Celiac Disease: Beyond Bowels, Blood, & Bones
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Celiac disease. One in 132 Americans has it. We know about the malabsorption, the anemia, the osteoporosis associated with celiac disease. But what of associations with neurological disease, reproductive health, and other organ systems? What DON'T you know about this common condition?
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Celiac Disease: Beyond Bowels, Blood, & Bones
- 1. Celiac Disease: Beyond Bowels, Blood & Bones Patricia Raymond MD FACP FACG
- 4. Celiac Disease Globally Prevalence on Screening Data http://www.istockphoto.com/janrysavy Worldwide 1:266 Brazil 1:400 Denmark 1:500 Finland 1:130 Germany 1:500 Italy 1:184 Netherlands 1:198 Norway 1:250 Sahara 1:70 Sweden 1:190 United Kingdom 1:112 USA 1:133
Notas do Editor
- Figure 3. Endoscopic and biopsy findings in patients with and without celiac disease. (A) High-definition endoscopic photo of normal small intestine. The villi are clearly visible with no evidence of atrophy or scalloping of the folds. (B) Biopsy specimen of normal small intestine (hematoxylin-eosin; original magnification, × 100). (C) PillCam image of small intestine in a patient with celiac disease, showing scalloping of the mucosal folds (arrows) characteristic of a malabsorption pattern. There is also evidence of villous atrophy compared with normal. (D) Biopsy specimen of small intestine in a patient with celiac disease (hematoxylin-eosin; original magnification, × 100). Note the loss of villous architecture.
- 8% Ackerman Study
- BMD is low in patients with clinically silent untreated coeliac disease, but it can be substantially improved by dietary treatment even within a year. With a view to the prevention of osteopenia screening for silent coeliac disease is thus warranted. The study group consisted of 19 consecutive patients with coeliac disease; six women and 13 men, median age 45 years, range 23–69 years. In all cases the disease was diagnosed through our routine screening programmes with the IgA-class endomysial antibody test as screening method; the risk groups were those having a 4–10% risk for coeliac disease. 15 were healthy family members of coeliacdisease patients, and four had disorders not indicative of coeliac disease—ie, two from oral ulcers, one from nonspecific arthritis, and one from ataxia. None of the clinically silent coeliac-disease patients had symptoms of malabsorption or anaemia, but two had mild abdominal symptoms. For comparison, data for 30 symptomatic untreated coeliac disease patients (23 women and seven men, median age 44 years, range 21–68 years) were used. 13 of these had abdominal distension, five loose stools, three weight loss, and nine anaemia as presenting symptoms. All coeliac patients were positive for endomysial antibodies, and had small-intestinal villous atrophy and crypt hyperplasia, which subsequently improved on a gluten-free diet. BMD was measured by dual-energy radiograph absorptiometry (Norland XR 26, Norland Corp, Fort Atkinson, WI, USA) in the lumbar spine and femoral neck before the start of gluten-free diet and 1 year thereafter. The baseline BMD data were expressed as t-scores with reference to data for sex-matched young individuals. The percentage change in BMD was calculated, and in individual change was judged significant if its magnitude exceeded 2Ö2 times the short-term in-vivo precision of the given measurement. In our laboratory, the significance levels were thus SD 2·0% for spine and SD 1·4% for f e m u r .5 At diagnosis, the median t-scores in symptom-free patients were –1·9 (95% CI –2·4 to –1·4) in the spine and – 0·9 (–1·5 to –0·7) in the femoral neck, and in patients with symptoms –1·1 (–1·5 to –0·7) and –0·8 (–1·1 to –0·5), respectively. Surprisingly, BMD was even lower in clinically silent than in symptomatic coeliac patients. This indicates that silent cases may have had a manifest mucosal lesion for a long time. After 1 year on a gluten-free diet, the spinal BMD increased significantly in eight out of 19 clinically silent coeliac disease patients (figure). In the femoral neck, ten patients showed significant increases in BMD.
- La¨hteenoja H, Toivanen A, Viander M, Ma¨ki M, Irjala K, Ra¨iha¨ I, Syrja¨nen S: Institute of Dentistry, University of Turku, Oral mucosal changes in coeliac patients on a gluten-free diet. Eur J Oral Sci Turku, Finland 1998; 106: 899–906. © Eur J Oral Sci, 1998 Oral mucosal lesions or dental enamel defects may be the only presenting features of coeliac disease. A series of 128 patients with coeliac disease (CD) on a gluten-free diet (GFD), 8 patients with a newly diagnosed CD, and 30 healthy controls participated in a clinical and histopathological study of their oral mucosa. Oral mucosal lesions occurred in 71/128 GFD-treated CD patients, in 4/8 untreated and in 10/30 controls, and oral symptoms in 85/128, in 6/8 and in 10/30, respectively. Five CD patients had aphthous ulcers. Moderate
- La¨hteenoja H, Toivanen A, Viander M, Ma¨ki M, Irjala K, Ra¨iha¨ I, Syrja¨nen S: Institute of Dentistry, University of Turku, Oral mucosal changes in coeliac patients on a gluten-free diet. Eur J Oral Sci Turku, Finland 1998; 106: 899–906. © Eur J Oral Sci, 1998 Oral mucosal lesions or dental enamel defects may be the only presenting features of coeliac disease. A series of 128 patients with coeliac disease (CD) on a gluten-free diet (GFD), 8 patients with a newly diagnosed CD, and 30 healthy controls participated in a clinical and histopathological study of their oral mucosa. Oral mucosal lesions occurred in 71/128 GFD-treated CD patients, in 4/8 untreated and in 10/30 controls, and oral symptoms in 85/128, in 6/8 and in 10/30, respectively. Five CD patients had aphthous ulcers. Moderate
- Cronin study: 1 in 20 pts c insulin dependant diabetes has celiac
- Ludvigsson, Sweedon
- Selective IgA deficiency was observed in 12 of 688 (1.7%) patients with celiac disease who were clinically undistinguishable from patients with celiac disease with normal IgA levels. This high prevalence of IgA deficiency in patients with celiac disease makes serum IgA assay advisable when screening for celiac disease is performed by measurement of antigliadin antibodies or anti-IgA endomysium antibodies. Similarly, subjects with IgA deficiency should be considered at risk ofceliac disease. (J Pediatr 1997;l31 :306-8) Selective IgA deficiency is the most common primary immunodeficiency, with a prevalence of 1 case in 500 to 700 subjects, I It is an important risk factor for recurrent infections and for diseases with autoimmune response, although many subjects seem to have no sequelae of IgA deficiency.e Selective IgA deficiency is significantly increased in celiac disease, but its prevalence and clinical and pathogenetic implications in patients with celiac disease are still unclear,3.& We report the prevalence and the clinical features ofsubjects with IgA deficiency in a group of 688 children with CD who were the object of a recent multicenterstudy.