Abstract:Background: Adults with celiac disease (CeD) show low bone mineral density (BMD) and high fracture risk. CeD guidelines suggest measurements of serum minerals and vitamin D. However, studies on vitamin levels in CeD patients are contradictory. Aim: To investigate in CeD, 25-hydroxy-vitamin D [25(OH)D], 1,25-dihydroxy-vitamin D [1,25(OH)2D], and related analytes and to evaluate their relationships to peripheral BMD as assessed by peripheral quantitative computed tomography (pQCT). Methods: Gluten-free diet (GFD… Show more
“…This has led to the hypothesis that vitamin D deficiency in early life may predispose to celiac disease due to seasonal differences in UVB exposure and subsequent 25(OH)D concentrations or via dysregulation of the immune response leading to an abnormal intestinal mucosa with increasing permeability ( 21 , 22 ). Although low 25(OH)D concentrations have been reported at the time of celiac disease diagnosis ( 23 – 26 ), this can be attributed to deranged dietary absorption from a damaged gut epithelium.…”
Objectives: An observed variation in the risk of celiac disease, according to the season of birth, suggests that vitamin D may affect the development of the disease. The aim of this study was to investigate if vitamin D concentration is associated with the risk of celiac disease autoimmunity (CDA) in genetically at-risk children.Study Design: Children prospectively followed in the multinational The Environmental Determinants of Diabetes in the Young study, conducted at six centers in Europe and the US, were selected for a 1-to-3 nested case–control study. In total, 281 case–control sets were identified. CDA was defined as positivity for tissue transglutaminase autoantibodies (tTGA) on two or more consecutive visits. Vitamin D was measured as 25-hydroxyvitamin D [25(OH)D] concentrations in all plasma samples prior to, and including, the first tTGA positive visit. Conditional logistic regression was used to examine the association between 25(OH)D and risk of CDA.Results: No significant association was seen between 25(OH)D concentrations (per 5 nmol/L increase) and risk for CDA development during early infancy (odds ratio [OR] 0.99, 95% confidence interval [CI] 0.95–1.04) or childhood (OR 1.02, 95% CI 0.97–1.07). When categorizing 25(OH)D concentrations, there was an increased risk of CDA with 25(OH)D concentrations <30 nmol/L (OR 2.23, 95% CI 1.29, 3.84) and >75 nmol/L (OR 2.10, 95% CI 1.28–3.44) in early infancy, as compared with 50–75 nmol/L.Conclusion: This study indicates that 25(OH)D concentrations <30 nmol/L and >75 nmol/L during early infancy were associated with an increased risk of developing CDA in genetically at-risk children. The non-linear relationship raises the need for more studies on the possible role of 25(OH)D in the relation to celiac disease onset.
“…This has led to the hypothesis that vitamin D deficiency in early life may predispose to celiac disease due to seasonal differences in UVB exposure and subsequent 25(OH)D concentrations or via dysregulation of the immune response leading to an abnormal intestinal mucosa with increasing permeability ( 21 , 22 ). Although low 25(OH)D concentrations have been reported at the time of celiac disease diagnosis ( 23 – 26 ), this can be attributed to deranged dietary absorption from a damaged gut epithelium.…”
Objectives: An observed variation in the risk of celiac disease, according to the season of birth, suggests that vitamin D may affect the development of the disease. The aim of this study was to investigate if vitamin D concentration is associated with the risk of celiac disease autoimmunity (CDA) in genetically at-risk children.Study Design: Children prospectively followed in the multinational The Environmental Determinants of Diabetes in the Young study, conducted at six centers in Europe and the US, were selected for a 1-to-3 nested case–control study. In total, 281 case–control sets were identified. CDA was defined as positivity for tissue transglutaminase autoantibodies (tTGA) on two or more consecutive visits. Vitamin D was measured as 25-hydroxyvitamin D [25(OH)D] concentrations in all plasma samples prior to, and including, the first tTGA positive visit. Conditional logistic regression was used to examine the association between 25(OH)D and risk of CDA.Results: No significant association was seen between 25(OH)D concentrations (per 5 nmol/L increase) and risk for CDA development during early infancy (odds ratio [OR] 0.99, 95% confidence interval [CI] 0.95–1.04) or childhood (OR 1.02, 95% CI 0.97–1.07). When categorizing 25(OH)D concentrations, there was an increased risk of CDA with 25(OH)D concentrations <30 nmol/L (OR 2.23, 95% CI 1.29, 3.84) and >75 nmol/L (OR 2.10, 95% CI 1.28–3.44) in early infancy, as compared with 50–75 nmol/L.Conclusion: This study indicates that 25(OH)D concentrations <30 nmol/L and >75 nmol/L during early infancy were associated with an increased risk of developing CDA in genetically at-risk children. The non-linear relationship raises the need for more studies on the possible role of 25(OH)D in the relation to celiac disease onset.
“…Several studies have shown that GFD may restore skeletal defects, particularly in children ( Figure 2 ), thus decreasing the risk of fracture in patients with celiac disease [ 78 , 79 , 80 , 81 , 82 , 83 ]. Generally, from a clinical point of view, after starting GFD, systemic inflammation decreases, the intestinal mucosa heals progressively, and normal gastrointestinal absorption is re-established.…”
Section: Celiac Diseasementioning
confidence: 99%
“…Generally, from a clinical point of view, after starting GFD, systemic inflammation decreases, the intestinal mucosa heals progressively, and normal gastrointestinal absorption is re-established. Consequently, bone resorption decreases, in part explaining the increase in BMD [ 83 ] and, ultimately, the decrease in fracture risk. Moreover, celiac disease patients on GFD undergo a significant decrease in the parathyroid hormone (PTH) levels, together with a significant increase in the calcium and vitamin D concentrations, thus allowing adequate skeletal mineralization.…”
Osteoporosis is a common systemic disease of the skeleton, characterized by compromised bone mass and strength, consequently leading to an increased risk of fragility fractures. In women, the disease mainly occurs due to the menopausal fall in estrogen levels, leading to an imbalance between bone resorption and bone formation and, consequently, to bone loss and bone fragility. Moreover, osteoporosis may affect men and may occur as a sequela to different diseases or even to their treatments. Despite their wide prevalence in the general population, the skeletal implications of many gastrointestinal diseases have been poorly investigated and their potential contribution to bone fragility is often underestimated in clinical practice. However, proper functioning of the gastrointestinal system appears essential for the skeleton, allowing correct absorption of calcium, vitamins, or other nutrients relevant to bone, preserving the gastrointestinal barrier function, and maintaining an optimal endocrine-metabolic balance, so that it is very likely that most chronic diseases of the gastrointestinal tract, and even gastrointestinal dysbiosis, may have profound implications for bone health. In this manuscript, we provide an updated and critical revision of the role of major gastrointestinal disorders in the pathogenesis of osteoporosis and fragility fractures.
“…The antitissue transglutaminase (anti-tTG) antibody is a key criterion for establishing the diagnosis of celiac disease and monitoring the adherence to a gluten-free diet (GFD) (1). The presence of anti-tTG autoantibodies is associated with small bowel mucosal damage, whereas celiac serology normalization is associated with mucosal healing and improvement in metabolic outcomes such as anemia and bone density (11,12). Celiac autoimmunity has been associated with other comorbidities and subsequent poor health outcomes, aside from small intestinal inflammation.…”
INTRODUCTION: We evaluated whether persistent-positive celiac serology is associated with the risk of hypothyroidism.
METHODS:We extracted a cohort of subjects aged 1-80 years with a positive IgA anti-tissue transglutaminase between January 1, 2008, and December 31, 2012, and a repeat anti-tissue transglutaminase test within 6-36 months from a large population-based electronic medical record database. Based on serology tests, we categorized the pediatric (age <21 years) and adult cohorts into normalized or persistent-positive serology groups. All subjects were followed up for incident diagnosis of hypothyroidism from the last serology date up to December 31, 2017. Hazard ratio (HR) along 95% confidence intervals (CIs) were prepared to evaluate the association of celiac serology group with a diagnosis of hypothyroidism, crude, and adjusted for age, sex, and diagnosis of type 1 diabetes mellitus.
RESULTS:Among the pediatric cohort (n 5 2,687), during a median follow-up of 64 months (interquartile range 48-80), 2.3% (16/681) of the persistent-positive serology group and 1.0% (20/2,006) of the normalized serology group developed hypothyroidism (HR 2.07 [95% CI 1.07-4.44], adjHR ). The rate among the pediatric cohort with an established diagnosis of celiac disease was 3.4% (10/486) vs 1.0% (5/481), HR 2.83 (0.96-8.32). In the adult cohort (n 5 1,286), 4.5% (20/442) of the persistent-positive group and 3.9% (33/811) of the normalized serology group developed hypothyroidism ).
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