scholarly journals Celiac disease: Understandings in diagnostic, nutritional, and medicinal aspects

2021 ◽  
Vol 35 ◽  
pp. 205873842110087
Author(s):  
Taoufik Ben Houmich ◽  
Brahim Admou
Keyword(s):  
Celiac Disease ◽  
Villous Atrophy ◽  
Current Trend ◽  
Diagnostic Delay ◽  
General Medicine ◽  
Iga Deficiency ◽  
Health Concern ◽  
Intestinal Biopsy ◽  
Antibody Testing ◽  
Main Challenge

Celiac disease (CD) is characterized by clinical polymorphism, with classic, asymptomatic or oligosymptomatic, and extra-intestinal forms, which may lead to diagnostic delay and exposure to serious complications. CD is a multidisciplinary health concern involving general medicine, pediatric, and adult gastroenterology, among other disciplines. Immunology and pathology laboratories have a fundamental role in diagnosing and monitoring CD. The diagnosis consists of serological testing based on IgA anti-transglutaminase (TG2) antibodies combined with IgA quantification to rule out IgA deficiency, a potential misleading factor of CD diagnosis. Positive TG2 serology should be corroborated by anti-endomysium antibody testing before considering an intestinal biopsy. Owing to multiple differential diagnoses, celiac disease cannot be confirmed based on serological positivity alone, nor on isolated villous atrophy. In children with classical signs or even when asymptomatic, with high levels of CD-linked markers and positive HLA DQ2 and/or DQ8 molecules, the current trend is to confirm the diagnosis on basis of the non-systematic use of the biopsy, which remains obligatory in adults. The main challenge in managing CD is the implementation and compliance with a gluten-free diet (GFD). This explains the key role of the dietitian and the active participation of patients and their families throughout the disease-management process. The presence of the gluten in several forms of medicine requires the sensitization of physicians when prescribing, and particularly when dispensing gluten-containing formulations by pharmacists. This underlines the importance of the contribution of the pharmacist in the care of patients with CD within the framework of close collaboration with physicians and nutritionists.

Nutritional Management of Celiac Disease

2018 ◽  
Author(s):  
Ciarán P Kelly ◽  
Satya Kurada ◽  
Mariana Urquiaga
Keyword(s):  
Immune Response ◽  
Celiac Disease ◽  
Tight Junction ◽  
Villous Atrophy ◽  
Gastrointestinal Symptoms ◽  
Gluten Free Diet ◽  
Intestinal Biopsy ◽  
Nutritional Management ◽  
Gluten Free ◽  
Antigliadin Antibodies

Celiac disease (CD) is an autoimmune disorder characterized by an immune response to gluten peptides in wheat, barley, and rye. The diagnosis of celiac disease is confirmed by three important characteristics: consistent symptoms, positive celiac-specific serology, and small intestinal biopsy findings of inflammation, crypt hyperplasia, and villous atrophy. CD may present with overt gastrointestinal symptoms, including diarrhea (or constipation), weight loss, and abdominal bloating and discomfort, or covertly with micronutrient deficiencies such as iron deficiency with anemia. A gluten-free diet (GFD) remains the mainstay of treatment. The aim of this review is to highlight the pathogenesis of CD, concepts and challenges associated with a GFD, and nutritional management of CD applicable in clinical practice to internists, gastroenterologists, and dietitians. Patients should be referred to an expert celiac dietitian for education on adherence to a GFD to address gluten contamination in the diet, the psychosocial implications of following a GFD, and macro- and micronutrient disequilibria arising from celiac disease and the GFD. Several novel therapeutics are on the horizon in various stages of development, including glutenases, antigliadin antibodies, tight junction regulators, modulation of the immune response to gliadin, and efforts to engineer less toxic gluten-containing foodstuffs. This review contains 3 figures, 5 tables, and 61 references. Key words: celiac disease, genetic engineering, food engineering, gluten, glutenases, gluten-free diet, oats, IgY, nutrition, tight junction regulators, wheat

Nutritional Management of Celiac Disease

2017 ◽  
Author(s):  
Ciarán P Kelly ◽  
Satya Kurada ◽  
Mariana Urquiaga
Keyword(s):  
Immune Response ◽  
Celiac Disease ◽  
Tight Junction ◽  
Villous Atrophy ◽  
Gastrointestinal Symptoms ◽  
Gluten Free Diet ◽  
Intestinal Biopsy ◽  
Nutritional Management ◽  
Gluten Free ◽  
Antigliadin Antibodies

Celiac disease (CD) is an autoimmune disorder characterized by an immune response to gluten peptides in wheat, barley, and rye. The diagnosis of celiac disease is confirmed by three important characteristics: consistent symptoms, positive celiac-specific serology, and small intestinal biopsy findings of inflammation, crypt hyperplasia, and villous atrophy. CD may present with overt gastrointestinal symptoms, including diarrhea (or constipation), weight loss, and abdominal bloating and discomfort, or covertly with micronutrient deficiencies such as iron deficiency with anemia. A gluten-free diet (GFD) remains the mainstay of treatment. The aim of this review is to highlight the pathogenesis of CD, concepts and challenges associated with a GFD, and nutritional management of CD applicable in clinical practice to internists, gastroenterologists, and dietitians. Patients should be referred to an expert celiac dietitian for education on adherence to a GFD to address gluten contamination in the diet, the psychosocial implications of following a GFD, and macro- and micronutrient disequilibria arising from celiac disease and the GFD. Several novel therapeutics are on the horizon in various stages of development, including glutenases, antigliadin antibodies, tight junction regulators, modulation of the immune response to gliadin, and efforts to engineer less toxic gluten-containing foodstuffs. This review contains 3 figures, 5 tables, and 61 references. Key words: celiac disease, genetic engineering, food engineering, gluten, glutenases, gluten-free diet, oats, IgY, nutrition, tight junction regulators, wheat

scholarly journals The Broad Spectrum of Celiac Disease and Gluten Sensitive Enteropathy

2016 ◽  
Vol 89 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Oana Mocan ◽  
Dan L. Dumitrașcu
Keyword(s):  
Celiac Disease ◽  
Viral Infections ◽  
Villous Atrophy ◽  
Intraepithelial Lymphocytes ◽  
Intestinal Biopsy ◽  
Gluten Free ◽  
Serological Tests ◽  
Genetic Transmission ◽  
Intestinal Involvement ◽  
Gluten Sensitive Enteropathy

The celiac disease is an immune chronic condition with genetic transmission, caused by the intolerance to gluten. Gluten is a protein from cereals containing the following soluble proteins: gliadine, which is the most toxic, and the prolamins. The average prevalence is about 1% in USA and Europe, but high in Africa: 5.6% in West Sahara. In the pathogenesis several factors are involved: gluten as external trigger, genetic predisposition (HLA, MYO9B), viral infections, abnormal immune reaction to gluten. Severity is correlated with the number of intraepithelial lymphocytes, cryptic hyperplasia and villous atrophy, as well as with the length of intestinal involvement. The severity is assessed according to the Marsh–Oberhuber staging. Diagnostic criteria are: positive serological tests, intestinal biopsy, the reversal after gluten free diet (GFD). Beside refractory forms, new conditions have been described, like the non celiac gluten intolerance. In a time when more and more people adhere to GFD for nonscientific reasons, practitioners should be updated with the progress in celiac disease knowledge.       

Nutritional Management of Celiac Disease

2017 ◽  
Author(s):  
Ciarán P Kelly ◽  
Satya Kurada ◽  
Mariana Urquiaga
Keyword(s):  
Immune Response ◽  
Celiac Disease ◽  
Tight Junction ◽  
Villous Atrophy ◽  
Gastrointestinal Symptoms ◽  
Gluten Free Diet ◽  
Intestinal Biopsy ◽  
Nutritional Management ◽  
Gluten Free ◽  
Antigliadin Antibodies

Celiac disease (CD) is an autoimmune disorder characterized by an immune response to gluten peptides in wheat, barley, and rye. The diagnosis of celiac disease is confirmed by three important characteristics: consistent symptoms, positive celiac-specific serology, and small intestinal biopsy findings of inflammation, crypt hyperplasia, and villous atrophy. CD may present with overt gastrointestinal symptoms, including diarrhea (or constipation), weight loss, and abdominal bloating and discomfort, or covertly with micronutrient deficiencies such as iron deficiency with anemia. A gluten-free diet (GFD) remains the mainstay of treatment. The aim of this review is to highlight the pathogenesis of CD, concepts and challenges associated with a GFD, and nutritional management of CD applicable in clinical practice to internists, gastroenterologists, and dietitians. Patients should be referred to an expert celiac dietitian for education on adherence to a GFD to address gluten contamination in the diet, the psychosocial implications of following a GFD, and macro- and micronutrient disequilibria arising from celiac disease and the GFD. Several novel therapeutics are on the horizon in various stages of development, including glutenases, antigliadin antibodies, tight junction regulators, modulation of the immune response to gliadin, and efforts to engineer less toxic gluten-containing foodstuffs. This review contains 3 figures, 5 tables, and 61 references. Key words: celiac disease, genetic engineering, food engineering, gluten, glutenases, gluten-free diet, oats, IgY, nutrition, tight junction regulators, wheat

scholarly journals Celiac Disease and IgA Deficiency: Complications of Serological Testing Approaches Encountered in the Clinic

2008 ◽  
Vol 54 (7) ◽  
pp. 1203-1209 ◽  
Author(s):  
Kelly E McGowan ◽  
Martha E Lyon ◽  
J Decker Butzner
Keyword(s):  
Celiac Disease ◽  
Tissue Transglutaminase ◽  
False Negative ◽  
Transglutaminase 2 ◽  
Iga Deficiency ◽  
Intestinal Biopsy ◽  
Serological Testing ◽  
Gastrointestinal Pathology ◽  
Serum Iga ◽  
Testing Algorithms

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 <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.

scholarly journals Frequency of Celiac Disease in Patients with Hypothyroidism

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Mojtaba Mehrdad ◽  
Fariborz Mansour-Ghanaei ◽  
Fereshteh Mohammadi ◽  
Farahnaz Joukar ◽  
Salimeh Dodangeh ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Villous Atrophy ◽  
Intestinal Biopsy ◽  
Overt Hypothyroidism ◽  
Endocrine Disorders ◽  
Serological Tests ◽  
Autoimmune Thyroid ◽  
Small Intestinal Biopsy ◽  
Antigliadin Antibodies ◽  
North Of Iran

Background. Celiac disease (CD) is closely associated with other autoimmune endocrine disorders, particularly autoimmune thyroid disease. The aim of this study was to find the frequency of celiac disease in patients with hypothyroidism in Guilan province, north of Iran.Methods. A total of 454 consecutive patients with hypothyroidism underwent celiac serological tests antiGliadin antibodies (AGA), antitissue transglutaminase antibodies (IgA-tTG) and antiendomysial antibodies (EMA-IgA). Small intestinal biopsy was performed when any of celiac serological tests was positive.Results. Eleven (2.4%) patients were positive for celiac serology, and two patients with documented villous atrophy were diagnosed with classic CD (0.4%; 95%). Two patients with classic CD had Hashimoto's thyroiditis (HT) (0.6%; 95%). Six (54.5%) of 11 were suffering from overt hypothyroidism and 45.5% from subclinical hypothyroidism. Six (54.5%) had HT, and 45.5% had nonautoimmune hypothyroidism.Conclusions. In this study, prevalence of CD was lower than other studies. Most of the patients with CD were suffering from HT, but there was no significant statistical relation between CD and HT.

scholarly journals Comparison of Anti-Transglutaminase ELISAs and an Anti-Endomysial Antibody Assay in the Diagnosis of Celiac Disease: A Prospective Study

2002 ◽  
Vol 48 (9) ◽  
pp. 1546-1550 ◽  
Author(s):  
Antonio Carroccio ◽  
Giustina Vitale ◽  
Lidia Di Prima ◽  
Nadia Chifari ◽  
Salvatore Napoli ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Predictive Value ◽  
Villous Atrophy ◽  
Roc Curves ◽  
Intestinal Biopsy ◽  
Control Group ◽  
Intestinal Histology ◽  
Predictive Values ◽  
Sensitivity Specificity ◽  
A Prospective Study

Abstract Background: Most studies of anti-transglutaminase (anti-tTG) assays have considered preselected groups of patients. This study compared the sensitivity, specificity, and predictive value of an immunofluorescence method for anti-endomysial antibodies (EmAs) and two anti-tTG ELISAs, one using guinea pig tTG (gp-tTG) and the other human tTG (h-tTG) as antigen, in consecutive patients investigated for suspected celiac disease (CD). Methods: We studied 207 consecutive patients (99 men, 108 women; age range, 17–84 years) who underwent intestinal biopsy for suspected CD. Patients presented with one or more of the following: weight loss, anemia, chronic diarrhea, abdominal pain, dyspepsia, alternating bowel habits, constipation, pain in the joints, and dermatitis. At entry to the study, an intestinal biopsy was performed and a serum sample was taken for IgA EmAs, anti-gp-tTG, and anti-h-tTG. Results: Intestinal histology showed that 24 patients had partial or total villous atrophy; in these patients the diagnosis of CD was confirmed by follow-up. The remaining 183 patients had villous/crypt ratios that were within our laboratory’s reference values and were considered controls. Serum EmAs, anti-gp-tTG, and anti-h-tTG were positive in all 24 CD patients; in the control group, none were positive for serum EmAs, but 15 of 183 (8.2%) were positive for anti-gp-tTG, and 6 of 183 (3.3%) were positive for anti-h-tTG. Sensitivity was 100% for all assays, whereas specificity was 100% for the EmA, 92% for the anti-gp-tTG, and 97% for the anti-h-tTG assay. The negative predictive value was 100% for all assays; the positive predictive value was 100% for the EmA, 80% [95% confidence interval (CI), 65–95%] for the anti-h-tTG (P = 0.03 vs EmA) and 60% (95% CI, 44–76%) for the anti-gp-tTG assay (P = 0.0002 vs EmA). Areas (95% CIs) under the ROC curves were 0.987 (0.97–1.0) for anti-h-tTG and 0.965 (0.94–0.99) for anti-gp-tTG. Most of the patients testing false positive for anti-tTG had Crohn disease or chronic liver disease. Conclusions: Although both anti-tTG ELISAs showed optimum sensitivity, their lack of specificity yielded positive predictive values significantly lower than those for the EmA assay.

scholarly journals Anti-Transglutaminase Antibody Assay of the Culture Medium of Intestinal Biopsy Specimens Can Improve the Accuracy of Celiac Disease Diagnosis

2006 ◽  
Vol 52 (6) ◽  
pp. 1175-1180 ◽  
Author(s):  
Antonio Carroccio ◽  
Lidia Di Prima ◽  
Giuseppe Pirrone ◽  
Calogero Scalici ◽  
Ada M Florena ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Diagnostic Accuracy ◽  
Culture Medium ◽  
Villous Atrophy ◽  
Disease Diagnosis ◽  
Intraepithelial Lymphocytes ◽  
Duodenal Biopsy ◽  
Intestinal Biopsy ◽  
Serum Antibodies ◽  
Biopsy Specimens

Abstract Background: We measured anti-transglutaminase (anti-tTG) antibody in the culture medium of intestinal biopsy specimens from patients with suspected celiac disease (CD) and evaluated the relationship between antibody production and severity of intestinal mucosal damage. Methods: We performed diagnostic testing for CD on 273 consecutive patients. In addition to routine histologic evaluation of duodenal biopsy specimens, we assayed anti-tTG antibodies in serum and in the culture medium of duodenal biopsy specimens. Results: CD was diagnosed in 191 of the 273 patients. Sensitivity and specificity of the serum anti-endomysium (EmA) and anti-tTG assays were 83% and 85% and 99% and 95%, respectively, and both had 88% diagnostic accuracy. EmA and anti-tTG assayed in the culture medium had 98% sensitivity, 100% specificity, and 98% diagnostic accuracy (vs serum assays; P <0.0001). Twenty-nine CD patient specimens (16%) were negative for serum anti-tTG and EmA; for 24 of these patients, anti-tTG assay of the culture medium was positive. The CD patients whose biopsy specimens were positive for serum antibodies showed the following intestinal histologies: total villous atrophy, 35%; severe villous atrophy, 25%; mild atrophy, 25%; villi with no atrophy but with increased intraepithelial lymphocytes, 15%. None of the CD patients whose specimens were negative for serum antibodies showed total or severe villous atrophy; 77% had mild villous atrophy, and 23% had no villous atrophy but had increased intraepithelial lymphocyte counts. Mild villous atrophy was also seen in specimens from ∼15% of patients without CD. Conclusion: Anti-tTG assay of the culture medium of biopsy specimens can improve the accuracy of CD diagnosis in patients negative for serum antibodies.

scholarly journals SAT-071 Autoimmune Polyglandular Syndrome Type 1 with Common Variable Immunodeficiency

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Yasamen Abdulmannan Shikdar ◽  
Abdullah Almazrooa ◽  
Shaza Samargandy
Keyword(s):  
Common Variable Immunodeficiency ◽  
Villous Atrophy ◽  
Tissue Transglutaminase ◽  
Iga Deficiency ◽  
Primary Hypothyroidism ◽  
Intestinal Biopsy ◽  
Autoimmune Polyglandular Syndrome ◽  
Autoimmune Polyglandular Syndrome Type ◽  
Common Variable

Abstract BACKGROUND: Autoimmune polyglandular syndrome (APS) is a rare disorder. It’s co-existence with common variable immunodeficiency (CVID) was reported in 5 cases before but, none of them was APS type 1up to our knowledge. The overlap between the 2 conditions indicates a possible association between Autoimmunity and immunodeficiency. CLINICAL CASE: A 21-year-old lady was diagnosed to have CVID since infancy, as she was presenting to the hospital with recurrent infections and sepsis. At the age of 7 months, she was diagnosed with type 1 diabetes and was started on insulin. Furthermore, at 2 years of age she was found to have primary hypothyroidism and in her teenage she was diagnosed with primary adrenal insufficiency. Her history became more complicated when she also started to develop recurrent oral and esophageal candidiasis that required systemic anti-fungal therapy. Later in her life, she was incidentally found to have hypoparathyroidism when her labs showed hypocalcemia with inappropriately normal parathyroid hormone. She had chronic diarrhea which was thought to be due to celiac disease based on intestinal biopsy showing villous atrophy. With her IgA deficiency, her Tissue transglutaminase IgA antibodies were not reliable. Splenic atrophy was also detected on abdominal imaging. She never reached puberty and elected with her parents to not start combined hormonal therapy. With the constellation of these features, we concluded that she has type 1 APS along with CVID. CONCLUSION: Autoimmunity and immunodeficiency might be interconnected. Early diagnosis will affect the quality of life and early targeted treatment will prevent morbidity and early mortality. KEY WORDS: Autoimmune Polyglandular Syndrome, Common Variable Immunodeficiency.

scholarly journals Diagnostic Accuracy of Ten Second-Generation (Human) Tissue Transglutaminase Antibody Assays in Celiac Disease

2004 ◽  
Vol 50 (11) ◽  
pp. 2125-2135 ◽  
Author(s):  
Britta Van Meensel ◽  
Martin Hiele ◽  
Ilse Hoffman ◽  
Severine Vermeire ◽  
Paul Rutgeerts ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Diagnostic Accuracy ◽  
Sensitivity And Specificity ◽  
Second Generation ◽  
Tissue Transglutaminase ◽  
Iga Deficiency ◽  
Intestinal Biopsy ◽  
Technical Performance ◽  
Antibody Assays ◽  
Endomysium Antibodies

Abstract Background: Anti-tissue transglutaminase (tTG) assays that use human tTG as antigen have recently become available. We evaluated commercially available assays with human tTG antigen to estimate their diagnostic accuracies and to determine whether they agree sufficiently to be used interchangeably. Methods: Ten commercially available second-generation anti-tTG assays were evaluated. The following populations were studied: celiac disease (CD) patients at the time of diagnosis without (n = 70) or with (n = 5) IgA deficiency; diseased controls (n = 70); and CD patients without (n = 28) or with (n = 2) IgA deficiency during follow-up. All individuals included in the study underwent intestinal biopsy. Technical performance (linearity, interference, precision, correlation, and agreement) and diagnostic accuracy (sensitivity and specificity) were compared. Anti-gliadin and anti-endomysium antibodies were also measured. Results: IgA anti-tTG results correlated well overall, but numerical values differed. Diagnostic sensitivity ranged between 91% and 97% and specificity between 96% and 100%. These were higher than the sensitivity and specificity of the IgA endomysium assay and the IgA gliadin assay. Generally, IgG anti-tTG was less sensitive but more specific than IgG anti-gliadin for the diagnosis of CD in the small group of IgA-deficient patients. Conclusions: Overall diagnostic performance of IgA tTG assays is acceptable and comparable among the different assays, but numerical values differ. Standardization is needed.

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