American Gastroenterological Association (AGA) Institute Technical Review on the Diagnosis and Management of Celiac Disease
Division of Gastroenterology, Foothills Medical Centre, University of Calgary, Calgary, Alberta, Canada. Gastroenterology
(Impact Factor: 16.72).
01/2007; 131(6):1981-2002. DOI: 10.1053/j.gastro.2006.10.004
This technical review addresses the state of evidence for celiac disease epidemiology, detection by serologic testing, diagnosis by biopsy, treatment, and outcome. It updates the previous American Gastroenterological Association (AGA) Institute technical review on celiac disease published in 2001.
Available from: PubMed Central
- "Individuals with a high risk for celiac disease include first-degree, and to a lesser extent second degree, relatives of patients with celiac disease [7,8]. In addition, individuals with co-morbid diseases such as type I diabetes mellitus, autoimmune thyroid disease, dermatitis herpetiformis, Sjogren’s disease, microscopic colitis, and autoimmune liver disease have an increased prevalence of celiac disease [8,9]. Celiac disease has also been reported to be increased in those with dental enamel hypoplasia , cerebellar ataxia , and migraine headaches , and in a subset of individuals with irritable bowel syndrome, although the latter has been controversial . "
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ABSTRACT: Celiac disease is present in ~1% of the general population in the United States and Europe. Despite the availability of inexpensive serologic screening tests, ~85% of individuals with celiac disease remain undiagnosed and there is an average delay in diagnosis of symptomatic individuals with celiac disease that ranges from ~5.8-11 years. This delay is often attributed to the use of a case-based approach for detection rather than general population screening for celiac disease, and deficiencies at the level of health care professionals. This study aimed to assess if patient-centered barriers have a role in impeding serologic screening for celiac disease in individuals from populations that are clinically at an increased risk for celiac disease.
119 adults meeting study inclusion criteria for being at a higher risk for celiac disease were recruited from the general population. Participants completed a survey/questionnaire at the William K. Warren Medical Research Center for Celiac Disease that addressed demographic information, celiac disease related symptoms (gastrointestinal and extraintestinal), family history, co-morbid diseases and conditions associated with celiac disease, and patient-centered barriers to screening for celiac disease. All participants underwent serologic screening for celiac disease using the IgA tissue transglutaminase antibody (IgA tTG) and, if positive, testing for IgA anti-endomysial antibody (IgA EMA) as a confirmatory test.
Two barriers to serologic testing were significant across the participant pool. These were participants not knowing they were at risk for celiac disease before learning of the study, and participants not knowing where to get tested for celiac disease. Among participants with incomes less than $25,000/ year and those less than the median age, not having a doctor to order the test was a significant barrier, and this strongly correlated with not having health insurance. Symptoms and co-morbid conditions were similar among those whose IgA tTG were negative and those who tested positive.
There are significant patient-centered barriers that impede serologic screening and contribute to the delayed detection and diagnosis of celiac disease. These barriers may be lessened by greater education of the public and health care professionals about celiac disease symptoms, risk factors, and serologic testing.
BMC Gastroenterology 03/2014; 14(1):42. DOI:10.1186/1471-230X-14-42 · 2.37 Impact Factor
Available from: Mohammad rostami nejad
- "Clinical presentation of disorder can vary from a classic malabsorption syndrome to extra-intestinal symptoms such as infertility, iron deficiency anaemia, and osteoporosis. CD may also be presented subclinical and diagnosed unexpectedly on routine investigations foriron deficiency anaemia or symptoms of irritable bowel syndrome (1, 4, 5). "
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Celiac disease (CD) is defined as a permanent intolerance to ingested gluten. The intolerance to gluten results in immune-mediated damage of small intestine mucosa manifested by villous atrophy and crypt hyperplasia. These abnormalities resolve with initiationa gluten-free diet.
PubMed, Ovid, and Google were searched for full text articles published between 1963 and 2012. The associated keywords were used, and papers described particularly the impact of celiac disease on severity of liver disorder were identified.
Recently evidence has emerged revealingthat celiac disease not only is associated with small intestine abnormalities and malabsorption, but is also a multisystem disorder affecting other systems outside gastrointestinal tract, including musculo-skeletal, cardiovascular and nervous systems. Some correlations have been assumed between celiac and liver diseases. In particular, celiac disease is associated with changes in liver biochemistry and linked to alter the prognosis of other disorders. This review will concentrate on the effect of celiac disease and gluten-free diets on the severity of liver disorders.
Although GFD effect on the progression of CD associated liver diseases is not well defined, it seems that GFD improves liver function tests in patients with a hypertransaminasemia.
Hepatitis Monthly 10/2013; 13(10):e11893. DOI:10.5812/hepatmon.11893 · 1.93 Impact Factor
Available from: Juha Taavela
- "Soon after the discovery of the gluten-induced detrimental effect on the mucosal architecture in celiac disease it became clear that great care should be taken in orienting specimens in order to ensure representative vertical sections , . One of the main reasons for missing a celiac disease diagnosis is incorrect biopsy orientation, resulting in cross-sectioning of the crypts and thus loss of evidence of crypt hyperplasia , . In contrast, the IEL densities are mainly unaffected by the biopsy orientation as shown here in Figure 3. "
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ABSTRACT: Assessment of the gluten-induced small-intestinal mucosal injury remains the cornerstone of celiac disease diagnosis. Usually the injury is evaluated using grouped classifications (e.g. Marsh groups), but this is often too imprecise and ignores minor but significant changes in the mucosa. Consequently, there is a need for validated continuous variables in everyday practice and in academic and pharmacological research.
We studied the performance of our standard operating procedure (SOP) on 93 selected biopsy specimens from adult celiac disease patients and non-celiac disease controls. The specimens, which comprised different grades of gluten-induced mucosal injury, were evaluated by morphometric measurements. Specimens with tangential cutting resulting from poorly oriented biopsies were included. Two accredited evaluators performed the measurements in blinded fashion. The intraobserver and interobserver variations for villus height and crypt depth ratio (VH:CrD) and densities of intraepithelial lymphocytes (IELs) were analyzed by the Bland-Altman method and intraclass correlation.
Unevaluable biopsies according to our SOP were correctly identified. The intraobserver analysis of VH:CrD showed a mean difference of 0.087 with limits of agreement from -0.398 to 0.224; the standard deviation (SD) was 0.159. The mean difference in interobserver analysis was 0.070, limits of agreement -0.516 to 0.375, and SD 0.227. The intraclass correlation coefficient in intraobserver variation was 0.983 and that in interobserver variation 0.978. CD3(+) IEL density countings in the paraffin-embedded and frozen biopsies showed SDs of 17.1% and 16.5%; the intraclass correlation coefficients were 0.961 and 0.956, respectively.
Using our SOP, quantitative, reliable and reproducible morphometric results can be obtained on duodenal biopsy specimens with different grades of gluten-induced injury. Clinically significant changes were defined according to the error margins (2SD) of the analyses in VH:CrD as 0.4 and in CD3(+)-stained IELs as 30%.
PLoS ONE 10/2013; 8(10):e76163. DOI:10.1371/journal.pone.0076163 · 3.23 Impact Factor
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