摘要
Introduction: Pubertal development is a process leading to the acquisition of reproductive capacities. Among the factors that inhibit pubertal development are chronic diseases including sickle cell anemia, which is a public health problem. Objectives: Describe the sociodemographic and clinical characteristics of adolescents with sickle cell disease. Report the prevalence of abnormalities of pubertal development. Identify associated factors that delay pubertal development. Patients and Methods: This was a multicenter analytical cross-sectional study over 7 months at the National Reference Center for Sickle Cell Disease and, at the Brazzaville University Hospital. It concerned adolescents with sickle cell disease aged between 10 to 19 years. The study focused on the sociodemographic characteristics of adolescents, the natural history of sickle cell anemia and the evaluation of secondary sexual characteristics using the Tanner classification. Nutritional status was assessed by calculating body mass index (BMI) and height/age and weight/age ratios. Results: Of the 347 adolescents included, the average age of the adolescents was 15.1 ± 2.5 years, 56.5% had normal puberty, 42.6% had delayed puberty and 0.9% had impuberty. The associated factors were under-nutrition with less than 3 meals/day (p = 0.0000), social status with more marked pubertal delay in orphans (p = 0.00127), more than 5 hospitalizations per year (p = 0.0013), pubertal delay was statistically significant in adolescents who had more than 3 vaso-occlusive crises (p = 0.0000), and those who had more than 5 blood transfusions since the discovery of the disease (p = 0.0127). Conclusion: The factors that hinder pubertal development in sickle cell patients are intrinsic (sickle cell anemia with its complications) and extrinsic (environmental: diet, social status). The appearance of secondary sexual characteristics is delayed on average by two years compared to the general population.
Introduction: Pubertal development is a process leading to the acquisition of reproductive capacities. Among the factors that inhibit pubertal development are chronic diseases including sickle cell anemia, which is a public health problem. Objectives: Describe the sociodemographic and clinical characteristics of adolescents with sickle cell disease. Report the prevalence of abnormalities of pubertal development. Identify associated factors that delay pubertal development. Patients and Methods: This was a multicenter analytical cross-sectional study over 7 months at the National Reference Center for Sickle Cell Disease and, at the Brazzaville University Hospital. It concerned adolescents with sickle cell disease aged between 10 to 19 years. The study focused on the sociodemographic characteristics of adolescents, the natural history of sickle cell anemia and the evaluation of secondary sexual characteristics using the Tanner classification. Nutritional status was assessed by calculating body mass index (BMI) and height/age and weight/age ratios. Results: Of the 347 adolescents included, the average age of the adolescents was 15.1 ± 2.5 years, 56.5% had normal puberty, 42.6% had delayed puberty and 0.9% had impuberty. The associated factors were under-nutrition with less than 3 meals/day (p = 0.0000), social status with more marked pubertal delay in orphans (p = 0.00127), more than 5 hospitalizations per year (p = 0.0013), pubertal delay was statistically significant in adolescents who had more than 3 vaso-occlusive crises (p = 0.0000), and those who had more than 5 blood transfusions since the discovery of the disease (p = 0.0127). Conclusion: The factors that hinder pubertal development in sickle cell patients are intrinsic (sickle cell anemia with its complications) and extrinsic (environmental: diet, social status). The appearance of secondary sexual characteristics is delayed on average by two years compared to the general population.
作者
Nestor Ghislain Andzouana Mbamognoua
John Claude Edzan
Farel Ongoth Elilie Mawa
Judicael Kambourou
Lydie Ocini Ngolet
Henri Germain Monabeka
Nestor Ghislain Andzouana Mbamognoua;John Claude Edzan;Farel Ongoth Elilie Mawa;Judicael Kambourou;Lydie Ocini Ngolet;Henri Germain Monabeka(Department of Metabolic and Endocrine Diseases, Brazzaville University Hospital, Brazzaville, Congo;Faculty of Health Sciences, Marien Ngouabi University, Brazzaville, Congo;Pediatric Intensive Care Department, Brazzaville University Hospital, Brazzaville, Congo;Hematology Department, Brazzaville University Hospital, Brazzaville, Congo)
