GLUTEN-FREE DIET

Description
The Gluten-Free Diet is the primary treatment for celiac disease, which is also called gluten-sensitive enteropathy or celiac sprue.  The only treatment for celiac disease is lifelong adherence to a gluten-free meal pattern, including strict avoidance of prolamins, which are proteins found in wheat, rye, barley, and triticale (1).  Dermatitis herpetiformis is the term for the skin manifestation of celiac disease. The Gluten-Free Diet also helps to control most cases of dermatitis herpetiformis associated with gluten-sensitive enteropathy (1-6).

Celiac disease is an immune-mediated disease characterized by chronic inflammation of the small intestine mucosa that results in malabsorption due to atrophy of the intestinal villa (1-6).  Although celiac disease was once thought to be a rare childhood disease, it is now recognized as a fairly common multisystem disorder that occurs in one in 133 people (1,6).  Individuals with celiac disease have an immunologic reaction to proteins termed prolamins, which are found in wheat, rye, and barley (1).When foods containing gluten are consumed by a person with celiac disease, the digestive process fails and an immunologically reactive protein fragment remains (1).  Research suggests that a 33–amino acid molecule may be the cause of the inflammatory response (1,4-6).  This molecule enters the intestinal mucosa and cannot be degraded by digestive enzymes or pancreatic enzymes.  The molecule then enters the lamina propria, where it causes the release of T cells (1).  The presence of the T cells in the lamina propria triggers cytokine activation, antibody production, and inflammatory responses (1).  The resulting villous atrophy and inflammation of the mucosa result in malabsorption (1-6).  The proximal bowel (duodenum) is the first area of the gastrointestinal tract to be exposed to the immunologically reactive peptide. Therefore, it is exposed to the highest concentration of the peptide and is often the most severely injured section of the small intestine.  The jejunum and occasionally the ileum may also be affected.   

    Although the classic presentation of celiac disease is diarrhea, wasting, malabsorption, failure to grow, bloating, and abdominal cramps, not all individuals with celiac disease have these symptoms.  Many individuals with celiac disease are diagnosed when seeking medical care for other problems such as anemia, osteoporosis, peripheral neuropathy, and fatigue (1,6).  Celiac disease is categorized into four main classes according to the National Institutes of Health Consensus Conference Statement (6):

Classical celiac disease: This class is characterized by predominant gastrointestinal symptoms and sequelae including malabsorption, significant weight loss or gain, failure to grow (in children), diarrhea, constipation, excessive gas, bloating, and abdominal pain.  The diagnostic testing reveals positive serologic test results and biopsy-proven intestinal atrophy.  Symptoms improve after a patient adopts a gluten-free diet.

Celiac disease with atypical symptoms:  This class is characterized by predominantly extraintestinal manifestations and few or no gastrointestinal symptoms. Non-gastrointestinal symptoms include anemia, osteoporosis, peripheral neuropathy or neurological symptoms, dental enamel defects, and fatigue.  The diagnostic test results and treatment response are consistent with classical celiac disease.

Silent celiac disease: This disease is characterized by a lack of clinical symptoms in spite of positive serologic test results and biopsy-proven villous atrophy.  Diagnosis of silent celiac disease usually results from screening high-risk individuals, eg, family members and individuals with associated conditions such as type I diabetes mellitus, Down syndrome, or Williams syndrome.  A clear outcome benefit of treating these individuals has not emerged from current data analysis.  

Latent celiac disease: This class is characterized by positive serologic test results, the absence of villous atrophy on intestinal biopsy, and no clinical symptoms of celiac disease.  These individuals may develop intestinal changes and symptoms of celiac disease later in life.

Dermatitis herpetiformis: This condition is the skin manifestation of celiac disease, which is characterized by a bilateral, symmetric rash or eruptions primarily on pressure points of the skin that may evolve into blisters or bullae (fluid-filled sacs).  These lesions are painfully itchy and do not respond well to topical treatment.  Dermatitis herpetiformis is diagnosed from a skin biopsy taken from a site next to a lesion.  Ninety percent of individuals with dermatitis herpetiformis have no gastrointestinal symptoms characteristic of celiac disease, but 75% have biopsy-proven villous atrophy that responds well to a gluten-free dietary pattern.  Topical treatment of the lesions with sulfapyridine is effective in treating this form of bullous atopic dermatitis.  Although oral medications may also be used, adherence to a gluten-free diet is the most effective way to prevent dermatitis herpetiformis. 

    Compliance with a gluten-free dietary pattern reduces the prevalence of diarrhea, constipation, abdominal pain and bloating, nausea or vomiting, reduced gut motility, delayed gastric emptying, and prolonged transit time (Grade II) (7).  Evidence is limited regarding the effect of a gluten-free dietary pattern on indigestion, dysphagia, and reflux (Grade II) (7).  Individuals who comply with a gluten-free dietary pattern have substantial improvement in villous atrophy; however, mucosal abnormalities may persist in some individuals (Grade II) (7).  Although normalization of abnormalities may occur within 1 year, it generally takes longer, depending on the severity of villous atrophy, level of compliance, and age at diagnosis (Grade II) (7).  Recovery in children may progress faster and more completely than in adults (Grade II) (7).  People with celiac disease are more likely than healthy controls to experience neurological symptoms such as depression, cerebellar ataxia, headaches, migraines, and neuropathy (Grade II) (7).  Early diagnosis and compliance with a gluten-free dietary pattern may reduce the prevalence of symptoms related to cerebellar ataxia, headaches, and migraines (Grade II) (7).  The evidence is less conclusive or limited regarding the effect of a gluten-free diet on depression, anxiety, and epilepsy (Grade II) (7).

Nutrition Assessment and Diagnosis
Biopsy of the small intestine is the gold standard for diagnosing celiac disease (1-6).   Several biopsies should be taken because mucosal abnormalities may be localized (6).  Criteria for diagnosis include mucosal abnormalities (eg, increased density of intraepithelial lymphocytes, partial to total villous atrophy, and crypt hyperplasia) and clinical improvement after a period of time on a gluten-free nutrition prescription (6,8).  Tests for genetic markers are available to determine the likelihood that a person has celiac disease (1).  The DQ2 and DQ8 markers are highly correlated with celiac disease and are tools for assessing a person’s risk for celiac disease (6).  Persons who exhibit symptoms of irritable bowel syndrome or who have undiagnosed gastrointestinal complaints (eg, diarrhea, bloating, gas, and abdominal pain), especially when accompanied by fatigue and weight loss, should be assessed for celiac disease.  In a survey of adults with celiac disease, 37% of cases reported an initial diagnosis of irritable bowel syndrome (9).  Serologic markers that can be used by dietitians to screen for celiac disease include immunoglobulin A, antihuman tissue transglutaminase, and immunoglobulin A endomysial antibody (1).  Tests for these markers have a high sensitivity and specificity and are the best available tests in terms of diagnostic accuracy (1,6).

    A comprehensive nutritional assessment is critical in determining whether recurrent symptoms are related to gluten sensitivity or to an unrelated problem.  Damage to the intestinal mucosa may cause various degrees of malabsorption that leads to deficiencies of key vitamins and minerals, including calcium, vitamin D, iron, and folate (4).  The following discussion reviews the evidence regarding the long-term effects of following a gluten-free dietary pattern after a diagnosis of celiac disease (7).      

Calcium:  Clinical trials and cross-sectional studies have found reduced bone mineral content and bone mineral density in untreated children, adolescents, and adults (7).  Both of these parameters improve significantly with compliance to a gluten-free dietary pattern for at least 1 year (Grade I) (7).  Compliance with dietary treatment initiated during childhood or adolescence allows the achievement of normal bone mineralization (Grade I) (7).  However, in adults who received no treatment or delayed treatment in childhood or adolescence, a gluten-free meal pattern may improve bone density but not normalize bone mineral density (Grade I) (7).  Successful treatment depends on the age at diagnosis, as patients who do not receive treatment in childhood and adolescence may never reach peak bone mass (Grade I) (7).  Further studies are needed to evaluate the effects of calcium and vitamin D supplementation on bone mineral content and bone mineral density, as well as the effects of hormone replacement therapy for postmenopausal women (7).  Adults with celiac disease should have a bone density test (dual energy X-ray absorptiometry scan) at the time of the diagnosis (6).

Iron:  For most children and adults with celiac disease, compliance with a gluten-free dietary pattern results in significant improvement in hematological parameters including serum hemoglobin, iron, ferritin, mean corpuscular volume, mean corpuscular hemoglobin, and red cell distribution width (Grade II) (7).  Recovery from anemia, as indicated by the normalization of hemoglobin concentrations, generally occurs within 6 months; recovery from iron deficiency, as indicated by the normalization of ferritin concentrations, may take longer than 1 year (Grade II) (7). Iron supplementation in the form of a multivitamin with iron may be necessary to achieve normal values for these hematological variables within these time periods (Grade II) (7). 

Lactose:  Patients may need to be evaluated for lactose intolerance, which can appear secondary to celiac disease.  If the patient is lactose intolerant, see the discussion of the Lactose-Controlled Diet later in this section.  Usually lactose intolerance will normalize within weeks to months of adopting a gluten-free diet pattern (1).
 
Contraindications
One form of celiac disease, refractory sprue, does not respond to the Gluten-Free Diet or responds only temporarily. 

Nutritional Adequacy
The Gluten-Free Diet can be planned to meet the Dietary Reference Intakes as outlined in the Statement on Nutritional Adequacy.  Compliance with a gluten-free dietary pattern results in significant improvements in nutritional laboratory values, such as serum hemoglobin, iron, zinc, and calcium, as a result of intestinal healing and improved absorption (Grade II) (7).  Often, supplementation may be required to treat deficiencies secondary to celiac disease (1).  Anemia may be treated with folate, iron, or vitamin B12.  Patients who are dehydrated due to severe diarrhea require electrolytes and fluids.  Vitamin K may be prescribed for patients who develop purpura, bleeding, or prolonged prothrombin time.  Calcium and vitamin D supplementation may be necessary to correct osteomalacia.  Vitamins A and D may be necessary to replenish stores depleted by steatorrhea.  Daily consumption of a gluten-free, multivitamin-mineral supplement containing the Dietary Reference Intakes is recommended for patients who continue to have suspected deficiencies or malabsorption (1,7). 

How to Order the Diet
Order as “Gluten-Free Diet.”

Nutrition Intervention and Prescription
The Gluten-Free Diet is based on the avoidance of the grains, chemicals, and natural or artificial ingredients that are toxic for patients with celiac disease or dermatitis herpetiformis (1). This diet eliminates all foods containing wheat, rye, barley, triticale, and their derivatives (1,6).  Derivatives of these grains include wheat-based spelt, semolina, and kamut.  Quinoa, buckwheat, amaranth, and teff are now allowed on a gluten-free diet, based on plant taxonomy and limited scientific evidence for the need to exclude these items (1).  Millet, sorghum, Job’s tears, teff, ragi, and wild rice are more closely related to corn than to wheat.  The American Dietetic Association, Dietitians of Canada, and other organizations such as the Gluten Intolerance Group and the Celiac Disease Foundation consider these plants to be acceptable in a gluten-free diet (1,6,10).   The following grains and plant foods can be included in a gluten-free prescription (1):

• Rice, corn, amaranth, quinoa, teff (or tef), millet, finger millet (ragi), sorghum, Indian rice grass (Montina), arrowroot, buckwheat, flax, Job’s tears, sago, potato, soy, legumes, tapioca, wild rice, cassava (manioc), yucca, and nuts
• Nonmalt vinegars, including cider vinegar, wine vinegar, and distilled vinegar

Oats:  Studies have shown that incorporating oats uncontaminated with wheat, barley, or rye into a gluten-free dietary pattern at intake levels of approximately 50 g of dry oats per day is generally safe for people with celiac disease and improves their compliance (Grade II) (7,11-15).  However, the introduction of oats may result in gastrointestinal symptoms such as diarrhea and abdominal discomfort (7,16-18).  Additional adverse effects include dermatitis herpetiformis, villous atrophy, and an increased density of intraepithelial lymphocytes, indicating that some persons with celiac disease may be unable to tolerate oats (Grade II) (7).  The risk of cross-contamination with gluten-containing products remains a substantial concern in the United States.  Some food companies such as Gluten Free Oats and Cream Hill Estates are attempting to improve the purity of oat production and may be a resource for persons with celiac disease (1).  Until oats are proven safe, the inclusion of oats in a gluten-free diet should be at the discretion of patients in consultation with their physicians and dietitians (1).  Patients who consume oats should be advised to limit their daily consumption to approximately 50 g of dry oats, an amount found to be safe in studies (19).  Ideally, patients should only consume oats that have been tested and found to be free of gluten contamination (1,19).

Wheat starch–based gluten-free foods:  Both natural and wheat starch–based gluten-free foods (as defined by the Codex Alimentarius (20)) produce similar histological and clinical recovery in people with celiac disease (Grade III) (7).  Overall compliance with a gluten-free diet may be more important than the specific type of diet (eg, natural or wheat starch–based), as evidenced by the incomplete bowel mucosal recovery and positive serological test results generally seen in study subjects who have dietary lapses (Grade III) (7).

Alcohol:  Beer, ale, porter, stout, and other fermented beverages should be avoided because they are derived from barley (1).  Distilled alcoholic beverages (eg, gin and vodka) may be included in a gluten-free nutrition prescription.  Although these beverages may be derived from gluten-containing grain, the process of distillation should prevent any protein from remaining in the final distillate (1).   Checking the manufacturer’s label is important with all types of alcoholic products because gluten-containing additives may be added after the alcohol is distilled. 

    The following guidelines should be considered when determining the nutrition prescription (1):

• The daily protein intake for adults should be 1 to 2 g/kg of body weight (1).  Use high–biological value proteins. 
• Adequate energy intake should be determined by using the Ireton-Jones or Mifflin–St. Jeor equations, or as outlined in Estimation of Energy Expenditures. Consider the need for weight gain if weight loss is unintentional and associated with disease. 
• Evaluate the need for gluten-free vitamin and mineral supplementation.
• Evaluate the need for a medium-chain triglyceride supplement in adults who are diagnosed with steatorrhea.

    The long-term nutritional adequacy of a gluten-free diet has been investigated.  Adherence to the gluten-free dietary pattern may result in a diet that is high in fat and low in carbohydrates and fiber, as well as low in iron, folate, niacin, vitamin B12, calcium, phosphorus, and zinc (Grade II) (7).  A food intake survey of persons with celiac disease found that less than 50% of the female participants consumed the recommended amounts of fiber, iron, and calcium (21).  A small number of studies of adults show a trend toward weight gain after diagnosis (Grade II) (7).  These factors may need to be considered during long-term patient management.  The following dietary guidelines may be suggested to persons with celiac disease (1):

• Consume 5- to 10-oz equivalent servings from the grain food group each day.
• Choose whole grain, gluten-free products whenever possible.
• Choose enriched, gluten-free products over refined, unenriched products whenever possible.
• Increase intake of gluten-free products made from alternative plant foods (eg, amaranth, buckwheat, quinoa, teff, and flaxseed) to provide good sources of fiber, iron, and some B vitamins.
• Increase intake of other enriched, gluten-free foods, such as rice and energy bars.
• Increase intake of noncereal sources of thiamin, riboflavin, niacin, folate, iron, and fiber.
• Consider taking a gluten-free multivitamin and mineral supplement.  Gluten-free brands include Freeda (www.freedavitamins.com) and Nature’s Bounty (www.naturesbounty.com).

   
Cross-contamination with gluten-containing grains or gluten-containing products during processing, preparation, or food handling should be avoided.  Patients will need to become proficient in the evaluation of food and manufacturers’ labels to screen the ingredients in food products, dietary or medical food supplements, and medications.  Hidden sources of gluten in food products include: hydrolyzed vegetable protein, flavorings, malt flavoring (includes malt syrup, malt extract, malt milk, and malt vinegar), brown rice syrup, modified food starch, dextrin, caramel color, vegetable gum, soy sauce, monoglycerides and diglycerides in dry products, emulsifiers, alcohol-based extracts (eg, vanilla extract), prepared meats, and flavored coffees.  The following additional components contain gluten and are often overlooked: broth, breading, croutons, pasta, stuffing, flours, sauces, coating mixes, marinades, thickeners, roux, soup base, self-basting poultry, imitation seafood, and imitation bacon (1).   According to the U.S. Food and Drug Administration’s Code of Federal Regulations (21CFR137), the following terms on a food label or ingredient list indicate the presence of wheat (22):

• flour, white flour, plain flour, bromated flour, enriched flour, phosphate flour, self-rising flour, durum flour, farina, semolina, and graham flour (1)

    Effective January 1, 2006, under the Food Allergen Labeling and Consumer Protection Act of 2004 (FALCPA), if a food or an ingredient contains wheat or protein derived from wheat, the word “wheat” must be clearly stated on the food label (1,22).  FALCPA applies not only to food products but also to dietary supplements, infant formulas, and medical foods.  This regulation includes products that contain dextrin, caramel color, or modified food starch found in food products containing protein derived from wheat (1,22).  All prescribed and over-the-counter medications should be evaluated by a knowledgeable pharmacist or physician prior to use. Ingredients used as part of the packaging are not required to be listed on the label.  Persons with celiac disease should be aware of the potential for cross-contamination with gluten-containing foods that may occur as result of preparing or cooking foods (eg, frying or grilling).    

Nutrition Evaluation and Monitoring
Persons with celiac disease may experience an improvement in symptoms after 3 to 6 days of consuming a gluten-free diet, with full improvement of the intestinal mucosa within 6 months (23).  Individuals with celiac disease demonstrate improved quality of life after compliance with a gluten-free dietary pattern for at least 1 year (Grade II) (7).  Celiac disease is a chronic disease.  An asymptomatic state depends on lifelong maintenance of the Gluten-Free Diet.  Patients should be cautioned against ingesting gluten once they start to gain weight and feel better.  The ingestion of gluten damages the mucosa and causes recurrent symptoms, although several weeks may lapse before the patient observes symptoms.  Villous atrophy is significantly associated with dietary compliance (Grade II) (7).  Therefore, an assessment of dietary adherence is critical in determining whether recurrent symptoms are related to gluten sensitivity or to an unrelated problem.  Individuals who are diagnosed with celiac disease and are not treated or do not adhere to a gluten-free diet are at greater risk of developing osteoporosis and benign and malignant complications including lymphoma and other autoimmune diseases such as type 1 diabetes mellitus (1-6). 

FOOD GUIDE – GLUTEN-FREE DIET

Substitutions for Wheat Flour
Most patients find special cookbooks helpful.  Recipes can be modified by the following substitutions:

For baking, 1 cup wheat flour may be replaced by:
1 cup corn flour (finely milled)
1 scant cup fine cornmeal
¾ cup coarse cornmeal
5/8 cup (10 tbsp) potato starch flour
7/8 cup (14 tbsp) rice flour (white or brown)
1 cup soy flour plus ¼ cup potato starch flour
½ cup soy flour plus ½ cup potato starch flour

For thickening, 1 tbsp of wheat flour may be replaced by:
1½  teaspoons of cornstarch, potato starch, rice, flour arrowroot starch, or gelatin
2 teaspoons of quick-cooking tapioca
1 tbsp rice flour (white or brown)

Support Groups

Suppliers of Gluten-Free Products

 References

1. Celiac disease.  In:  Nutrition Care Manual. American Dietetic Association; 2007.  Available at: http://www.nutritioncaremanual.org.  Accessed November 15, 2007.
2. Abdulkarim AS, Murray JA.  Review article:  the diagnosis of coeliac disease.  Aliment Pharmacol Ther.  2003;17:987-995.
3. Alaedini A, Green PH.  Narrative review: celiac disease: understanding a complex autoimmune disorder.  Ann Intern Med.  2005;142:289-298.
4. Farrell RJ, Kelly CP.  Celiac sprue.  N Engl J Med.  2002;346:180-188.
5. Fasano A, Catassi I.  Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum.  Gastroenterology.  2001;120:636-651.
6. National Institutes of Health Consensus Development Conference Statement. NIH Consensus Development Conference on Celiac Disease. June 28-30, 2004; Bethesda, Md.  Final Statement August 9, 2004. Available at: http://consensus.nih.gov/2004/2004CeliacDisease118html.htm. Accessed November 27, 2007.
7. Gluten Intolerance/Celiac Disease and Nutrition Evidence Analysis Project.  American Dietetic Association Evidence Analysis Library.  American Dietetic Association; 2007. Available at: http://www.adaevidencelibrary.org.  Accessed November 15, 2007.
8. Maki M, Collin P. Coeliac disease. Lancet. 1997;349:1755-1759.
9. Zipser RD, Patel S, Yahya KZ, Baisch DW, Monarch E.  Presentations of adult celiac disease in a nationwide patient support group.  Dig Dis Sci.  2003;48:761-764.
10. Thompson T.  Case Problem: questions regarding the acceptability of buckwheat, amaranth, quinoa, and oats from a patient with celiac disease.  J Am Diet Assoc.  2001;101:586-587.
11. Janatuinen EK, Kemppainen TA, Pikkarainen PH, Holm KH, Kosma V-M, Uusitupa MIJ, Maki M, Julkunen RJK. Lack of cellular and humoral immunological responses to oats in adults with coeliac disease. Gut. 2000;46:327-331.
12. Hoffenberg EJ, Haas J, Drescher A, Barnhurst R, Osberg I, Bao F, Eisenbarth G. A trial of oats in children with newly diagnosed celiac disease. J Pediatr. 2000;137:361-366.
13. Janatuinen EK, Kemppainen TA, Julkunen RJK, Kosma V-M, Maki M, Heikkinen M, Uusitupa MIJ. No harm from five year ingestion of oats in coeliac disease. Gut. 2002;50:332-335.
14. Storsrud S, Olsson M, Arvidsson LR, Nilsson LA, Kilander A. Adult coeliac patients do tolerate large amounts of oats. Eur J Clin Nutr. 2003;57:163-169.
15. Hogberg L, Laurin P, Faith-Magnusson K, Grant C, Grodzinsky E, Jansson G, Ascher H, Browaldh L, Hammersjo JA, Lindberg E, Myrdal U, Stenhammer L. Oats to children with newly diagnosed coeliac disease: a randomised double blind study. Gut. 2004;53:649-654.
16. Lundin KE, Nilsen EM, Scott HG, Loberg EM, Gjoen A, Bratlie J, Skar V, Mendez, E, Lovik A, Kett K. Oats induced villous atrophy in coeliac disease. Gut. 2003;52:1649-1652.
17. Peraaho M, Kaukinen K, Mustalahti K, Vuolteenaho N, Maki M, Laippala P, Collin P. Effect of oats-containing gluten-free diet on symptoms and quality of life in coeliac disease: a randomized study. Scand J Gastroenterol. 2004;39:27-31.
18. Arentz-Hansen H, Fleckenstein B, Molberg O, Scott H, Koning F, Jung G, Roepstorff P, Lundin KEA, Sollid LM. The molecular basis for oat intolerance in patients with celiac disease. PLoS Med. 2004;1:e1.
19. Thompson T. Oats and the gluten-free diet. J Am Diet Assoc. 2003;103:376-379.
20. Joint FAO/WHO Food Standards Program. Codex Committee on Nutrition and Foods for Special Dietary Uses. Draft revised standard for gluten-free foods. CX/NFSDU 98/4. July 1998:1-4.
21. Thompson T, Dennis M, Higgins L, Lee A, Sharrett M. Gluten-free diet survey: are Americans with coeliac disease consuming recommended amounts of fibre, iron, calcium and grain foods? J Hum Nutr Diet. 2005;18:163-169.
22. US Food and Drug Administration’s (FDA) Code of Federal Regulations (21CFR137).  Available at: http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=108_cong_bills&docid=f:s741es.txt.pdf. Accessed November 29, 2007.
23. Godkin A, Jewell D.  The pathogenesis of celiac disease.  Gastroenterology.  1998;115:206-210.

Bibliography

Green PH, Jabri B. Coeliac disease.  Lancet.  2003;362:383-391.
Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, Elitsur Y, Green PH, Guandalini S, Hill ID, Pietzak M, Ventura A, Thorpe M, Kry D, Fornardi F, Wasserman SS, Murray JA, Horvath K.  Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study.  Arch Intern Med.  2003;163:286-292.
Murray JA.  The widening spectrum of celiac disease.  Am J Clin Nutr.  1999;69:354-365.
Thompson T.  Thiamin, riboflavin, and niacin contents of the gluten-free diet: is there cause for concern?  J Am Diet Assoc.  1999; 99: 858-862.
American Gastroenterological Association medical position statement: Celiac Sprue.  Gastroenterology.  2001; 120:1522- 1525.

Manual of Clinical Nutrition Management                                                     
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