Tossea Stephane Koui, Adji Eric Gbessi, Coulibaly Baba, Ako Berenger Ako, Coulibaly David Ngolo, Joly Philippe, Assi Serge-Brice, Toure Andre, Jambou Ronan
Departement de Parasitologie Mycologie, Institut Pasteur de Côte d'Ivoire, BP 490, Abidjan 01, Côte d'Ivoire.
Univ Lyon, University Claude Bernard Lyon 1, EA 7424, Lyon, France.
BMC Res Notes. 2018 Apr 2;11(1):215. doi: 10.1186/s13104-018-3296-7.
Sickle cell anemia is due to a mutations on the betaglobin gene, inducing abnormal hemoglobin. In West Africa the main mutations lead to S or C types of hemoglobin. Patients with homozygote mutations seem protected against severe malaria, but not against mild disease. The prevalence of abnormal hemoglobin among patients attending dispensaries for mild malaria is thus unknown. A retrospective study was conducted to update data on the prevalence of S and C hemoglobin among patients attending dispensaries with mild malaria. Enrolment of patients was conducted during in vivo malaria treatment efficacy survey following the 42 days WHO protocol. A group of non-infected pregnant women and a group of patients with fever different from malaria, were also recruited in the same dispensaries.
794 blood samples were included. S and C genotypes were found in all the regions of Ivory Coast with the highest prevalence in the Northern region (S and C genotypes, 27%). In non-infected patients, prevalence of mutations was higher than in malaria patients.
A high proportion of patients with mild malaria carried genetic hemoglobin disorder. This population of high risk must be better investigated to control treatment efficacy and to manage complications.
镰状细胞贫血是由β珠蛋白基因突变引起的,会导致异常血红蛋白。在西非,主要的突变会导致血红蛋白出现S型或C型。纯合子突变患者似乎对严重疟疾有抵抗力,但对轻度疾病没有抵抗力。因此,在治疗轻度疟疾的诊所就诊的患者中,异常血红蛋白的患病率尚不清楚。进行了一项回顾性研究,以更新在治疗轻度疟疾的诊所就诊的患者中S型和C型血红蛋白患病率的数据。在按照世界卫生组织42天方案进行的体内疟疾治疗疗效调查期间招募患者。在同一诊所还招募了一组未感染的孕妇和一组患有非疟疾发热的患者。
共纳入794份血样。在科特迪瓦的所有地区均发现了S型和C型基因型,其中北部地区的患病率最高(S型和C型基因型,27%)。在未感染患者中,突变的患病率高于疟疾患者。
很大一部分轻度疟疾患者携带遗传性血红蛋白疾病。必须对这一高危人群进行更好的调查,以控制治疗效果并处理并发症。