CD36 deficiency is frequent and can cause platelet immunization in Africans

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Abstract
BACKGROUND: CD36 is expressed on several cell lineages. About 5 to 10 percent of Asians lack platelet membrane CD36 (pCD36), but the frequency of pCD36 deficiency in other ethnic groups is not known. Persons who are pCD36‐negative are apparently healthy but can develop CD36 isoimmunization. STUDY DESIGN AND METHODS: The pCD36 phenotype was studied in 1885 subjects belonging either to a group of 1127 healthy French blood donors (almost all of whom were white Europeans) or to a group of 758 patients of known ethnic origin. RESULTS: No pCD36‐negative persons were found among the blood donors. Only 1 of the 301 white European patients was pCD36‐negative. In contrast, 16 of the 206 sub‐Saharan Africans was pCD36‐negative, a proportion higher than that among that black Caribbeans (1/148, p<0.01). The frequency of pCD36‐negative patients was similar in blacks with and without sickle cell disease. Monocyte CD36 (mCD36) expression was studied in 15 of 22 pCD36‐negative individuals: it was <10 percent in 7 subjects (type I deficiency) and between 12 and 100 percent in 8 others (type II deficiency). Thirteen pCD36‐negative individuals had risk factors for immunization, and 4 had anti‐CD36. Some had a history resembling posttransfusion purpura (n = 2), platelet transfusion refractoriness (n = 1), and recurrent miscarriage (n = 1). No correlation was found between immunization and the amount of mCD36. Anti‐CD36 from an immunized type II‐deficient woman reacted with monocytes from normal controls but not with monocytes from type I‐ or type II‐deficient individuals, and thus it is postulated that mCD36 could be structurally different in normal and type II CD36‐deficient individuals. CONCLUSION: CD36 deficiency is frequent in sub‐Saharan Africans; development of anti‐CD36 can lead to serious complications in multiply transfused patients, such as those with sicke cell disease.