Videocapsule Endoscopy in Celiac Disease: Indications and Timing

2015 ◽  
Vol 33 (2) ◽  
pp. 244-251 ◽  
Author(s):  
Emanuele Rondonotti ◽  
Silvia Paggi

Background: Because of its technical characteristics (i.e. 8-fold magnification, capability to inspect the entire small bowel) and minimal invasiveness, videocapsule endoscopy (VCE) has been proposed as a useful tool for managing patients with celiac disease (CD). Key Messages: Although VCE has been found to be highly sensitive and specific in identifying CD endoscopic markers, it is still inadequate to replace esophagogastroduodenoscopy (EGD) with biopsies in the diagnosis of CD. Nevertheless, it represents a reliable alternative in patients unable or unwilling to undergo EGD. Up to now, available studies have failed to identify any correlation between the length of small bowel involvement and the severity of symptoms. The available evidence on the use of VCE in diagnosing CD in equivocal cases (patients with positive serology and negative or nonspecific histology or those with negative serology and histologically proven villous atrophy) is limited, and its role is still under discussion. In CD patients not improving on gluten-free diet, a complete workup is necessary. In patients with nonresponsive (NRCD) or refractory CD (RCD), VCE has been shown to be able not only to detect significant findings, driving further management, but also to rule out major complications. Nevertheless, in this setting, the inability of VCE to take tissue samples and the risk of capsule retention can represent major limitations. Conclusions: At the present time, for diagnostic purposes, VCE can be proposed only in patients unable or unwilling to undergo EGD, whereas it could be useful in some equivocal cases. Conversely, there is no room for VCE either to estimate the length of the small bowel affected by villous atrophy or to follow up patients improving on gluten-free diet. In patients with NRCD or RCD, VCE can play a role, but it should be combined with other diagnostic techniques.

2018 ◽  
Author(s):  
Ciarán P Kelly ◽  
Satya Kurada ◽  
Mariana Urquiaga

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


2017 ◽  
Author(s):  
Ciarán P Kelly ◽  
Satya Kurada ◽  
Mariana Urquiaga

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


2002 ◽  
Vol 23 (4) ◽  
pp. 464-483 ◽  
Author(s):  
Pekka Collin ◽  
Katri Kaukinen ◽  
Matti Välimäki ◽  
Jorma Salmi

Abstract Celiac disease is a permanent intolerance to dietary gluten. Its well known features are abdominal symptoms, malabsorption of nutrients, and small-bowel mucosal inflammation with villous atrophy, which recover on a gluten-free diet. Diagnosis is challenging in that patients often suffer from subtle, if any, symptoms. The risk of clinically silent celiac disease is increased in various autoimmune conditions. The endocrinologist, especially, should maintain high suspicion and alertness to celiac disease, which is to be found in 2–5% of patients with insulin-dependent diabetes mellitus or autoimmune thyroid disease. Patients with multiple endocrine disorders, Addison’s disease, alopecia, or hypophysitis may also have concomitant celiac disease. Similar heredity and proneness to autoimmune conditions are considered to be explanations for these associations. A gluten-free diet is essential to prevent celiac complications such as anemia, osteoporosis, and infertility. The diet may also be beneficial in the treatment of the underlying endocrinological disease; prolonged gluten exposure may even contribute to the development of autoimmune diseases. The diagnosis of celiac disease requires endoscopic biopsy, but serological screening with antiendomysial and antitissue transglutaminase antibody assays is an easy method for preliminary case finding. Celiac disease will be increasingly detected provided the close association with autoimmune endocrinological diseases is recognized.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Gianpiero Stefanelli ◽  
Sara Navisse ◽  
Marco Valvano ◽  
Filippo Vernia ◽  
Antonio Ciccone ◽  
...  

2017 ◽  
Author(s):  
Ciarán P Kelly ◽  
Satya Kurada ◽  
Mariana Urquiaga

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


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1665-1665
Author(s):  
R.K. Marwaha ◽  
Deepak Bansal ◽  
Amita Trehan ◽  
Akash Patel

Abstract Celiac disease (CD) is a malabsorptive disorder wherein the proximal small bowel mucosa is damaged as a result of dietary exposure to gluten. Children with intractable diarrhea and failure to thrive are diagnosed with relative ease. Diagnosis can however be challenging and is often delayed when children present with ‘difficult to treat anemia’, without overt gastrointestinal manifestations. The case records of 77 patients with CD were scrutinized retrospectively. Diagnosis was established with serology (tissue transglutaminase-IgA assay) in 46 (59.7%), serology along with small bowel mucosal biopsy in 23 (29.9%) and with biopsy alone in the remaining 8 (10.4%). All children belonged to the predominantly wheat consuming northern Indian states. The mean age at presentation was 99.1±34.8 months (median: 102, range: 22–168). Males outnumbered females in a ratio of 1.96:1. The mean duration of symptoms was 41±31.2 months (median: 36, range: 1–132). The overwhelming majority, i.e., 75 (97.4%) children had anemia (Hemoglobin <11 g/dL). Mean hemoglobin (Hb) was 7.0±2.2 g/dL (median: 7.2, range: 2.3–12.5). 52 (67.5%) had received iron supplements for sufficient lengths, without benefit. The red cell morphology was microcytic hypochromic in 37 (48%) and dimorphic in 33 (42.9%). A history of diarrhea was not forthcoming in 32 (41.6%) cases. 59 (76.6%) were malnourished, with a weight less than 80 % of expected for the age and 30 (39 %) were stunted, with a height falling below the 90% of expected. Two children had skin bleeds secondary to coagulopathy, due to Vitamin K malabsorption. In another 2, recurrent anemia was attributed to pulmonary hemosiderosis; further investigations for secondary causes unearthed CD. All children were initiated on an austere gluten free diet, along with iron and folic acid supplements for the initial 6–9 months. Mean duration of follow was 17.7±20.9 months. Improvement was perceptible within days of initiating gluten free diet. Of the 38 (49.4%) children who had a follow up of a year or longer, the mean Hb at the last visit had risen to 12.9±1.2 g/dL. Conclusions: Hematologists need to be aware of the mono-symptomatic presentation of CD with anemia. The typical period of presentation of CD is described to be between 6 mo and 2 yr of age. Prolonged duration of symptoms and a diagnosis at a relatively older age is striking in the index study. In a suggestive clinical background, identification of CD with serodiagnosis alone, without resorting to small bowel biopsy is increasingly gaining acceptance, as the specificity of newer serological assays is 95–98%. This is particularly true in tropical countries, where some degree of flattening of villi may be attributed to malnutrition and or infections, such as rotavirus enteritis, Giardia lamblia, or tropical sprue. A biopsy may be misleading in such cases. Heightened awareness is essential to identify CD at an early age, especially, in children in whom anemia is the dominant manifestation. The benefits of gluten free diet are apparent with the rise in hemoglobin and the improvement in growth parameters are gratifying both for physicians and the caretakers.


2013 ◽  
Vol 37 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Md Rukunuzzaman ◽  
ASM Bazlul Karim ◽  
SM Baqui Billah ◽  
Md Atiar Rahman ◽  
Md Mahbubul Islam ◽  
...  

Celiae disease is an immunological disorder precipitated by gluten in genetically susceptible persons. Its prevalence is not known in Bangladesh because of unavailability of its screening test. There is diversity in the presentation of celiac disease. Two children of 5 and 8 years of age who were diagnosed as celiac disease are reported here. One presented typically with chronic diarrhoea & growth failure. Another child presented with features of chronic liver disease. In both the cases IgA tTGA were positive and duodenal biopsy showed villous atrophy. After diagnosis, both the patients were kept on gluten free diet (GFD). After six months of GFD, IgA tTGA came down to normal in both the cases. They were then given gluten containing diet again & after few months IgA tTGA again raised in both the cases. Thereafter the cases were finally diagnosed as celiac disease and were advised life long gluten free diet. Celiac disease is not uncommon in Bangladesh and screening test should be done to diagnose or rule out celiac disease when there is a suspicion. DOI: http://dx.doi.org/10.3329/bjch.v37i1.15351 BANGLADESH J CHILD HEALTH 2013; VOL 37 (1) : 45-48


2017 ◽  
Vol 49 (4) ◽  
pp. 412-416 ◽  
Author(s):  
Konstantinos Efthymakis ◽  
Angelo Milano ◽  
Francesco Laterza ◽  
Mariaelena Serio ◽  
Matteo Neri

2007 ◽  
Vol 22 (8) ◽  
pp. 1300-1305 ◽  
Author(s):  
Surender K Yachha ◽  
Anshu Srivastava ◽  
Samir Mohindra ◽  
Narendra Krishnani ◽  
Rakesh Aggarwal ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Esko Kemppainen ◽  
Teea Salmi ◽  
Katri Lindfors

Dermatitis herpetiformis is a cutaneous form of celiac disease manifesting as an itching rash typically on the elbows, knees and buttocks. It is driven by the ingestion of gluten-containing cereals and characterized by granular deposits of immunoglobulin A in the papillary dermis. These antibodies target transglutaminase (TG) 3 and in the majority of patients they are also found in circulation. The circulating antibodies disappear and skin symptoms resolve as a result of gluten-free diet but the cutaneous anti-TG3 IgA deposits may persist for several years. In dermatitis herpetiformis, plasma cells secreting antibodies against TG3 are located in the intestinal mucosa similarly to those producing TG2 antibodies characteristic for celiac disease. In fact, both TG2- and TG3-specific plasma cells and gluten responsive T cells are found in dermatitis herpetiformis patients but the interplay between these cell populations is unknown. The small bowel mucosal damage in celiac disease is believed to be mediated by co-operation of cytotoxic intraepithelial T cells and the inflammatory milieu contributed by gluten-reactive CD4+ T cells, whereas the skin lesions in dermatitis herpetiformis appear to be devoid of gluten reactive T cells. Thus, how celiac disease-type intestinal T and B cell responses develop into an autoimmune condition affecting the skin is still incompletely understood. Finally, the skin and small bowel lesions may reappear upon reintroduction of gluten in patients treated with gluten-free diet but virtually nothing is known about the long-lived B cell and memory T cell populations activating in response to dietary gluten in dermatitis herpetiformis.


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