{"title":"镰状细胞特征(AS)个体对恶性疟原虫感染的耐药性是否与高频率接触珠蛋白Hp2-1有关?","authors":"A. Elagib, Hiba Mirgani","doi":"10.5251/AJSIR.2013.4.2.253.256","DOIUrl":null,"url":null,"abstract":"Sickle cell anemia is a haemoglobinpathy due to a single point mutation in the -chain of human haemoglobin. A hospital based case control study was done on the paediatric section in Khartoum Teaching hospital to investigate the role of haptoglobin phenotypes among sickle cell disease patients. A total number of 127 sickle disease patients and 34 healthy controls were screened for Hb phenotypes. Out of 88 homozygous sickle cell anaemia patients (HbSS), 77.3% patients had the Hp 1-1 phenotype, 22.7% had the Hp 2-1 phenotype, and none of them had Hp 2-2 type. Out of the 39 sickle cell trait (HbAS) individuals, 41% individuals had Hp1-1 phenotype, 59% had Hp21 phenotype and none of them had the Hp 2-2 phenotypes. Out of the 34 healthy controls (HbAA), 44% had Hp 1-1 phenotype, 38% had Hp 2-1 phenotype and 18% had Hp2-2 phenotype. There was a highly significant difference in the distribution of haptoglobin phenotypes among the three groups (P = 0.0001). The sickle cell trait (AS) had high frequency of Hp2-1. The sickle cell disease individuals (SS) had higher frequencies of Hp1-1. In conclusion, Malaria infection among the sickle cell homozygous (SS) individuals may be related to the high frequency of Hp1-1 and the protection of sickle cell trait (AS) against malaria infection may be due to the high frequency of haptoglobin phenotype 2-1.","PeriodicalId":7661,"journal":{"name":"American Journal of Scientific and Industrial Research","volume":"100 1","pages":"253-256"},"PeriodicalIF":0.0000,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Is resistance to P. falciparum infection in sickle cell trait (AS) individuals is related to presence of high frequencies of haptoglobin Hp2-1?\",\"authors\":\"A. Elagib, Hiba Mirgani\",\"doi\":\"10.5251/AJSIR.2013.4.2.253.256\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Sickle cell anemia is a haemoglobinpathy due to a single point mutation in the -chain of human haemoglobin. A hospital based case control study was done on the paediatric section in Khartoum Teaching hospital to investigate the role of haptoglobin phenotypes among sickle cell disease patients. A total number of 127 sickle disease patients and 34 healthy controls were screened for Hb phenotypes. Out of 88 homozygous sickle cell anaemia patients (HbSS), 77.3% patients had the Hp 1-1 phenotype, 22.7% had the Hp 2-1 phenotype, and none of them had Hp 2-2 type. Out of the 39 sickle cell trait (HbAS) individuals, 41% individuals had Hp1-1 phenotype, 59% had Hp21 phenotype and none of them had the Hp 2-2 phenotypes. Out of the 34 healthy controls (HbAA), 44% had Hp 1-1 phenotype, 38% had Hp 2-1 phenotype and 18% had Hp2-2 phenotype. There was a highly significant difference in the distribution of haptoglobin phenotypes among the three groups (P = 0.0001). The sickle cell trait (AS) had high frequency of Hp2-1. The sickle cell disease individuals (SS) had higher frequencies of Hp1-1. In conclusion, Malaria infection among the sickle cell homozygous (SS) individuals may be related to the high frequency of Hp1-1 and the protection of sickle cell trait (AS) against malaria infection may be due to the high frequency of haptoglobin phenotype 2-1.\",\"PeriodicalId\":7661,\"journal\":{\"name\":\"American Journal of Scientific and Industrial Research\",\"volume\":\"100 1\",\"pages\":\"253-256\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2013-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American Journal of Scientific and Industrial Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5251/AJSIR.2013.4.2.253.256\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Scientific and Industrial Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5251/AJSIR.2013.4.2.253.256","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Is resistance to P. falciparum infection in sickle cell trait (AS) individuals is related to presence of high frequencies of haptoglobin Hp2-1?
Sickle cell anemia is a haemoglobinpathy due to a single point mutation in the -chain of human haemoglobin. A hospital based case control study was done on the paediatric section in Khartoum Teaching hospital to investigate the role of haptoglobin phenotypes among sickle cell disease patients. A total number of 127 sickle disease patients and 34 healthy controls were screened for Hb phenotypes. Out of 88 homozygous sickle cell anaemia patients (HbSS), 77.3% patients had the Hp 1-1 phenotype, 22.7% had the Hp 2-1 phenotype, and none of them had Hp 2-2 type. Out of the 39 sickle cell trait (HbAS) individuals, 41% individuals had Hp1-1 phenotype, 59% had Hp21 phenotype and none of them had the Hp 2-2 phenotypes. Out of the 34 healthy controls (HbAA), 44% had Hp 1-1 phenotype, 38% had Hp 2-1 phenotype and 18% had Hp2-2 phenotype. There was a highly significant difference in the distribution of haptoglobin phenotypes among the three groups (P = 0.0001). The sickle cell trait (AS) had high frequency of Hp2-1. The sickle cell disease individuals (SS) had higher frequencies of Hp1-1. In conclusion, Malaria infection among the sickle cell homozygous (SS) individuals may be related to the high frequency of Hp1-1 and the protection of sickle cell trait (AS) against malaria infection may be due to the high frequency of haptoglobin phenotype 2-1.