RESUMO
An earlier onset of puberty is associated with increased cardiometabolic risk. We investigated whether this relation was independent of faster childhood growth or current size in an Afro-Caribbean birth cohort (n=259). Anthropometry was measured at birth and then 6-monthly. Tanner staging started at age 8 years. Cardiometabolic risk factors were measured at mean age 11.5 years. In boys, pubarchal stage and testicular size were associated with lower high-density lipoprotein cholesterol, higher systolic blood pressure, and higher homeostasis model assessment of insulin resistance score, but not after adjusting for current body mass index (BMI) or rate of growth (up to age 8 years). In girls, earlier menarche and greater breast development were associated with higher fasting glucose even after adjusting for current BMI or prior growth. Pubarchal stage was associated with systolic blood pressure, even after adjusting for current BMI and prior growth. We concluded that earlier puberty is independently associated with cardiometabolic risk in girls but not in boys.
Assuntos
Cardiopatias/epidemiologia , Cardiopatias/metabolismo , Puberdade/fisiologia , Adolescente , Adulto , População Negra , Glicemia/metabolismo , Pressão Sanguínea/fisiologia , Criança , Estudos de Coortes , Feminino , Humanos , Resistência à Insulina , Jamaica/epidemiologia , Lipídeos/sangue , Masculino , Gravidez , Puberdade Precoce/complicações , Fatores de Risco , Distribuição por Sexo , Adulto JovemRESUMO
BACKGROUND: Albuminuria is a marker of glomerular damage in Sickle Cell Disease (SCD). In this study, we sought to determine the possible predictors of albuminuria in the two more prevalent genotypes of SCD among the Jamaica Sickle Cell Cohort Study participants. METHODS: An age-matched cohort of 122 patients with HbSS or HbSC genotypes had measurements of their morning urine albumin concentration, blood pressure, body mass index, haematology and certain biochemistry parameters done. Associations of albuminuria with possible predictors including hematological parameters, reticulocyte counts, aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels were examined using multiple regression models. RESULTS: A total of 122 participants were recruited (mean age 28.6 years ±2.5 years; 85 HbSS, 37 HbSC). 25.9% with HbSS and 10.8% with HbSC disease had microalbuminuria (urine albumin/creatinine ratio â=â 30-300 mg/g of creatinine) whereas 16.5% of HbSS and 2.7% of HbSC disease had macroalbuminuria (urine albumin/creatinine ratio>300 mg/g of creatinine). Mean arterial pressure, hemoglobin levels, serum creatinine, reticulocyte counts and white blood cell counts were statistically significant predictors of albuminuria in HbSS, whereas white blood cell counts and serum creatinine predicted albuminuria in HbSC disease. Both markers of chronic hemolysis, i.e. AST and LDH levels, showed no associations with albuminuria in either genotype. CONCLUSIONS: Renal disease, as evidenced by excretion of increased amounts of albumin in urine due to a glomerulopathy, is a common end-organ complication in SCD. It is shown to be more severe in those with HbSS disease than in HbSC disease. Rising blood pressure, lower hemoglobin levels and higher white blood cell counts are hints to the clinician of impending renal disease, whereas higher rates of hemolysis do not appear to play a role in this complication of SCD.
Assuntos
Albuminúria/complicações , Anemia Falciforme/complicações , Hemólise , Adulto , Albuminúria/sangue , Anemia Falciforme/sangue , Estudos de Coortes , Estudos Transversais , Feminino , Humanos , Jamaica , MasculinoRESUMO
Clinical and hematological features are presented for 261 patients with identified ß-thalassemia (ß-thal) mutations. Mutations causing Hb S [ß6(A3)GluâVal]-ß(0)-thal were IVS-II-849 (A>G) in 44%, frameshift codon (FSC) 6 (-A) in 14%, Hb Monroe [ß30(B12)ArgâThr] in 14%, and IVS-II-1 (G>A) in 10%. Mutations causing Hb S-ß(+)-thal with 14-25% Hb A (type III) were -29 (A>G) mutation in 60%, -88 (C>T) in 22% and the polyadenylation signal site (polyA) (T>C) mutation in 14%, and in Hb S-ß(+)-thal with 1-7% Hb A (type I), all had the IVS-I-5 (G>C) mutation. Hematologically, only minor differences occurred between the four Hb S-ß(0)-thal mutations, but among the three mutations causing Hb S-ß(+)-thal type III, levels of Hb A(2), Hb F, hemoglobin (Hb), MCV and MCH were highest in the -88 and lowest in the polyA mutations. Clinically, Hb S-ß(0)-thal and Hb S-ß(+)-thal type I were generally severe, and Hb S-ß(+)-thal type III disease with the -88 mutation was milder than that caused by the polyA mutation.
Assuntos
Talassemia beta/genética , Adulto , Anemia Falciforme/genética , Anemia Falciforme/mortalidade , Anemia Falciforme/fisiopatologia , Criança , Códon , Hemoglobina Fetal/genética , Estudos de Associação Genética , Testes Hematológicos , Hemoglobina A2/genética , Hemoglobinas Anormais/genética , Humanos , Recém-Nascido , Mutação , Triagem Neonatal , Análise de Sequência de DNA , Taxa de Sobrevida , Talassemia beta/mortalidade , Talassemia beta/fisiopatologiaRESUMO
Both intra-uterine and early childhood development contribute to the risk of developing CVD in adult life. We therefore evaluated the maternal, placental, fetal, birth, infant and childhood determinants of cardiovascular risk in a cohort of Afro-Jamaican children. The Vulnerable Windows Cohort is a longitudinal survey of 569 mothers and their offspring recruited from the first trimester. The offspring's anthropometry was measured at birth, at 6 weeks, every 3 months to 1 year and then every 6 months. At mean age 11.5 years, fasting blood was sampled for glucose, insulin and lipids. Analyses were confined to 296 women and their offspring who had complete data. Waist circumference (WC) was related to maternal weight and BMI, placental weight and to the size of the offspring in utero, at birth and the rate of growth in childhood (P < 0.05). Total cholesterol, TAG and glucose concentrations were unrelated to maternal, placental, fetal, neonatal and childhood measurements. Fasting insulin and homeostasis model assessment of insulin resistance were related to maternal weight and BMI (P < 0.05), but not after adjusting for WC. HDL-cholesterol was inversely related to placental and birth weight, and inversely related to weight and BMI throughout childhood (P < 0.001), but not after adjusting for WC. Systolic blood pressure was directly related to maternal weight, child's height, weight and BMI (P < 0.05), but not after adjustment for WC. Systolic blood pressure and fasting glucose concentration were inversely related to birth weight in boys but directly associated in girls. We concluded that maternal anthropometry during pregnancy, fetal size, and childhood growth rate contribute to cardiovascular risk factors in childhood.
Assuntos
Peso ao Nascer , Peso Corporal , Doenças Cardiovasculares/etiologia , HDL-Colesterol/sangue , Desenvolvimento Fetal , Crescimento , Adulto , África/etnologia , Glicemia/metabolismo , Pressão Sanguínea , Índice de Massa Corporal , Criança , Feminino , Humanos , Recém-Nascido , Insulina/sangue , Resistência à Insulina , Jamaica , Masculino , Tamanho do Órgão , Placenta/anatomia & histologia , Gravidez , Fatores de Risco , Fatores Sexuais , Circunferência da Cintura , Adulto JovemRESUMO
CONTEXT: Childhood growth and body composition may influence the onset of puberty. OBJECTIVE: We examined the effects of birth size, growth rates throughout childhood, and body composition on the onset of puberty in Afro-Caribbean children. DESIGN AND SETTING: This was a longitudinal birth cohort study (the Vulnerable Windows Cohort Study) in Jamaica. SUBJECTS AND MEASUREMENTS: The anthropometry (weight, height, skinfold measurements, and waist circumference) of 259 children was measured at birth, at 6 wk, every 3 months to 2 yr, and then every 6 months. Tanner staging for puberty and orchidometry were performed every 6 months starting at approximately age 8 yr. Bioelectrical impedance was done at age 11 yr. RESULTS: In the girls, thelarche, pubarche, and menarche occurred at median ages of 8.8, 9.9, and 12.0 yr, respectively. Pubarche in boys occurred at a median age of 11.3 yr when the median testicular volume was 2.8 ml. Faster weight gain during infancy (age 0-6 months) and childhood, but not birth size, was associated with more advanced puberty (P values <0.05). Fat mass at age 8 yr was associated with more advanced puberty (P values <0.001) in both sexes. At age 11 yr, lean mass, but not fat mass, was associated with more advanced puberty (P values <0.001). CONCLUSION: These data support the hypothesis that faster growth throughout childhood, especially with fat mass accretion, is associated with more advanced puberty apart from menarche. With the onset of puberty, lean mass accretion significantly increases.