Aetiology of nutritional rickets in rural Bangladeshi children.


Journal

Bone
ISSN: 1873-2763
Titre abrégé: Bone
Pays: United States
ID NLM: 8504048

Informations de publication

Date de publication:
07 2020
Historique:
received: 25 02 2020
revised: 01 04 2020
accepted: 03 04 2020
pubmed: 11 4 2020
medline: 22 6 2021
entrez: 11 4 2020
Statut: ppublish

Résumé

A high prevalence of rickets of unknown aetiology has been reported in Chakaria, Bangladesh. Classically, rickets is caused by vitamin D deficiency but increasing evidence from Africa and Asia points towards other nutritional deficiencies or excessive exposure to some metals. The aim of this study was to investigate the aetiology of rickets in rural Bangladeshi children. 64 cases with rickets-like deformities were recruited at first presentation together with age-sex-village matched controls. Data and sample acquisition included anthropometry, radiographs, fasted plasma and urinary samples, 24 h weighed dietary intake together with a 24 h urine collection, and One child had active rickets and frank hypovitaminosis D (F, n = 1) and one had deformities with radiological features of Blount disease (M, n = 1). The remaining cases were grouped into those with active rickets, defined as a radiographic Thacher score ≥1.5 (Group A, n = 24, 12M, 12F) and rickets-like bone deformities but not active rickets (Group B, n = 38, 28M, 10F). All children had a low dietary calcium intake, but this was lower in Group A than their controls (mean (SD): 156 (80) versus 323 (249) mg/day, p = 0.005). Plasma 25-hydroxyvitamin D (25OHD) was lower in Group A compared to controls; 63% of Group A and 8% of controls had a concentration <25 nmol/L (p ≤ 0.0001). There was, however, no evidence of differences in skin sunshine exposure. Group A had lower plasma calcium and phosphate and higher 1,25-dihydroxyvitamin D (1,25(OH) Nutritional rickets in this region is likely to be predominantly due to low calcium intake in the context of poor vitamin D status and exposure to environmental metals, but not H. pylori infection, anaemia or iron deficiency.

Identifiants

pubmed: 32276153
pii: S8756-3282(20)30137-X
doi: 10.1016/j.bone.2020.115357
pmc: PMC7262584
pii:
doi:

Substances chimiques

FGF23 protein, human 0
Parathyroid Hormone 0
Phosphates 0
Vitamin D 1406-16-2
Fibroblast Growth Factor-23 7Q7P4S7RRE
Calcium SY7Q814VUP

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

115357

Subventions

Organisme : Medical Research Council
ID : U105960371
Pays : United Kingdom

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest None.

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Auteurs

Sonia Ahmed (S)

MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, UK; International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR,B), Dhaka 1000, Bangladesh. Electronic address: sonia.ahmed@durham.ac.uk.

Gail R Goldberg (GR)

MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, UK.

Rubhana Raqib (R)

International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR,B), Dhaka 1000, Bangladesh.

Swapan Kumar Roy (SK)

International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR,B), Dhaka 1000, Bangladesh.

Shahidul Haque (S)

Social Assistance and Rehabilitation for the Physically Vulnerable (SARPV), Dhaka 1207, Bangladesh.

Vickie S Braithwaite (VS)

MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, UK; MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Cambridge CB2 0SL, UK.

John M Pettifor (JM)

SAMRC/Wits Developmental Pathways for Health Research Unit, Department of Paediatrics, University of the Witwatersrand, Johannesburg, South Africa.

Ann Prentice (A)

MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, UK.

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