American Gastroenterological AssociationAmerican Gastroenterological Association medical position statement: Celiac sprue☆,☆☆,★
Introduction
The objective is to define celiac sprue, document the prevalence, and summarize available therapy.
Celiac sprue or gluten-sensitive enteropathy is a chronic malabsorption disorder of the small intestine caused by exposure to dietary gluten in genetically predisposed individuals. The condition is characterized by villous atrophy, a lowering of the villous height to crypt depth ratio (normal, 3–5:1), an increase in intraepithelial lymphocytes (normal, 10–30 per 100 epithelial cells), and extensive surface cell damage and infiltration of the lamina propria with inflammatory cells. There are a wide range of presentations from asymptomatic through fatigue, and vague abdominal symptoms, weight loss, and diarrhea to frank malabsorption with steatorrhea. Both the symptoms and abnormal small intestinal mucosal morphology resolve on removal of gluten from the diet.
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Epidemiology
The age of presentation and prevalence of celiac sprue have altered over the last 30–40 years. The condition was previously thought to be a disease of childhood. However, adult presentation is increasingly common and celiac sprue can occur at any age.
The prevalence in different countries ranges widely. Several European studies have recently revealed values between 1:152 to 1:300 in countries that include Ireland, the United Kingdom, Italy, and Sweden. Previous figures from the United States
Clinical features
Adult presentation usually involves weight loss, diarrhea, lassitude, and anemia. Children frequently present with failure to thrive, vomiting, diarrhea, muscle wasting, signs of hypoproteinemia including possible ascites, and general irritability and unhappiness.
Patients may present at any hospital department with associated conditions. One important example is insulin-dependent diabetes mellitus, in which 6%–8% of sufferers have concomitant celiac sprue. Other conditions include cerebral
Diagnosis
The mainstay of diagnosis of celiac sprue is a small intestinal biopsy specimen, which is usually taken at endoscopy. At least 3 biopsy specimens preferably should be taken with “jumbo” forceps from the distal duodenum. Some individuals, especially pediatricians, use a dedicated Watson or Crosby capsule. The characteristic changes involve damage to the normal villous morphology with decreased villous height to crypt depth, decreased epithelial surface cell height, and increased lymphocytic
Treatment
The cornerstone of treatment is a gluten-free diet. This should involve the advice of a dietician who is experienced in this field. Patients should omit wheat, rye, and barley from their diet. Oats may be permitted, although it should not be forgotten that the majority of commercially available oat flour is contaminated with wheat gluten.
It is important to explain the disease and the toxicity of gluten-containing foods to the patient. This should include information on the avoidance of future
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2013, Journal of Taibah University Medical SciencesCitation Excerpt :Extra intestinal manifestations such as short stature, delayed puberty, rickets, dental enamel defect, and arthralgia may occur as monosymptomatic manifestations.8,9 The diagnosis of CD was based on clinical symptoms, positive serology sub as serum IgA-class, antireticulum, antigliadin and antiendomysial antibodies and a small bowel biopsy.10–12 Histological evidence of CD was usually reported according to the Oberhuber classification.13
Celiac Disease
2012, Gastroenterology Clinics of North America
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Address requests for reprints to: Chair, Clinical Practice and Practice Economics Committee, AGA National Office, c/o Membership Department, 7910 Woodmont Avenue, 7th Floor, Bethesda, Maryland 20814. Fax: (301) 654-5920.
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This work was supported by the American Gastroenterological Association.
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The Clinical Practice and Practice Economics Committee acknowledges the following individuals whose critiques of this review paper provided valuable guidance to the authors: Sumner Bell, M.D.; Peter H. R. Green, M.D.; Martin F. Kagnoff, M.D.