Recent PubMed Articles on Coeliac Disease (External)

Prevalence and Natural History of Celiac Disease in a Cohort of At-risk Children.

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Prevalence and Natural History of Celiac Disease in a Cohort of At-risk Children.

J Pediatr Gastroenterol Nutr. 2016 May;62(5):739-45

Authors: Cilleruelo ML, Fernández-Fernández S, Jiménez-Jiménez J, Rayo AI, de Larramendi CH

Abstract
OBJECTIVES: To assess the prevalence and clinical presentation of celiac disease (CD) in a cohort of children with HLA-DQ2 positive and evaluate the risk factors in the development of CD.
METHODS: Between July 2004 and July 2005, parents of all healthy full-term newborns in our hospital were invited to participate. HLA-DQ2 was tested in blood sample of the umbilical cord. A point of contact serological test was performed on children between 2 and 3 years of age. Positive results were confirmed by serum anti-transglutaminase 2 and endomysial antibodies. Children with high autoantibody titers underwent an intestinal biopsy. Children of the cohort diagnosed with CD before the screening study were included. Sex, mode of delivery, breast-feeding duration, and age of gluten introduction were studied.
RESULTS: Of 1291 children, 362 were HLA-DQ2 positive and 262 participated in the study. CD was diagnosed in 4.1% (95% confidence interval (CI) 1.9-6.3). In the whole cohort, 60% had gastrointestinal symptoms, 7% poor weight gain, and 33% were asymptomatic. Five children with potential CD and 6 with CD autoimmunity became negative (42.3%) and are still negative after 5 to 7 years. Female sex was at-risk factor odds ratio 5.7 (95% CI 1.5-20.9), whereas breast-feeding during gluten introduction had a protective effect odds ratio 0.1 (95% CI 0.01-0.8).
CONCLUSIONS: Prevalence of CD in this cohort was 4%, half of whom had digestive symptoms. Because a high proportion of children showed a spontaneous disappearance of antibodies, prevalence studies of CD in young children should be based on intestinal damage so as not to overestimate results.

PMID: 26485606 [PubMed - indexed for MEDLINE]

Persistent mucosal damage and the risk of epilepsy in people with celiac disease.

Persistent mucosal damage and the risk of epilepsy in people with celiac disease.

Eur J Neurol. 2018 Jan 05;:

Authors: Kurien M, Ludvigsson JF, Sanders DS, Zylberberg HM, Green PH, Sundelin HEK, Lebwohl B

Abstract
BACKGROUND: Celiac disease (CD) is associated with an increased risk of developing epilepsy, a risk that persists after CD diagnosis. A significant proportion of CD patients have persistent villous atrophy (VA) on follow-up biopsy. This study's objective was to determine whether persistent VA on follow-up biopsy affects long-term epilepsy risk and epilepsy-related hospital emergency admissions.
METHODS: Nationwide Cohort Study. We identified all people in Sweden with histological evidence of CD who underwent a follow-up small intestinal biopsy (1969-2008). We compared those with persistent VA to those who showed histological improvement, assessing the development of epilepsy and related emergency hospital admissions (defined according to relevant ICD codes in the Swedish Patient Register). Cox regression analysis was used to assess outcome measures.
RESULTS: Of 7590 people with CD who had a follow-up biopsy, VA was present in 43%. The presence of persistent VA was significantly associated with a reduced risk of developing newly-diagnosed epilepsy (hazard ratio [HR] 0.61; 95% confidence interval [CI] 0.38-0.98). On stratified analysis this effect was primarily amongst males (HR 0.35; 95 CI 0.15-0.80). Among the 58 CD patients with a prior diagnosis of epilepsy, those with persistent VA were less likely to visit an emergency department with epilepsy (HR 0.37; 95%CI 0.09-1.09).
CONCLUSIONS: In a population-based study of CD individuals, persisting VA on follow up biopsy was associated with reduced future risk of developing epilepsy but did not influence emergency epilepsy-related hospital admissions. Mechanisms as to why persistent VA confers this benefit requires further exploration. This article is protected by copyright. All rights reserved.

PMID: 29316034 [PubMed - as supplied by publisher]

Celiac Disease in South Jordan.

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Celiac Disease in South Jordan.

Pediatr Gastroenterol Hepatol Nutr. 2017 Dec;20(4):222-226

Authors: Altamimi E

Abstract
Purpose: Celiac disease, an autoimmune enteropathy triggered by exposure to gluten, is not uncommon in South Jordan. However, its prevalence is underestimated due to lack of physician awareness of the diversity of disease presentation. The clinical spectrum includes classic gastrointestinal manifestations, as well as rickets, iron-deficiency anemia, short stature, elevated liver enzymes, and edema. Our goal was to evaluate celiac disease presentation in clinically diagnosed children.
Methods: Retrospective study included all children diagnosed with celiac disease between September 2009 and September 2015. Hospital charts were reviewed. Demographic data, clinical characteristics, and follow-up were recorded.
Results: Thirty-five children were diagnosed with celiac disease during the study period. Mean age±standard deviation was 6.7±3.8 years (range, 2.0-14 years). There were 17 (48.6%) female patients. The average duration between onset of symptoms and diagnosis was 16.3±18.7 months. Fifteen (42.9%) patients presented with classic malabsorption symptoms, whereas 7 (20.0%) patients presented with short stature. Positive tissue transglutaminase antibodies (tTg)-immunoglobulin A (IgA) was seen in 34 (97.1%) patients. The one patient with negative tTg-IgA had IgA deficiency. Although tTG-IgA values were not available for objective documentation of compliance, clinical data (resolution of presenting abnormalities and growth improvement) assured acceptable compliance in 22 (62.9%) patients.
Conclusion: CD in children may present with diverse picture. Although of the small number, the non-classical presentations are not uncommon in our rural community. Gluten-free diet is the main strategy for treatment and associated with usually correction of laboratory abnormalities and improvement of growth.

PMID: 29302503 [PubMed]

Joint Involvement in Children with Celiac Disease.

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Joint Involvement in Children with Celiac Disease.

Indian Pediatr. 2017 Nov 15;54(11):946-948

Authors: Garg K, Agarwal P, Gupta RK, Sitaraman S

Abstract
OBJECTIVE: To determine early joint involvement as detected by ultrasonography in children with newly diagnosed celiac disease, and in children with celiac disease on gluten-free diet for more than 6 months.
METHODS: Cross-sectional comparative study evaluating joint abnormalities by ultrasonography.
Results: Ultrasonography showed abnormalities in 19 out of 60 (31.7%) children with newly diagnosed celiac disease as compared to 2 (3.3%) out of 60 in those on a gluten-free diet for more than 6 months.
CONCLUSION: Subclinical synovitis as detected by ultrasound is a frequent finding in newly diagnosed children with celiac disease.

PMID: 28849767 [PubMed - indexed for MEDLINE]

Non-IgE-mediated gastrointestinal food allergies in children.

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Non-IgE-mediated gastrointestinal food allergies in children.

Pediatr Allergy Immunol. 2017 Feb;28(1):6-17

Authors: Caubet JC, Szajewska H, Shamir R, Nowak-Węgrzyn A

Abstract
Non-IgE-mediated gastrointestinal food allergic disorders (non-IgE-GI-FA) including food protein-induced enterocolitis syndrome (FPIES), food protein-induced enteropathy (FPE), and food protein-induced allergic proctocolitis (FPIAP) are relatively uncommon in infants and young children, but are likely under-diagnosed. Non-IgE-GI-FA have a favorable prognosis, with majority resolving by age 3-5 years. Diagnosis relies on the recognition of symptoms pattern in FPIAP and FPIES and biopsy in FPE. Further studies are needed for a better understanding of the pathomechanism, which will lead eventually to the development of diagnostic tests and treatments. Limited evidence supports the role of food allergens in subsets of constipation, gastroesophageal reflux disease, irritable bowel syndrome, and colic. The immunologic pathomechanism is not fully understood and empiric prolonged avoidance of food allergens should be limited to minimize nutrient deficiency and feeding disorders/food aversions in infants.

PMID: 27637372 [PubMed - indexed for MEDLINE]

Unusual Onset of Celiac Disease and Addison's Disease in a 12-Year-Old Boy.

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Unusual Onset of Celiac Disease and Addison's Disease in a 12-Year-Old Boy.

Int J Environ Res Public Health. 2017 Jul 29;14(8):

Authors: Miconi F, Savarese E, Miconi G, Cabiati G, Rapaccini V, Principi N, Esposito S

Abstract
BACKGROUND: Celiac disease (CD) is an autoimmune disorder deriving from an aberrant adaptive immune response against gluten-containing grains in genetically predisposed subjects. In a number of patients, CD is associated with one or more other autoimmune diseases. Primary Addison's disease (AD) and CD may co-exist, although this association is relatively uncommon in children. In addition, it is not precisely defined whether a gluten-free diet influences the course of AD.
CASE PRESENTATION: A case of CD in a 12-year-old boy presenting as acute adrenal insufficiency is described here. A gluten-free diet had a significant therapeutic role in this case, wherein most of the clinical signs and symptoms of AD disappeared in a few days. In addition, the dosage of cortisol acetate, initially administered to treat the AD, was able to be rapidly reduced.
CONCLUSION: This case highlights that CD can be associated with AD in children, and a gluten-free diet seems to positively influence the course of AD.

PMID: 28758924 [PubMed - indexed for MEDLINE]

Factors That Increase Risk of Celiac Disease Autoimmunity After a Gastrointestinal Infection in Early Life.

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Factors That Increase Risk of Celiac Disease Autoimmunity After a Gastrointestinal Infection in Early Life.

Clin Gastroenterol Hepatol. 2017 May;15(5):694-702.e5

Authors: Kemppainen KM, Lynch KF, Liu E, Lönnrot M, Simell V, Briese T, Koletzko S, Hagopian W, Rewers M, She JX, Simell O, Toppari J, Ziegler AG, Akolkar B, Krischer JP, Lernmark Å, Hyöty H, Triplett EW, Agardh D, TEDDY Study Group

Abstract
BACKGROUND & AIMS: Little is known about the pathogenic mechanisms of gluten immunogenicity in patients with celiac disease. We studied temporal associations between infections and the development of celiac disease autoimmunity, and examined effects of HLA alleles, rotavirus vaccination status, and infant feeding.
METHODS: We monitored 6327 children in the United States and Europe carrying HLA risk genotypes for celiac disease from 1 to 4 years of age for presence of tissue transglutaminase autoantibodies (the definition of celiac disease autoimmunity), until March 31, 2015. Parental reports of gastrointestinal and respiratory infections were collected every third month from birth. We analyzed time-varying relationships among reported infections, rotavirus vaccination status, time to first introduction of gluten, breastfeeding, and risk of celiac disease autoimmunity using proportional hazard models.
RESULTS: We identified 13,881 gastrointestinal infectious episodes (GIE) and 79,816 respiratory infectious episodes. During the follow-up period, 732 of 6327 (11.6%) children developed celiac disease autoimmunity. A GIE increased the risk of celiac disease autoimmunity within the following 3 months by 33% (hazard ratio [HR], 1.33; 95% confidence interval [CI], 1.11-1.59). This risk increased 2-fold among children born in winter and introduced to gluten before age 6 months (HR, 2.08; 95% CI, 1.46-2.98), and increased 10-fold among children without HLA-DQ2 alleles and breastfed for fewer than 4 months (HR, 9.76; 95% CI, 3.87-24.8). Risk of celiac disease autoimmunity was reduced in children vaccinated against rotavirus and introduced to gluten before age 6 months (HR, 0.57; 95% CI, 0.36-0.88).
CONCLUSIONS: Gastrointestinal infections increase the risk of celiac disease autoimmunity in children with genetic susceptibility to this autoimmune disorder. The risk is modified by HLA genotype, infant gluten consumption, breastfeeding, and rotavirus vaccination, indicating complex interactions among infections, genetic factors, and diet in the etiology of celiac disease in early childhood.

PMID: 27840181 [PubMed - indexed for MEDLINE]

Celiac Disease and Wheat Intolerance Syndrome: A Critical Update and Reappraisal.

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Celiac Disease and Wheat Intolerance Syndrome: A Critical Update and Reappraisal.

J Pediatr Gastroenterol Nutr. 2017 Jan;64(1):15-21

Authors: Jericho H, Assiri A, Guandalini S

Abstract
Since the first description of celiac disease (CeD) by Samuel Gee in 1888 and the later "miraculous discovery" that bread was responsible for this condition following World War II in Europe, there has been an exponential growth of knowledge regarding CeD. Just when we thought that we knew everything there was to know about it, the disease is, however, offering new challenges, with its presentation having significantly morphed over the years from cases of overt gastrointestinal symptoms, malnutrition, and atrophic villi on duodenal biopsies to that of largely extraintestinal, subtle, or mild symptoms. Along with these changes, unexpectedly a new parallel entity appeared a few years ago and is gaining ground: the so-called nonceliac gluten sensitivity, an improper name because it should actually be referred to as wheat intolerance syndrome given that the role of gluten in all such cases is far from demonstrated and the implication of an immune involvement suggested by the term "sensitivity" is still unfounded. Lastly, wheat can be an offender also through an immunoglobulin E-mediated allergy, whose presence must also be evaluated and ruled out in selected cases.The practicing physician is therefore now challenged with the task of discerning which patients need to be assessed for one or the other of these disorders, and how.This review aims at providing an updated, critical reassessment of these 2 entities.

PMID: 27322560 [PubMed - indexed for MEDLINE]

Adherence to the gluten free diet and health related quality of life in an ethnically diverse pediatric population with Celiac Disease.

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Adherence to the gluten free diet and health related quality of life in an ethnically diverse pediatric population with Celiac Disease.

J Pediatr Gastroenterol Nutr. 2017 Dec 28;:

Authors: Mager DM, Marcon M, Brill H, Liu A, Radmanovich K, Mileski H, Nasser R, Alzaben A, Carroll MW, Yap J, Persad R, Turner JM

Abstract
OBJECTIVES: Celiac disease (CD) is an autoimmune disease that requires life-long adherence to a gluten-free diet (GFD). Adherence to the GFD in childhood may be poor and adversely influence health related quality of life (HRQOL). The study purpose was to determine socio-demographic and socio-economic factors influencing adherence to the GFD and HRQOL in a multi-ethnic cohort of youth with CD.
METHODS: A multi-site (Edmonton, Hamilton, Toronto) study examining child-parent HRQOL in youth with CD (n=243) and /or mild gastrointestinal complaints (GI-CON; n = 148) was conducted. Socio-demographic (age, child-parental age/education/ethnicity/place of birth), anthropometric (weight, height, BMI), disease (diagnosis, age at diagnosis, duration, Marsh score, serology), household characteristics (income, family size, region, number of children/total household size), HRQOL (Peds TM/Kindl and CDDUX), GI Complaints (PedsQLGastrointestinal Symptom Scale [GSS]) and gluten intake were measured.
RESULTS: Younger age (<10 years), non-Caucasian ethnicity (parent/child) and presence of GI symptoms were associated with the highest rates of adherence to the GFD in CD children (p < 0.05). CD children (parent/child) had higher HRQOL (average, composite domains) than GI-CON (p < 0.05), but CD children were comparable to healthy children. Lack of GI symptoms, non-Caucasian ethnicity and age (<10 yrs) were associated with increased HRQOL in composite/average domains for CD (p < 0.05).
CONCLUSIONS: Child-parent perceptions of HRQOL in a multiethnic population with CD are comparable to healthy reference populations, but significantly higher than in parent/child GI-CON. Adherence to the GFD in ethnically diverse youth with CD was related to GI symptoms, age of the child and ethnicity of the parent-child.

PMID: 29287009 [PubMed - as supplied by publisher]

Transglutaminase 2-specific coeliac disease autoantibodies induce morphological changes and signs of inflammation in the small-bowel mucosa of mice.

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Transglutaminase 2-specific coeliac disease autoantibodies induce morphological changes and signs of inflammation in the small-bowel mucosa of mice.

Amino Acids. 2017 Mar;49(3):529-540

Authors: Kalliokoski S, Piqueras VO, Frías R, Sulic AM, Määttä JA, Kähkönen N, Viiri K, Huhtala H, Pasternack A, Laurila K, Sblattero D, Korponay-Szabó IR, Mäki M, Caja S, Kaukinen K, Lindfors K

Abstract
Coeliac disease is hallmarked by an abnormal immune reaction against ingested wheat-, rye- and barley-derived gluten and the presence of transglutaminase 2 (TG2)-targeted autoantibodies. The small-bowel mucosal damage characteristic of the disorder develops gradually from normal villus morphology to inflammation and finally to villus atrophy with crypt hyperplasia. Patients with early-stage coeliac disease have TG2-autoantibodies present in serum and small-intestinal mucosa and they may already suffer from abdominal symptoms before the development of villus atrophy. Previously, we have shown that intraperitoneal injections of coeliac patient-derived sera or purified immunoglobulin fraction into mice induce a condition mimicking early-stage coeliac disease. In the current study, we sought to establish whether recombinantly produced patient-derived TG2-targeted autoantibodies are by themselves sufficient for the development of such an experimentally induced condition in immune-compromised mice. Interestingly, mice injected with coeliac patient TG2-antibodies had altered small-intestinal mucosal morphology, increased lamina propria cellular infiltration and disease-specific autoantibodies deposited in the small bowel, but did not evince clinical features of the disease. Thus, coeliac patient-derived TG2-specific autoantibodies seem to be sufficient for the induction of subtle small-bowel mucosal alterations in mice, but the development of clinical features probably requires additional factors such as other antibody populations relevant in coeliac disease.

PMID: 27503559 [PubMed - indexed for MEDLINE]

Symptoms and Mucosal Changes Stable During Rapid Increase of Pediatric Celiac Disease in Norway.

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Symptoms and Mucosal Changes Stable During Rapid Increase of Pediatric Celiac Disease in Norway.

J Pediatr Gastroenterol Nutr. 2017 Apr;64(4):586-591

Authors: Beitnes AR, Vikskjold FB, Jóhannesdóttir GB, Perminow G, Olbjørn C, Andersen SN, Bentsen BS, Rugtveit J, Størdal K

Abstract
OBJECTIVES: We aimed to study whether the incidence of pediatric celiac disease (CD) in South-Eastern Norway changed from 2000 to 2010. We also examined whether there was a change in symptoms and histopathological morphology in the duodenal biopsies during the same period.
METHODS: In 3 hospitals in South-Eastern Norway, records from pediatric patients (0-14.9 years) diagnosed with CD during two 3-year periods (2000-2002 and 2008-2010) were reviewed. Only cases with a duodenal biopsy diagnosis of CD classified as Marsh grade 2 and 3a-c were included. Frequencies of symptoms, anthropometric data, and laboratory results were compared, in addition to re-examinations of histological sections from one of the hospitals.
RESULTS: A total of 400 cases were diagnosed with a female to male ratio of 1.5:1. The incidence rate for 2000 to 2002 was 15.9 cases per 100,000 person-years (95% confidence interval 12.8-19.4), compared with 45.5 cases per 100,000 person-years during 2008 to 2010 (95% confidence interval 40.5-50.9), P < 0.001. The relative frequencies of symptoms and the distribution of histopathological changes were similar in the 2 periods, whereas weight z scores and hemoglobin levels were significantly lower in the first period.
CONCLUSIONS: We found a 3-fold increase in the incidence rate for CD in the Norwegian pediatric population during the decade 2000 to 2010. Slightly higher weight and hemoglobin levels at diagnosis in the latter period may be due to improved CD awareness. Unaltered relative frequencies of symptoms and histopathological changes in the gut, however, suggest a true increase of CD in Norwegian children.

PMID: 27299421 [PubMed - indexed for MEDLINE]

Comprehensive Computational Analysis of GWAS Loci Identifies CCR2 as a Candidate Gene for Celiac Disease Pathogenesis.

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Comprehensive Computational Analysis of GWAS Loci Identifies CCR2 as a Candidate Gene for Celiac Disease Pathogenesis.

J Cell Biochem. 2017 Aug;118(8):2193-2207

Authors: Banaganapalli B, Rashidi O, Saadah OI, Wang J, Khan IA, Al-Aama JY, Shaik NA, Elango R

Abstract
Celiac disease (CD) is a gluten intolerance disorder with known genetic contribution. The recent fine mapping and genome-wide association studies (GWAS) have identified up to 57 non-HLA CD susceptibility SNPs, majority of which are non-coding variants lacking any functional annotation. Therefore, we adopted multidimensional computational approach for uncovering the plausible mechanisms through which these GWAS SNPs are connected to CD pathogenesis. At initial phase, we identified that 25 (43.85%) out of 57 CD-SNPs lies in evolutionarily constrained genetic element regions. In follow-up phases, through computational (CADD, GWAVA, and FATHMM algorithms) deleterious intensity measurements, we have discovered that 42 (3.94%) out of 1065 variants (57 CD-lead and 1008-linked SNPs; r2  ≥ 0.8) are differentially deleterious in nature to CD. Further functional scrutinization of these CD variants by public domain eQTL mapping, gene expression, knockout mouse model, and pathway analyses revealed that deleterious SNPs of CCR2 gene influences its expression levels and may also elicit a cascade of T-cell-mediated immunological events leading to intestinal gluten intolerance in genetically susceptible individuals. This study demonstrates the utility of integrated in silico analysis of annotations, gene expression, and pathways in prioritizing the potential complex disease variants from large-scale open source genomic data. J. Cell. Biochem. 118: 2193-2207, 2017. © 2017 Wiley Periodicals, Inc.

PMID: 28059456 [PubMed - indexed for MEDLINE]

Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling.

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Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling.

Schizophr Res. 2016 Sep;176(1):23-35

Authors: Severance EG, Yolken RH, Eaton WW

Abstract
Autoimmunity, gastrointestinal (GI) disorders and schizophrenia have been associated with one another for a long time. This paper reviews these connections and provides a context by which multiple risk factors for schizophrenia may be related. Epidemiological studies strongly link schizophrenia with autoimmune disorders including enteropathic celiac disease. Exposure to wheat gluten and bovine milk casein also contribute to non-celiac food sensitivities in susceptible individuals. Co-morbid GI inflammation accompanies humoral immunity to food antigens, occurs early during the course of schizophrenia and appears to be independent from antipsychotic-generated motility effects. This inflammation impacts endothelial barrier permeability and can precipitate translocation of gut bacteria into systemic circulation. Infection by the neurotropic gut pathogen, Toxoplasma gondii, will elicit an inflammatory GI environment. Such processes trigger innate immunity, including activation of complement C1q, which also functions at synapses in the brain. The emerging field of microbiome research lies at the center of these interactions with evidence that the abundance and diversity of resident gut microbiota contribute to digestion, inflammation, gut permeability and behavior. Dietary modifications of core bacterial compositions may explain inefficient gluten digestion and how immigrant status in certain situations is a risk factor for schizophrenia. Gut microbiome research in schizophrenia is in its infancy, but data in related fields suggest disease-associated altered phylogenetic compositions. In summary, this review surveys associative and experimental data linking autoimmunity, GI activity and schizophrenia, and proposes that understanding of disrupted biological pathways outside of the brain can lend valuable information regarding pathogeneses of complex, polygenic brain disorders.

PMID: 25034760 [PubMed - indexed for MEDLINE]

Celiac disease and Down syndrome mortality: a nationwide cohort study.

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Celiac disease and Down syndrome mortality: a nationwide cohort study.

BMC Pediatr. 2017 Jan 31;17(1):41

Authors: Ludvigsson JF, Lebwohl B, Green PH, Chung WK, Mårild K

Abstract
BACKGROUND: Individuals with Down syndrome (DS) have increased mortality and are also at increased risk of celiac disease (CD). It is unknown if CD influences mortality in DS. In this study we examined the risk of death in individuals with DS according to celiac status.
METHODS: In this nationwide population-based cohort study, we first identified individuals with CD (diagnosed 1969-2008) through small intestinal biopsy report data showing villous atrophy (Marsh stage III) from Sweden's 28 pathology departments. Celiac individuals were then matched with up to five reference individuals from the general population. In these cohorts we identified individuals with DS using International Classification of Disease codes (ICD) registered in the Swedish Patient Register (includes inpatients and hospital-based outpatients), the Medical Birth Register, and the Register of Congenital Malformations. Of 29,096 individuals with CD, 201 (0.7%) had DS compared to 124 of the 144,522 reference individuals (0.09%). Data on mortality were obtained from the Swedish Cause of Death Registry. Hazard ratios (HRs) for death were calculated using Cox regression.
RESULTS: During follow-up, there were seven deaths among individuals with DS and CD (7/201, 3.5%) as compared with 14 deaths among DS individuals without a record of CD (14/124, 11.3%). Adjusting for potential confounders, CD did not influence the risk of death in DS (HR = 1.36; 95%CI = 0.33-5.59). Cardiovascular death occurred in two individuals with CD and three individuals without CD, while death from malignancy occurred in one individual with CD and two individuals without CD.
CONCLUSION: While both DS and CD have been linked to increased risk of death, this study found no excess mortality in DS patients with a concurrent diagnosis of CD, however confidence intervals were wide.

PMID: 28143429 [PubMed - indexed for MEDLINE]

Prevalence of selective immunoglobulin A deficiency in Greek children and adolescents with type 1 diabetes.

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Prevalence of selective immunoglobulin A deficiency in Greek children and adolescents with type 1 diabetes.

World J Pediatr. 2016 Nov;12(4):470-476

Authors: Giza S, Kotanidou E, Papadopoulou-Alataki E, Antoniou MC, Maggana I, Kyrgios I, Galli-Tsinopoulou A

Abstract
BACKGROUND: The association of selective immunoglobulin A (IgA) deficiency with type 1 diabetes (T1D) remains unclear. This study was to evaluate serum IgA concentrations in Greek children and adolescents with T1D.
METHODS: In two hundred individuals with T1D, serum IgA concentrations were quantitatively determined using nephelometry.
RESULTS: Immunoglobulin A deficiency was detected in 6 (3.0%) of 200 patients who were subjected to immunological evaluation. Recurrent infections were not recorded, but human papilloma virus infection was clinically suspected and confirmed by laboratory examination in a 5-year-old girl. In regard to coincidence of selective IgA deficiency with autoimmune diseases, celiac disease was detected in a girl and juvenile idiopathic arthritis in a boy. Serum IgA concentrations differed significantly when patients were grouped according to age at the beginning of the study (P<0.001), age at diagnosis of T1D (P=0.015) and coincidence of celiac disease (CD) (P=0.038). However, when the age of the patients was adjusted, difference in serum IgA concentrations was not statistically significant despite CD was present or not. Moreover, serum IgA concentrations were positively correlated with serum IgG (P<0.001) and IgE (P=0.001) concentrations and negatively correlated with serum antigliadin antibody IgG (P=0.035) concentrations. There was no association or correlation of serum IgA concentrations with glycemic control.
CONCLUSION: The prevalence of selective IgA deficiency in Greek children and adolescents with T1D is high (3.0%). The correlation of serum IgA concentrations with serum IgG, IgE and anti-gliadin antibody IgG concentrations needs further investigation.

PMID: 27286692 [PubMed - indexed for MEDLINE]

E-Healthcare for Celiac Disease-A Multicenter Randomized Controlled Trial.

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E-Healthcare for Celiac Disease-A Multicenter Randomized Controlled Trial.

J Pediatr. 2017 Dec 21;:

Authors: Vriezinga S, Borghorst A, van den Akker-van Marle E, Benninga M, George E, Hendriks D, Hopman E, de Meij T, van der Meulen-de Jong A, Putter H, Rings E, Schaart M, Schweizer J, Smit M, Tabbers M, Weijerman M, Wessels M, Mearin ML

Abstract
OBJECTIVE: To evaluate the (cost-)effectiveness of online consultations in follow-up of patients with celiac disease (CD).
STUDY DESIGN: Multicenter randomized, controlled trial involving 304 patients aged ≤25 years with CD for ≥1 year, randomized to an online (n = 156) or outpatient consultation (n = 148). An online consultation included questionnaires for symptom and growth measurement. Antitransglutaminase-type-2 antibodies were determined using a point-of-care (POC) test. Controls had a traditional consultation with antitransglutaminase-type-2 antibodies testing in laboratories. Both groups completed questionnaires concerning CD-specific health-related quality of life (HRQOL), gluten-free diet adherence, and patient satisfaction. Six months later, participants repeated HRQOL and patient satisfaction questionnaires and the POC test. The primary outcome was anti-transglutaminase-type-2 antibodies after 6 months, and the secondary outcomes were health problems, dietary adherence, HRQOL, patient satisfaction, and costs.
RESULTS: The performance of the POC test was inferior to laboratory testing (2/156 positive POC tests vs 13/148 positive laboratory tests; P = .003). Health problems were detected significantly more frequently using online consultation. The detection of growth problems and dietary transgressions was similar. HRQOL (from 1 [good] to 5 [poor]) improved after online consultation (from 3.25 to 3.16 [P = .013] vs controls from 3.10 to 3.23; P = .810). Patient satisfaction (from 1 [low] to 10 [high]) was 7.6 (online) vs 8.0 (controls; P = .001); 58% wished to continue online consultations. Mean costs per participant during the studied period were €202 less for the online group (P < .001).
CONCLUSIONS: The primary outcome could not be tested because the POC test was unreliable. Nevertheless, our results indicate that online consultations for children and young adults with CD are cost saving, increase CD-specific HRQOL, and are satisfactory for the majority.
TRIAL REGISTRATION: Trialregister.nl: NTR3688.

PMID: 29275927 [PubMed - as supplied by publisher]

Sex- and age-dependent effects of celiac disease on growth and weight gain in children with type 1 diabetes: Analysis of the type 1 diabetes Exchange Clinic Registry.

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Sex- and age-dependent effects of celiac disease on growth and weight gain in children with type 1 diabetes: Analysis of the type 1 diabetes Exchange Clinic Registry.

Pediatr Diabetes. 2017 Dec 22;:

Authors: Simmons JH, Foster NC, Riddlesworth TD, DuBose SN, Redondo MJ, Liu E, Freemark M, T1D Exchange Clinic Network

Abstract
BACKGROUND: Celiac disease (CD) is common in patients with type 1 diabetes (T1D) and effects of CD on growth in children with T1D remain unclear.
METHODS: We analyzed heights, weights, and body mass index (BMI) in 215 matched pediatric CD/control pairs in the T1D Exchange Clinic Registry. CD was defined by a clinic-reported diagnosis and positive celiac serology (n = 80) and/or positive small bowel biopsy (n = 135). Cases and controls were matched by age (mean: 14 years), diabetes duration (median: 7 years), sex (57% female), and clinic site. There were 5569 height/weight measurements.
RESULTS: Gluten was restricted for varying periods of time in 61% of females and 51% of males with CD. Females with CD were shorter than female controls at all ages (P = 0.01). Weight z-scores were initially lower in preschool females with CD but similar to controls by middle childhood. Males with CD were initially shorter but adult heights were similar. Height in both sexes and weight in males were lower in CD participants diagnosed at younger age. Growth in T1D children with biopsy-proven CD, 76% of them were gluten-restricted, was comparable to that of T1D controls.
CONCLUSION: Concurrent CD impairs linear growth in T1D females at all stages of development and in young T1D males. Young females with CD have lower weights, but both sexes have similar weights by middle childhood. Children younger at CD onset remain shorter throughout childhood; males younger at CD onset have persistently lower weights. Long-term gluten restriction may restore weight gain and linear growth in children with CD and T1D.

PMID: 29271067 [PubMed - as supplied by publisher]

A new ELISA for autoantibodies to steroid 21-hydroxylase.

A new ELISA for autoantibodies to steroid 21-hydroxylase.

Clin Chem Lab Med. 2017 Dec 21;:

Authors: Larosa MDP, Chen S, Steinmaus N, Macrae H, Guo L, Masiero S, Garelli S, Dalla Costa M, Bossowski A, Furmaniak J, Betterle C, Rees Smith B

Abstract
BACKGROUND: A new ELISA for autoantibodies to steroid 21-hydroxylase (21-OH Ab) is described.
METHODS: In the assay test sample autoantibodies form a bridge between 21-OH coated onto the plate well and liquid phase 21-OH-biotin. Bound 21-OH-biotin is detected by the addition of streptavidin peroxidase and colorogenic peroxidase substrate.
RESULTS: Of 100 samples from patients with autoimmune Addison's disease, 86 (86%) were positive for 21-OH Ab ELISA whereas 84 (84%) were positive in an immunoprecipitation assay based on 125I-labeled 21-OH. Six (0.6%) of 928 healthy adult blood donors and 1 (2.0%) of 49 adult patients with type 1 diabetes mellitus (T1DM) were positive by ELISA. No samples from adult patients with Graves' disease (GD; n=50), celiac disease (n=29), systemic lupus erythematosis (n=9) or rheumatoid arthritis (n=20) were positive by ELISA. However, 2/51 (3.9%) children with GD, 3/69 (4.3%) children with Hashimoto's thyroiditis (HT) and 3/119 (2.5%) children with T1DM alone or associated with autoimmune thyroid disorders were ELISA positive.
CONCLUSIONS: The new assay should be useful for screening patients known to be at increased risk of developing clinical autoimmune Addison's disease, in particular children with HT, GD and/or T1DM.

PMID: 29267164 [PubMed - as supplied by publisher]

Pediatric Celiac Disease: Follow-Up in the Spotlight.

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Pediatric Celiac Disease: Follow-Up in the Spotlight.

Adv Nutr. 2017 Mar;8(2):356-361

Authors: Valitutti F, Trovato CM, Montuori M, Cucchiara S

Abstract
The follow-up of celiac disease (CD) is challenging due to the scarcity of published data and the lack of standardized evidence-based protocols. The worldwide frequency and methods of CD follow-up appear to be heavily influenced by expert opinions of the individual physicians who assess children with CD. The aim of this review was to summarize the available studies on CD follow-up in children. We conducted a literature search with the use of PubMed, Medline, and Embase (from 1900 to 15 December 2016) for terms relevant to this review, including CD, follow-up, dietary adherence or dietary compliance, nutrition, comorbidities, complications, and quality of life. The aims of follow-up are as follows: to ensure strict adherence to a gluten-free diet, to ensure nutritional adequacy, to improve quality of life, and to prevent disease complications. For the correct evaluation of children with CD at follow-up, a clinical and biochemical evaluation is necessary on a regular basis. It is advisable to assess compliance, nutrition, comorbidities, or possible complications once a year at the referral center. Laboratory tests might be useful for a thorough evaluation of any patient with CD to rule out a micronutrient deficiency (full blood count, ferritin, folic acid, vitamin B-6, and vitamin B-12) and possible cardiovascular risk factors (glucose, LDL cholesterol, triglycerides). Biochemical evaluation is essential when there are clinical problems and should be customized on the basis of the specific clinical suspicion. Associated autoimmune thyroiditis should also be screened for yearly by measuring thyroid-stimulating hormone and thyroid autoantibody concentrations, regardless of symptoms, because hypothyroidism is often subtle and methods for early treatment are available and desirable. Although evidence-based recommendations for follow-up of pediatric patients with CD have not yet been established, we advise a yearly follow-up visit as the safest approach.

PMID: 28298278 [PubMed - indexed for MEDLINE]

Is Celiac Disease an Etiological Factor in Children With Migraine?

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Is Celiac Disease an Etiological Factor in Children With Migraine?

J Child Neurol. 2016 Jun;31(7):929-31

Authors: Balcı O, Yılmaz D, Sezer T, Hızlı Ş

Abstract
To determine the prevalence of celiac disease in children and adolescents with migraine, the authors investigated serum levels of tissue transglutaminase antibody immunoglobulin A and total immunoglobulin A from 81 children with migraine and in a healthy control group of 176 children. Study participants who were positive for tissue transglutaminase immunoglobulin A antibodies underwent a duodenal biopsy. Two patients in the migraine group (2.5%) and 1 in the control group (0.57%) tested positive for serum tissue transglutaminase immunoglobulin A antibodies (P > .05). Duodenal biopsy did not confirm celiac disease in both groups, and these patients were considered "potential celiac" cases. In the present study, children with migraine did not exhibit a higher prevalence rate of celiac disease compared with healthy controls. Therefore, the screening test for celiac disease is not a necessary part of the management of migraine in children.

PMID: 26887413 [PubMed - indexed for MEDLINE]

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