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Low prevalence of glucose intolerance in racially mixed children with cystic fibrosis

Authors

  • Crésio Alves,

    Corresponding author
    1. Federal University of Bahia, Salvador-Bahia, Brazil
    2. Pediatric Endocrinology Unit, Hospital Universitario Professor Edgard Santos, Federal University of Bahia, Salvador-Bahia, Brazil
      Dr. Crésio Alves, Rua Plínio Moscoso, No. 222, Apto. 601, CEP: 40157-190, Salvador-Bahia, Brazil.
      Tel: +55 71 9178 4055;
      Fax: +55 71 3797 9990;
      e-mail: cresio.alves@uol.com.br
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  • Daniela S Lima,

    1. Federal University of Bahia, Salvador-Bahia, Brazil
    2. Pediatric Endocrinology Unit, Hospital Universitario Professor Edgard Santos, Federal University of Bahia, Salvador-Bahia, Brazil
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  • Mauricio Cardeal,

    1. Biomedical Statistics Department, Federal University of Bahia, Salvador-Bahia, Brazil
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  • Angelica Santana

    1. Cystic Fibrosis Center, Hospital Octávio Mangabeira, Salvador-Bahia, Brazil
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Dr. Crésio Alves, Rua Plínio Moscoso, No. 222, Apto. 601, CEP: 40157-190, Salvador-Bahia, Brazil.
Tel: +55 71 9178 4055;
Fax: +55 71 3797 9990;
e-mail: cresio.alves@uol.com.br

Abstract

Alves C, Lima DS, Cardeal M, Santana A. Low prevalence of glucose intolerance in racially mixed children with cystic fibrosis.

Objective: To evaluate glucose tolerance in racially mixed Brazilian youth with cystic fibrosis (CF).

Methods: Cross-sectional study conducted between August and September 2007, at a reference service for CF, evaluating: glycated hemoglobin (HbA1c), blood glucose, and insulin levels, before and 2 h after a glucose overload.

Results: There were 46 patients aged between 6 yr and 16 yr and 2 months (median: 9 yr and 10 months) of whom 64% were boys. Of these, 26% were Whites; 54.4% Mulattoes; and 19.6% Blacks. HbA1c was normal in all patients. Only one participant (12-yr old) had glucose intolerance. Insulin levels ranged from 1 to 23 µIU/mL (median: 4.5 µIU/mL) at baseline and from 3.2 to 192.1 µIU/mL (median: 11 µIU/mL) after a glucose overload. Insulin resistance evaluated by the HOMA index, stratified by sex and age, was present in three patients. The ΔF508 mutation was present in only 4.3% of the sample, all of them being heterozygous.

Conclusions: The low prevalence of carbohydrate intolerance in this population is probably a result of their young age. Another possibility is the low frequency of the ΔF508 mutation. Although not conclusive, these data suggest that in addition to age, the genotype:phenotype ratio may influence the development of glucose intolerance in patients with CF.

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