Celiac disease and bone

Detalhes bibliográficos
Autor(a) principal: Kondapalli,Ananya V.
Data de Publicação: 2022
Outros Autores: Walker,Marcella Donovan
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Arquivos de Endocrinologia e Metabolismo (Online)
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972022000500756
Resumo: Abstract Celiac disease (CD) is an autoimmune disorder characterized by small intestinal inflammation triggered by gluten ingestion in genetically-predisposed individuals. A frequent extra-intestinal manifestation of CD is metabolic bone disease which contributes to an increased risk of fracture. The mechanisms underlying bone disease in CD remain incompletely understood, but multiple processes have been proposed including (1) malabsorption of calcium and vitamin D leading to secondary hyperparathyroidism and increased skeletal resorption, (2) pro-inflammatory cytokines altering the osteoprotegerin and receptor activator of nuclear kappa-B ligand ratio favoring osteoclastogenesis, (3) hypogonadism, and (4) low weight and malnutrition. Most studies show reduced bone mineral density in patients with CD. Bone microarchitecture is also deteriorated leading to reduced whole bone stiffness. Many, but not all investigations, have shown an increased risk of fracture associated with CD. The main stay of therapy for CD is maintaining a gluten-free diet. Improvement in bone mineral density with adherence to a gluten-free diet has been well-established. Bone mineral density remains lower, however, compared to controls and increased fracture risk can persist. There is no consensus on the timing of dual-energy x-ray absorptiometry for bone mineral density assessment in patients with CD. Routine screening for CD in patients with osteoporosis is not recommended. Little data are available on the use or efficacy of prescription osteoporosis therapeutics in patients with CD. Studies are needed to develop standardized guidelines for screening and treatment of metabolic bone disease in patients with CD to identify those who may need early intervention with prescription osteoporosis therapy. Arch Endocrinol Metab. 2022;66(5):756-64
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spelling Celiac disease and boneMicroarchitectureglutenfracturebone densityinflammationAbstract Celiac disease (CD) is an autoimmune disorder characterized by small intestinal inflammation triggered by gluten ingestion in genetically-predisposed individuals. A frequent extra-intestinal manifestation of CD is metabolic bone disease which contributes to an increased risk of fracture. The mechanisms underlying bone disease in CD remain incompletely understood, but multiple processes have been proposed including (1) malabsorption of calcium and vitamin D leading to secondary hyperparathyroidism and increased skeletal resorption, (2) pro-inflammatory cytokines altering the osteoprotegerin and receptor activator of nuclear kappa-B ligand ratio favoring osteoclastogenesis, (3) hypogonadism, and (4) low weight and malnutrition. Most studies show reduced bone mineral density in patients with CD. Bone microarchitecture is also deteriorated leading to reduced whole bone stiffness. Many, but not all investigations, have shown an increased risk of fracture associated with CD. The main stay of therapy for CD is maintaining a gluten-free diet. Improvement in bone mineral density with adherence to a gluten-free diet has been well-established. Bone mineral density remains lower, however, compared to controls and increased fracture risk can persist. There is no consensus on the timing of dual-energy x-ray absorptiometry for bone mineral density assessment in patients with CD. Routine screening for CD in patients with osteoporosis is not recommended. Little data are available on the use or efficacy of prescription osteoporosis therapeutics in patients with CD. Studies are needed to develop standardized guidelines for screening and treatment of metabolic bone disease in patients with CD to identify those who may need early intervention with prescription osteoporosis therapy. Arch Endocrinol Metab. 2022;66(5):756-64Sociedade Brasileira de Endocrinologia e Metabologia2022-10-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972022000500756Archives of Endocrinology and Metabolism v.66 n.5 2022reponame:Arquivos de Endocrinologia e Metabolismo (Online)instname:Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)instacron:SBEM10.20945/2359-3997000000561info:eu-repo/semantics/openAccessKondapalli,Ananya V.Walker,Marcella Donovaneng2022-11-30T00:00:00Zoai:scielo:S2359-39972022000500756Revistahttps://www.aem-sbem.com/https://old.scielo.br/oai/scielo-oai.php||aem.editorial.office@endocrino.org.br2359-42922359-3997opendoar:2022-11-30T00:00Arquivos de Endocrinologia e Metabolismo (Online) - Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)false
dc.title.none.fl_str_mv Celiac disease and bone
title Celiac disease and bone
spellingShingle Celiac disease and bone
Kondapalli,Ananya V.
Microarchitecture
gluten
fracture
bone density
inflammation
title_short Celiac disease and bone
title_full Celiac disease and bone
title_fullStr Celiac disease and bone
title_full_unstemmed Celiac disease and bone
title_sort Celiac disease and bone
author Kondapalli,Ananya V.
author_facet Kondapalli,Ananya V.
Walker,Marcella Donovan
author_role author
author2 Walker,Marcella Donovan
author2_role author
dc.contributor.author.fl_str_mv Kondapalli,Ananya V.
Walker,Marcella Donovan
dc.subject.por.fl_str_mv Microarchitecture
gluten
fracture
bone density
inflammation
topic Microarchitecture
gluten
fracture
bone density
inflammation
description Abstract Celiac disease (CD) is an autoimmune disorder characterized by small intestinal inflammation triggered by gluten ingestion in genetically-predisposed individuals. A frequent extra-intestinal manifestation of CD is metabolic bone disease which contributes to an increased risk of fracture. The mechanisms underlying bone disease in CD remain incompletely understood, but multiple processes have been proposed including (1) malabsorption of calcium and vitamin D leading to secondary hyperparathyroidism and increased skeletal resorption, (2) pro-inflammatory cytokines altering the osteoprotegerin and receptor activator of nuclear kappa-B ligand ratio favoring osteoclastogenesis, (3) hypogonadism, and (4) low weight and malnutrition. Most studies show reduced bone mineral density in patients with CD. Bone microarchitecture is also deteriorated leading to reduced whole bone stiffness. Many, but not all investigations, have shown an increased risk of fracture associated with CD. The main stay of therapy for CD is maintaining a gluten-free diet. Improvement in bone mineral density with adherence to a gluten-free diet has been well-established. Bone mineral density remains lower, however, compared to controls and increased fracture risk can persist. There is no consensus on the timing of dual-energy x-ray absorptiometry for bone mineral density assessment in patients with CD. Routine screening for CD in patients with osteoporosis is not recommended. Little data are available on the use or efficacy of prescription osteoporosis therapeutics in patients with CD. Studies are needed to develop standardized guidelines for screening and treatment of metabolic bone disease in patients with CD to identify those who may need early intervention with prescription osteoporosis therapy. Arch Endocrinol Metab. 2022;66(5):756-64
publishDate 2022
dc.date.none.fl_str_mv 2022-10-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
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dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972022000500756
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S2359-39972022000500756
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.20945/2359-3997000000561
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Sociedade Brasileira de Endocrinologia e Metabologia
publisher.none.fl_str_mv Sociedade Brasileira de Endocrinologia e Metabologia
dc.source.none.fl_str_mv Archives of Endocrinology and Metabolism v.66 n.5 2022
reponame:Arquivos de Endocrinologia e Metabolismo (Online)
instname:Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)
instacron:SBEM
instname_str Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)
instacron_str SBEM
institution SBEM
reponame_str Arquivos de Endocrinologia e Metabolismo (Online)
collection Arquivos de Endocrinologia e Metabolismo (Online)
repository.name.fl_str_mv Arquivos de Endocrinologia e Metabolismo (Online) - Sociedade Brasileira de Endocrinologia e Metabologia (SBEM)
repository.mail.fl_str_mv ||aem.editorial.office@endocrino.org.br
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