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Sökning: WFRF:(Alaedini Armin)

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1.
  • Alaedini, Armin, et al. (författare)
  • Borrelia infection and risk of celiac disease
  • 2017
  • Ingår i: BMC Medicine. - : BioMed Central. - 1741-7015. ; 15
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Environmental factors, including infectious agents, are speculated to play a role in the rising prevalence and the geographic distribution of celiac disease, an autoimmune disorder. In the USA and Sweden where the regional variation in the frequency of celiac disease has been studied, a similarity with the geographic distribution of Lyme disease, an emerging multisystemic infection caused by Borrelia burgdorferi spirochetes, has been found, thus raising the possibility of a link. We aimed to determine if infection with Borrelia contributes to an increased risk of celiac disease.Methods: Biopsy reports from all of Sweden's pathology departments were used to identify 15,769 individuals with celiac disease. Through linkage to the nationwide Patient Register, we compared the rate of earlier occurrence of Lyme disease in the patients with celiac disease to that in 78,331 matched controls. To further assess the temporal relationship between Borrelia infection and celiac disease, we also examined the risk of subsequent Lyme disease in patients with a diagnosis of celiac disease.Results: Twenty-five individuals (0.16%) with celiac disease had a prior diagnosis of Lyme disease, whereas 79 (0.5%) had a subsequent diagnosis of Lyme disease. A modest association between Lyme disease and celiac disease was seen both before (odds ratio, 1.61; 95% confidence interval (CI), 1.06-2.47) and after the diagnosis of celiac disease (hazard ratio, 1.82; 95% CI, 1.40-2.35), with the risk of disease being highest in the first year of follow-up.Conclusions: Only a minor fraction of the celiac disease patient population had a prior diagnosis of Lyme disease. The similar association between Lyme disease and celiac disease both before and after the diagnosis of celiac disease is strongly suggestive of surveillance bias as a likely contributor. Taken together, the data indicate that Borrelia infection is not a substantive risk factor in the development of celiac disease.
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2.
  • Lau, Nga M., et al. (författare)
  • Markers of Celiac Disease and Gluten Sensitivity in Children with Autism
  • 2013
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:6, s. e66155-
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Gastrointestinal symptoms are a common feature in children with autism, drawing attention to a potential association with celiac disease or gluten sensitivity. However, studies to date regarding the immune response to gluten in autism and its association with celiac disease have been inconsistent. The aim of this study was to assess immune reactivity to gluten in pediatric patients diagnosed with autism according to strict criteria and to evaluate the potential link between autism and celiac disease. Methods: Study participants included children (with or without gastrointestinal symptoms) diagnosed with autism according to both the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADIR) (n = 37), their unaffected siblings (n = 27), and age-matched healthy controls (n = 76). Serum specimens were tested for antibodies to native gliadin, deamidated gliadin, and transglutaminase 2 (TG2). Affected children were genotyped for celiac disease associated HLA-DQ2 and -DQ8 alleles. Results: Children with autism had significantly higher levels of IgG antibody to gliadin compared with unrelated healthy controls (p<0.01). The IgG levels were also higher compared to the unaffected siblings, but did not reach statistical significance. The IgG anti-gliadin antibody response was significantly greater in the autistic children with gastrointestinal symptoms in comparison to those without them (p<0.01). There was no difference in IgA response to gliadin across groups. The levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2, did not differ between patients and controls. An association between increased anti-gliadin antibody and presence of HLA-DQ2 and/or -DQ8 was not observed. Conclusions: A subset of children with autism displays increased immune reactivity to gluten, the mechanism of which appears to be distinct from that in celiac disease. The increased anti-gliadin antibody response and its association with GI symptoms points to a potential mechanism involving immunologic and/or intestinal permeability abnormalities in affected children.
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3.
  • Lebwohl, Benjamin, et al. (författare)
  • Risk of Headache-Related Healthcare Visits in Patients With Celiac Disease : A Population-Based Observational Study
  • 2016
  • Ingår i: Headache. - Hoboken, USA : Wiley-Blackwell. - 0017-8748 .- 1526-4610. ; 56:5, s. 849-858
  • Tidskriftsartikel (refereegranskat)abstract
    • Background and Aims: Patients with celiac disease (CD) are reported to be at increased risk for headaches, though large studies are lacking. We aimed to examine the risk of headache-related healthcare encounters in patients with CD in a nationwide population-based setting.Methods: In this population-based retrospective cohort study, we searched all (n = 28) pathology departments in Sweden and identified patients with CD based on the presence of villous atrophy (VA). Each patient was matched to up to 5 controls, by age, gender, calendar period, and region. Using Cox proportional hazards, we tested for an association between CD and subsequent headache-related visit. We also tested this association for those with intestinal inflammation but normal villi, and subjects with positive CD serologies but normal histology.Results: Among 28,638 patients with CD and 143,126 controls, headache-related visit occurred in 1,337 (4.7%) and 4,102 (2.9%), respectively. The incidence of headache-related visit was 423 per 100,000 person-years in CD patients and 254 per 100,000 person-years in controls (HR 1.66; 95% CI 1.56-1.77; P < .0001). Individuals having inflammation without VA on small intestinal biopsy (n = 12,898; HR 2.08; 95% CI 1.90-2.27; P < .0001) and those with normal mucosa but positive CD serology (n = 3,617; HR 1.83; 95% CI 1.57-2.12; P < .0001) were also at increased risk for headache-related visit.Conclusions: In this population-based study we found a significantly increased risk of headache-related visits in patients with CD; this increase was also present in patients with intestinal inflammation and those with positive CD serology but with normal mucosal architecture on small bowel biopsy. Though limited by surveillance bias, this study indicates that headache-related visits are more common in these populations.
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4.
  • Moeller, Sina, et al. (författare)
  • Lack of association between autism and anti-GM1 ganglioside antibody
  • 2013
  • Ingår i: Neurology. - 0028-3878 .- 1526-632X. ; 81:18, s. 1640-1641
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Forty of 54 children with autism were reported to have an elevated antibody response to GM1 ganglioside that correlated with disease severity.1 Antiganglioside autoantibodies, especially those directed at GM1, are known to be associated with and play a pathogenic role in some immune-mediated peripheral neuropathies.2,3 The presumed link between autism and anti-GM1 antibodies, therefore, implies that testing may identify a sizable subset of patients who would benefit from immunomodulatory therapy. To evaluate the proposed association between autism and anti-GM1 antibodies, serum samples from children diagnosed with autism by strict clinical criteria and those without autism were analyzed using a standard, validated immunoassay protocol.
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5.
  • Stenberg, Reidun, 1954-, et al. (författare)
  • Associations Between Subclass Profile of IgG Response to Gluten and the Gastrointestinal and Motor Symptoms in Children with Cerebral Palsy
  • 2021
  • Ingår i: Journal of Pediatric Gastroenterology and Nutrition - JPGN. - : Lippincott Williams & Wilkins. - 0277-2116 .- 1536-4801. ; 73:3, s. 367-375
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: Gastrointestinal problems are often seen in children with cerebral palsy, although the etiology and underlying mechanisms are not fully understood. Recent data point to significantly elevated levels of IgG antibody to dietary gluten in cerebral palsy independent of celiac disease, a gluten-mediated autoimmune enteropathy. We aimed to further characterize this antibody response by examining its subclass distribution and target reactivity in the context of relevant patient symptom profile.METHODS: Study participants included children with cerebral palsy (n = 70) and celiac disease (n = 85), as well as unaffected controls (n = 30). Serum IgG antibody to gluten was investigated for subclass distribution, pattern of reactivity towards target proteins, and relationship with gastrointestinal symptoms and motor function.RESULTS: The anti-gluten IgG antibody response in the cerebral palsy cohort was comprised of all four subclasses. However, in comparison with celiac disease, IgG1, IgG2, and IgG3 subclasses were significantly lower, whereas the IgG4 response was significantly higher in cerebral palsy. Within the cohort of cerebral palsy patients, levels of anti-gluten IgG1, IgG3, and IgG4 were greater in those with gastrointestinal symptoms, and the IgG3 subclass antibody correlated inversely with gross motor function. The anti-gluten IgG antibodies targeted a broad range of gliadin and glutenin proteins.CONCLUSION: These findings reveal an anti-gluten IgG subclass distribution in cerebral palsy that is significantly different from that in celiac disease. Furthermore, the observed association between IgG subclass and symptom profile is suggestive of a relationship between the immune response and disease pathophysiology that may indicate a role for defects in gut immune and barrier function in cerebral palsy.
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