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Gut-bone cross talks and implications in Celiac disease
Aaron Lerner, Torsten Matthias
Language English Country United States
- MeSH
- Celiac Disease diagnosis diet therapy complications MeSH
- Child MeSH
- Adult MeSH
- Comorbidity MeSH
- Bone Density drug effects MeSH
- Humans MeSH
- Bone Diseases, Metabolic diagnosis epidemiology prevention & control MeSH
- Dietary Supplements MeSH
- Calcium, Dietary therapeutic use MeSH
- Life Style MeSH
- Check Tag
- Child MeSH
- Adult MeSH
- Humans MeSH
Metabolic bone disease is a frequent extra-intestinal co-morbidity in newly diagnosed, mostly adult patients who have 70% low bone mineral density. Musculoskeletal signs and symptoms, osteopenia, osteoporosis and fractures are the most frequent manifestations. The etiology is multifactorial, however, micronutrient malabsorption, mainly of calcium and vitamin D, secondary hyperparathyroidism and inflammation are the main driving forces. The diagnosis is based on signs and symptoms, biochemical and endocrinologic laboratory evaluation and imaging by dual x-ray absorptiometry. Treatment of low bone mineral density in CD comprises: a gluten free diet, coverage of nutritional deficiencies (including calcium and vitamin D), changes in life style and if necessary, pharmacologic and hormonal replacement therapy. The cost effectiveness of those therapy methods were barely assessed. Understanding the pathophysiology of bone loss in celiac disease might bring new therapeutical strategies for the patient’s benefit.
AESKU KIPP Institute Wendelsheim Germany
B Rappaport School of Medicine Technion Israel Institute of Technology Haifa Israel
References provided by Crossref.org
Literatura
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- $a Metabolic bone disease is a frequent extra-intestinal co-morbidity in newly diagnosed, mostly adult patients who have 70% low bone mineral density. Musculoskeletal signs and symptoms, osteopenia, osteoporosis and fractures are the most frequent manifestations. The etiology is multifactorial, however, micronutrient malabsorption, mainly of calcium and vitamin D, secondary hyperparathyroidism and inflammation are the main driving forces. The diagnosis is based on signs and symptoms, biochemical and endocrinologic laboratory evaluation and imaging by dual x-ray absorptiometry. Treatment of low bone mineral density in CD comprises: a gluten free diet, coverage of nutritional deficiencies (including calcium and vitamin D), changes in life style and if necessary, pharmacologic and hormonal replacement therapy. The cost effectiveness of those therapy methods were barely assessed. Understanding the pathophysiology of bone loss in celiac disease might bring new therapeutical strategies for the patient’s benefit.
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