against 16.7%) when compared to those with the Hp2-2 phenotype. The difference in the parasite density between women carrying the Hp1-1 and Hp2-2 phenotypes was statistically significant for placental infection (P=0.001) but not for maternal peripheral blood infection. Placental parasitaemias without peripheral blood parasitaemias were detected in 42.6% of all the P. falciparum positive women while 27.7% of the women had peripheral blood parasitaemias in the absence of placental infection and 29.8% of the women had both placental and peripheral blood parasitaemias. A statistically significant difference was observed between the primigravidae and multigravidae in the parasite density in placental biopsies (P=0.02) but not for maternal peripheral blood parasitaemia. Our data suggest that the Hp1-1 phenotype may play a role in susceptibility to placental infection by P. falciparum during pregnancy.
authors.affiliation: Department of Immunology, Wenner-Gren Institute, Stockholm University, SE-10691, Stockholm, Sweden.
authors.forename: Jacob T
authors.initials: JT
authors.lastname: Minang
authors.forename: Ben A
authors.initials: BA
authors.lastname: Gyan
authors.forename: Judith K
authors.initials: JK
authors.lastname: Anchang
authors.forename: Marita
authors.initials: M
authors.lastname: Troye-Blomberg
authors.forename: Hedvig
authors.initials: H
authors.lastname: Perlmann
authors.forename: Eric A
authors.initials: EA
authors.lastname: Achidi
mesh_terms: D000328:Adult; D002163:Cameroon / Q000453:epidemiology; D036861:Delivery, Obstetric; D004198:Disease Susceptibility / Q000097:blood / Q000469:parasitology; D004591:Electrophoresis, Polyacrylamide Gel; D005260:Female; D005312:Fetal Blood / Q000469:parasitology; D006242:Haptoglobins / Q000235:genetics*; D006801:Humans; D016778:Malaria, Falciparum / Q000097:blood* / Q000453:epidemiology / Q000517:prevention & control; D010641:Phenotype; D010920:Placenta / Q000469:parasitology; D011247:Pregnancy; D015995:Prevalence
chemical_list: D006242:Haptoglobins