scholarly journals Testing for Gluten-Related Disorders in Clinical Practice: The Role of Serology in Managing the Spectrum of Gluten Sensitivity

2011 ◽  
Vol 25 (4) ◽  
pp. 193-197 ◽  
Author(s):  
David Armstrong ◽  
Andrew C Don-Wauchope ◽  
Elena F Verdu

Immunoglobulin A tissue transglutaminase is the single most efficient serological test for the diagnosis of celiac disease. It is well known that immunoglobulin A tissue transglutaminase levels correlate with the degree of intestinal damage, and that values can fluctuate in patients over time. Serological testing can be used to identify symptomatic individuals that need a confirmatory biopsy, to screen at-risk populations or to monitor diet compliance in patients previously diagnosed with celiac disease. Thus, interpretation of serological testing requires consideration of the full clinical scenario. Antigliadin tests are no longer recommended for the diagnosis of classical celiac disease. However, our understanding of the pathogenesis and spectrum of gluten sensitivity has improved, and gluten-sensitive irritable bowel syndrome patients are increasingly being recognized. Studies are needed to determine the clinical utility of antigliadin serology in the diagnosis of gluten sensitivity.

2000 ◽  
Vol 14 (11) ◽  
pp. 919-921 ◽  
Author(s):  
Helen Rachel Gillett ◽  
Hugh James Freeman

Both collagenous and lymphocytic colitis have been described in patients with celiac disease, suggesting an association between the conditions. Over the past few years, the availability, sensitivity and specificity of serological markers for celiac disease have improved - the most recent advancement being the description of tissue transglutaminase as the major antigen for endomysium antibody. A quantitative ELISA was used to measure titres of immunoglobulin A (IgA) antibody to tissue transglutaminase (tTG) along with an immunofluorescent technique for IgA endomysium antibody (EmA) in 15 patients with lymphocytic colitis and eight with collagenous colitis to determine whether celiac disease latency could be detected. One patient with lymphocytic colitis demonstrated both elevated titres of tTG antibody and positive EmA, and small bowel biopsy confirmed celiac disease. One patient with collagenous colitis had a slightly elevated titre of tTG antibody with a negative EmA, and results of a small bowel biopsy were normal. Three other patients with lymphocytic colitis were already treated for previously diagnosed celiac disease. The prevalence of celiac disease occurring in lymphocytic colitis was found to be 27%, but no cases of celiac disease in association with collagenous colitis were found.


2006 ◽  
Vol 4 (6) ◽  
pp. 726-730 ◽  
Author(s):  
Julian A. Abrams ◽  
Pardeep Brar ◽  
Beverly Diamond ◽  
Heidrun Rotterdam ◽  
Peter H. Green

2010 ◽  
Vol 24 (2) ◽  
pp. 103-107 ◽  
Author(s):  
Donald R Duerksen ◽  
William D Leslie

BACKGROUND: Low bone density and osteoporosis have been demonstrated in celiac disease populations in Europe, South America and the United States. Serological testing with tissue transglutaminase (TTG) and immunoglobulin A endomysial (EMA) antibodies is highly specific for celiac disease, while antigliadin antibody (AGA) testing is less specific.OBJECTIVE: To evaluate the association of celiac serology with reduced bone density in adult women.METHODS: A clinical database containing all bone density testing data in the province of Manitoba was linked to a database containing all celiac serology data for the province. The study cohort consisted of 376 women older than 20 years of age with bone density measurements preceding initial celiac serology by six months or less. Bone density was assessed in relation to TTG/EMA and AGA seropositivity, and compared with seronegative controls in age-, height- and weight-adjusted models.RESULTS: There was significantly lower bone density in TTG/EMA seropositive women than with seronegative controls for all sites tested (lumbar spine, total hip, trochanter, femoral neck; all P<0.05). TTG/EMA seropositive women also had a significantly higher prevalence of osteoporosis (67.7% versus 44.8%; P<0.05). There was lower bone density at the three hip sites (all P<0.05) in AGA seropositive women, but after excluding TTG/EMA seropositive women, isolated AGA seropositivity showed no significant association with any bone density measurements.CONCLUSION: TTG/EMA seropositivity was associated with lower bone density and a higher prevalence of osteoporosis compared with seronegative controls.


2000 ◽  
Vol 14 (11) ◽  
pp. 915-918 ◽  
Author(s):  
PM Gillett ◽  
HR Gillett ◽  
DM Israel ◽  
DL Metzger ◽  
L Stewart ◽  
...  

OBJECTIVE: To establish the prevalence of celiac disease (CD) in girls with Turner syndrome (TS) in British Columbia.METHODS: Forty-five girls with TS were prospectively screened for CD using blinded testing with the current ’gold standard’ - immunoglobulin A (IgA) endomysium antibody (EmA) and the novel IgA tissue transglutaminase antibody (tTG). Those with positive results were offered small bowel biopsies, and a gluten-free diet was recommended if CD was confirmed.RESULTS: One asymptomatic prepubertal East Indian girl was positive for EmA, had an elevated tTG concentration of 560 U/mL and histological evidence of CD. Seven girls were negative for EmA but had elevated tTG concentrations (175 to 250 U/mL); five were white, one was Asian and one was East Indian. Small bowel biopsies were performed on three girls, and the histologies were normal. The remaining four patients declined biopsy.CONCLUSIONS: One girl with TS was identified with CD from 45 screened, giving an overall biopsy-confirmed prevalence of 2.2%. This study confirms previous observations placing girls with TS at higher risk for CD and suggests a similar high prevalence in British Columbia.


Author(s):  
Feridun Gurlek ◽  
Eyyup Tasdemir ◽  
Taskın Erkinuresin

Background: The aim of this study is to evaluate gluten sensitivity and/or celiac disease (CD) on the basis of serological tests and duodenal biopsy and to draw attention to the prevalence in the population and the correlation between serological tests and biopsy results.Methods: Patients who applied to Health Sciences University Bursa High Specialization Training and Research Hospital between 2015-2019 and who underwent serological tests and duodenal biopsies with a diagnosis of CD or gluten sensitivity were retrospectively analyzed.Results: The study was conducted with a total of 1137 cases, 61.2% (n = 696) of who were women and 38.8% (n = 441) were men. Their ages range from 17 to 91, with a mean of 40.16 ± 16.18 years. Of the 178 patients with gluten sensitivity, 122 (68%) were female and 56 (32%) were male. According to the results of duodenal biopsy, an average of 8% Marsh 3, 5% Marsh 1-2 was detected in the last five years. For the whole study, a significant difference was found between celiac autoantibody positivity rates according to the biopsy results (p = 0.001; p <0.01). The rate of serological test positivity was higher in patients with biopsy result Marsh 3 than those with normal biopsy result, peptic duodenitis and Marsh 1 and 2. No statistically significant difference was found between the rates of Marsh 3 biopsy results and serological test positivity by years (p> 0.05).Conclusions: The number of patients applied with a diagnosis of CD in the last five years has gradually increased (3.4-33.7%). Of the patients with Marsh 3 and Marsh 1-2 biopsy results, 78% were under 50 years old. This suggests that gluten enteropathy in young female patients having digestive system complaints should not be ignored during the diagnosis. Serological test results were highly correlated with the biopsy results in patients with Marsh 3 biopsy results. We think that if clinical findings are supported with serological tests and directed for biopsy in the diagnosis of celiac disease, it will be more cost effective and the workload and time loss will be prevented.


Author(s):  
Helmut Niederhofer ◽  
Klaus Pittschieler

Celiac disease (CD) is an immune-mediated chronic inflammatory disorder characterized by permanent gluten intolerance in genetically susceptible individuals. Exposure to gluten perpetuates an enteropathy leading to malabsorption with chronic diarrhea, weight loss, and abdominal distension. The small intestine mucosa is abnormal, and jejunal biopsy demonstrates various degrees of villous atrophy, absence of surface mucosa, and crypt hyperplasia. The diagnosis is based on the demonstration of a more or less pronounced villus atrophy in a jejunal biopsy. The villous atrophy improves after withdrawal of gluten from the diet. If undetected or neglected, CD may cause considerable late complications from malabsorption or secondary autoimmune diseases (Feigbery 1999; Maki and Collins 1997; Holmes 1996). The therapy consists of permanently excluding gluten from the diet and allows the healing of the mucosal lesion. Abnormalities of humeral and cell-mediated immunity suggest that celiac disease is an immunologic disorder (Walker-Smith 1996). It is caused by inappropriate immune response to the gliadin component in the dietary gluten (Dieterich 1997). Genetic susceptibility is present, and 90% of the patients have HLA DRG 3 DQ-2 haplotype, and some have the HLA DR4 DQ8 gene (Hadjivassiliou 1998). A close relationship exists between the biochemical properties of tissue transglutaminase and the basic molecular mechanisms responsible for CD, and possibly with the neuropsychiatric manifestations of CD (Gentile 2002). Anti–tissue transglutaminase antibody assay has been used as a serologic screening test for CD. In addition, antiendomysial, antigliadin, and antireticulin antibodies are associated with the disease. Nevertheless, the clinical symptomatology affecting the gastrointestinal (GI) system, histological abnormalities on gut biopsy, and presence of antiendomysial antibodies do not always coexist. Also, presentation with minor symptoms, such as irritable bowel syndrome, anaemia, slight weight loss, and fatigue, has become increasingly common, and in many cases the disease may be clinically silent, despite manifest small-bowel mucosal lesions. Therefore, CD is underdiagnosed (Catassi et al. 1996; Feigbery 1999; Holmes 1996; Kolho et al. 1998; Maki and Collins 1997).


2008 ◽  
Vol 54 (7) ◽  
pp. 1203-1209 ◽  
Author(s):  
Kelly E McGowan ◽  
Martha E Lyon ◽  
J Decker Butzner

AbstractBackground: IgA deficiency causes false-negative IgA-based celiac serology results in patients with celiac disease. Using a case-finding strategy, we examined the prevalence of IgA deficiency, physician evaluation, and management of IgA deficiency during serological testing for celiac disease.Methods: We reviewed consecutive IgA-endomysial antibody (EMA) and serum IgA results from the laboratory database over 17 months. We cross-referenced seronegative patients with IgA deficiency (IgA &lt;0.06 g/L) to the pathology database to evaluate intestinal biopsy results. Ordering physicians received a questionnaire regarding the management of seronegative patients with IgA deficiency who had no biopsy record.Results: Among the 9533 patients tested for IgA-EMA, 4698 (49%) were tested for IgA deficiency. IgA deficiency occurred in 35 of 4698 (0.75%) patients screened for IgA deficiency. Only 19 of 35 (54%) IgA-deficient patients were diagnosed appropriately with either intestinal biopsy (17 patients) or measurement of IgG-tissue transglutaminase (2 patients). Thirteen (76%) of the 17 IgA-deficient patients who underwent upper endoscopy with or without colonoscopy displayed gastrointestinal pathology on biopsies, including 3 (18%) with celiac disease. No further evaluation to exclude celiac disease was performed for the remaining 16 of 35 (46%) IgA-deficient, EMA-negative patients because of inappropriate management (6 patients), administrative error (7 patients), or patient/physician refusal (3 patients).Conclusions: IgA deficiency occurred in 1:131 patients tested for celiac disease, and celiac disease occurred in 1:6 of those properly evaluated. Inadequate evaluation of IgA deficiency while testing for celiac disease occurred frequently and resulted in the underdiagnosis of both. Changes in testing algorithms and reporting of results were made to improve testing for celiac disease and IgA deficiency.


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