scholarly journals Celiac Disease in Bangladesh – Two Case Reports

2013 ◽  
Vol 37 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Md Rukunuzzaman ◽  
ASM Bazlul Karim ◽  
SM Baqui Billah ◽  
Md Atiar Rahman ◽  
Md Mahbubul Islam ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Screening Test ◽  
Villous Atrophy ◽  
Case Reports ◽  
Growth Failure ◽  
Gluten Free Diet ◽  
Chronic Diarrhoea ◽  
Gluten Free ◽  
Immunological Disorder ◽  
Rule Out

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

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 A109 CELIAC DISEASE IS A RARE CAUSE OF BENIGN DUODENAL STRICTURE

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 126-127
Author(s):  
I Balubaid ◽  
N Khanna
Keyword(s):  
Weight Loss ◽  
Celiac Disease ◽  
Case Reports ◽  
Balloon Dilation ◽  
Gluten Free Diet ◽  
Gluten Free ◽  
Early Satiety ◽  
Ulcer Disease ◽  
Duodenal Stricture ◽  
H Pylori

Abstract Background Benign duodenal stricture is an uncommon problem encountered by gastroenterologists. The most common cause is peptic ulcer disease (PUD). With the diagnosis and eradication of H. Pylori, early diagnosis of PUD and the use of PPIs to treat upper gastrointestinal inflammation, the incidence of benign duodenal stricture has dramatically decreased. Patients with duodenal stricture may present with early satiety, nausea, vomiting and weight loss. We present the case of a man with a refractory web-like stricture in the second part of the duodenum (D2) caused by Celiac disease. Aims To describe a rare endoscopic finding in a patient with Celiac disease Methods Case report with literature review Results We present a case of a 64 year old male was referred for consideration of duodenal stenting of a refractory stricture in the second part of the duodenum D2. The patient had a 1 year history of abdominal pain, early satiety and weight loss (10 lbs). He also reported intermittent episodes of diarrhea. Investigations included a CT scan of the abdomen which showed a stricture at the level of proximal D2 described as a “duodenal band”. Previous attempts at balloon dilation had not resulted in prolonged symptomatic or endoscopic improvement. Testing for H. Pylori was negative and he did not use NSAIDs. Upper endoscopy was performed to assess the stricture prior to consideration of stenting. This showed a tight web-like stricture in proximal D2. The stricture was balloon dilated up to 16.5 mm, enabling the endoscope to pass beyond it. The mucosa in D2 was atrophic with flattening of the folds and scalloping. There was no inflammation seen. Biopsies from D2 revealed moderate villous blunting and intraepithelial lymphocytosis. Celiac serology testing was abnormal, with an anti-tTG Ab level of 32 RU/ml which confirmed the diagnosis of Celiac disease. The balloon dilation and gluten-free diet resulted in resolution of his symptoms. Follow up endoscopy revealed normalization of his duodenal folds and biopsies. In addition, anti-tTG Ab level was normalized. Although stricture improved with prolonged patency, he still has mild recurrence of his stricture requiring balloon dilation on an annual basis. Conclusions This case describes a very uncommon complication of Celiac disease. The likely pathophysiology involves inflammation and potentially ulceration from Celiac disease, resulting in a benign stricture. There have been a few case reports describing duodenal strictures as a complication of Celiac disease. Treatment involves a gluten-free diet and endoscopic therapy. More severe cases of obstruction would likely require surgical intervention. In our case, the gluten-free diet and balloon dilation were successful and duodenal stenting was not necessary. Given the possibility of Celiac disease as a cause of duodenal stricture, it would be reasonable to biopsy D2 and check anti-tTG Ab in cases of duodenal stricture. Funding Agencies None

Videocapsule Endoscopy in Celiac Disease: Indications and Timing

2015 ◽  
Vol 33 (2) ◽  
pp. 244-251 ◽  
Author(s):  
Emanuele Rondonotti ◽  
Silvia Paggi
Keyword(s):  
Celiac Disease ◽  
Small Bowel ◽  
Villous Atrophy ◽  
Diagnostic Techniques ◽  
Gluten Free Diet ◽  
Gluten Free ◽  
Positive Serology ◽  
Tissue Samples ◽  
Minimal Invasiveness ◽  
Videocapsule Endoscopy

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.

scholarly journals Endocrinological Disorders and Celiac Disease

2002 ◽  
Vol 23 (4) ◽  
pp. 464-483 ◽  
Author(s):  
Pekka Collin ◽  
Katri Kaukinen ◽  
Matti Välimäki ◽  
Jorma Salmi
Keyword(s):  
Celiac Disease ◽  
Villous Atrophy ◽  
Close Association ◽  
Gluten Free Diet ◽  
Mucosal Inflammation ◽  
Dependent Diabetes Mellitus ◽  
Endocrine Disorders ◽  
Gluten Free ◽  
Abdominal Symptoms ◽  
Autoimmune Conditions

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.

Treatment Failure in Celiac Disease Due to Coexistent Exocrine Pancreatic Insufficiency

PEDIATRICS ◽  
1987 ◽  
Vol 80 (6) ◽  
pp. 924-926
Author(s):  
Z. Weizman ◽  
J. R. Hamilton ◽  
H. R. Kopelman ◽  
G. Cleghorn ◽  
P. R. Dune
Keyword(s):  
Celiac Disease ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Age Determination ◽  
Growth Failure ◽  
Gluten Free Diet ◽  
Delayed Puberty ◽  
Partial Recovery ◽  
Gluten Free ◽  
Immunoreactive Trypsinogen

A 17-year-old white adolescent had a history of chronic diarrhea, delayed puberty, and growth failure. Investigations excluded cystic fibrosis, Shwachman syndrome, and endocrine causes of growth failure. Severe steatorrhea was diagnosed from fecal fat studies, and a jejunal suction biopsy showed total villus atrophy, consistent with a diagnosis of celiac disease. Following introduction of a gluten-free diet, his appetite and growth improved, but he continued to have abdominal discomfort and loose offensive bowel motions. One year later, severe steatorrhea was present. A repeat jejunal biopsy showed partial recovery of villus architecture. Serum immunoreactive trypsinogen level was low, which was highly suggestive of exocrine pancreatic failure. Results of quantitative pancreatic stimulation test confirmed the presence of primary pancreatic insufficiency. After introduction of oral pancreatic enzyme supplements with meals, his gastrointestinal symptoms resolved and growth velocity accelerated. Previously, primary pancreatic insufficiency has only been described in elderly patients with long-standing untreated celiac disease. This case, however, emphasizes that pancreatic failure can occur with celiac disease at any age. Determination of a serum immunoreactive trypsinogen level should be considered a useful screening tool for pancreatic insufficiency in patients with celiac disease who have not responded to a gluten-free diet.

Serum transglutaminase antibodies do not always detect the persistent villous atrophy in patients with celiac disease on a gluten-free diet

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Gianpiero Stefanelli ◽  
Sara Navisse ◽  
Marco Valvano ◽  
Filippo Vernia ◽  
Antonio Ciccone ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Villous Atrophy ◽  
Gluten Free Diet ◽  
Gluten Free

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

Natural Antibiotic Expression in Celiac Disease?Correlation with Villous Atrophy and Response to a Gluten-Free Diet

2005 ◽  
Vol 50 (4) ◽  
pp. 791-795 ◽  
Author(s):  
Ali S. Taha ◽  
Elena Faccenda ◽  
Wilson J. Angerson ◽  
Margaret Balsitis ◽  
Rodney W. Kelly
Keyword(s):  
Celiac Disease ◽  
Villous Atrophy ◽  
Gluten Free Diet ◽  
Gluten Free

scholarly journals Persistent Iron Deficiency Anemia in Patients with Celiac Disease Despite a Gluten-Free Diet

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2176
Author(s):  
Gianpiero Stefanelli ◽  
Angelo Viscido ◽  
Salvatore Longo ◽  
Marco Magistroni ◽  
Giovanni Latella
Keyword(s):  
Celiac Disease ◽  
Iron Deficiency ◽  
Iron Deficiency Anemia ◽  
Villous Atrophy ◽  
Gluten Free Diet ◽  
Deficiency Anemia ◽  
Gluten Free ◽  
Anemia Of Chronic Disease ◽  
Therapeutic Implications ◽  
Molecular Alterations

Celiac disease (CD) is an autoimmune disorder characterized by intolerance to dietary gluten in genetically predisposed subjects. Iron deficiency anemia (IDA) is a common sign in CD, being the only abnormality in approximately 40% of celiac patients. A multifactorial etiology leads to IDA in CD. The two main causes are the villous atrophy of the mucosa at the site of iron absorption (the duodenum) and the resulting inflammation, which triggers the mechanism that leads to the anemia of chronic disease. Until now, it has been unclear why some patients with CD continue to have IDA despite a careful gluten-free diet (GFD) and the normalization of villous atrophy. Furthermore, some celiac patients are refractory to oral iron supplementation despite the healing of the mucosa, and they thus require periodic intravenous iron administration. The Marsh classification evaluates the degree of inflammation and villous atrophy, but it does not assess the possible persistence of ultrastructural and molecular alterations in enterocytes. The latter was found in CD in remission after adopting a GFD and could be responsible for the persistently reduced absorption of iron and IDA. Even in non-celiac gluten sensitivity, anemia is present in 18.5–22% of patients and appears to be related to ultrastructural and molecular alterations in intestinal microvilli. It is possible that a genetic component may also play a role in IDA. In this review, we evaluate and discuss the main mechanisms of IDA in CD and the possible causes of its persistence after adopting a GFD, as well as their therapeutic implications.

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