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CELIAC
Description
Celiac sprue is an inherited digestive disease. In this disorder, gluten (protein fraction) found in wheat, rye, oats and barley damages the lining of the small intestine. The symptoms can be overt with diarrhea, weight loss and malnutrition or it can be subclinical with isolated weight loss and nutritional deficiencies, but no gastrointestinal symptoms. Diagnosis is confirmed by a biopsy of the small intestine and a rapid response to the gluten-restricted diet. 1
Causes
Celiac disease is caused by a genetic disorder.
Types
Celiac disease is also referred to as gluten-induced enteropathy, gluten-induced sprue and idiopathic steatorrhea (loose, fatty stools). These conditions are lifelong. Gluten intolerance may occur as a temporary condition secondary to intestinal damage in other disorders. 2
At Risk
Celiac disease typically appears in infancy when cereals are added to the diet or in adults 20 to 30 years of age.
Prevention and Maintenance
General:
There is no prevention of celiac
disease since it is a genetic disorder. Patients must follow a gluten free
diet, which is essential and life-long. The gluten-free diet involves avoiding
wheat, rye, oats and barley and any products made with these grains. A gluten
free diet allows the intestine to heal, eliminating problems with malabsorption.
3
Restricting fat and avoiding lactose may be necessary initially. Once the
intestinal tract heals, fat and lactose may be reintroduced.
Nutritional Influences:
In
one study, patients on a gluten free diet with documented magnesium depletion
showed increased bone mineral density with magnesium supplementation.4
Bone mineral density in the celiac patient has been shown to be significantly
lower than that of age-matched controls when not following a gluten free
diet. 5
Healthier Lifestyles Product Recommendations
Additional Information
Disclaimer: These websites, addresses and/or phone numbers are provided for information purposes only. USANA, Inc. makes no claim, actual or implied, regarding the content or validity of the information obtained from these outside sources.
Gluten
Intolerance Group of North America
PO Box 23053
Seattle WA 98102-0353
Celiac Disease Foundation
13251 Ventura Blvd #3
Studio City, CA 91604
http://cpmcnet.columb.edu/dept/gi/celiac.html
http://www.mc.vanderbilt.edu/peds/pidl/gi/celiac.html
Abstracts
Corazza GR, Di Sario A, Cecchetti L, Jorizzo RA, Di Stefano M, Minguzzi L, Brusco G, Bernardi M, Gasbarrini G. Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult celiac disease. Bone 1996 Jun;18:525-30. Since no information is available on bone derangements in subclinical celiac disease (CD), we evaluated bone mineral density (BMD, expressed as z score) at lumbar spine, by x-ray dual-photon bsorptiometry and serum indices of bone metabolism and remodeling in 14 subclinical or silent patients, 10 classical patients and 15 healthy volunteers all on a gluten-containing diet. In the subclinical group, BMD at lumbar spine was significantly higher than in the classical group (-1.3 +/ 0.8, 73% vs. 2.6+/- 0.6, 88%, respectively; p<0.001), but significantly lower than in volunteers (+0.4 +/- 1.1, 104%; p<0.001). Similar changes were observed in serum calcium, whereas, as regards parathyroid hormone, no significant difference was found between subclinical and classical patients. 25-vitamin D was significantly lower, and 1,25-vitamin D was significantly higher in subclinical and classical patients than in healthy volunteers. Indices of bone remodeling were higher in the subclinical and classical groups than in the volunteers, but lower in the subclinical than in classical patients. Eight subclinical and 8 classical patients were reexamined after a period of gluten-free diet (GFD) and in both groups BMD had significantly improved. Our results show that osteopenia is a frequent feature also in subclinical CD, although the extent of bone and mineral metabolism derangements is lower than in classical CD> GFD is able to normalize BMD in subclinical and to significantly improve it in classical patients.
References
1
Zeman FJ. Clinical Nutrition and Dietetics. 2nd Ed. New York:MacMillan Publishing
Company; 1991. p 240-241.
2 Zeman FJ. Clinical Nutrition and Dietetics. 2nd Ed. New York:MacMillan
Publishing Company; 1991. p 240-241.
3 Kemppainen T, Uusitupa M, Janatuinen, Jarvinen R, Julkunen R, Pikkarainen
P. Intakes of nutrients and nutritional status in coeliac patients. Scand
J Gastroenterol. 1995;30:575-9.
4 Rude RK, Olerich M. Magnesium deficiency: possible role in osteoporosis
associated with gluten-senstive enteropathy. Osteoporos Int. 1996;6:453-61.
5 Valimnarsson T, Lofman O, Toss G, Strom M. Reversal of osteopenia with
diet in adult coeliac disease. Gut 1996;38:322-7
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