eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Celiac Disease: Treatment & Medication

Author: Stefano Guandalini, MD, Director, University of Chicago Celiac Disease Program, Section Chief of Gastroenterology, Hepatology and Nutrition; Professor, Department of Pediatrics, University of Chicago Comer Children's Hospital
Coauthor(s): Phyllis A Vallee, MD, Associate Program Director, Department of Emergency Medicine, Henry Ford Hospital
Contributor Information and Disclosures

Updated: Sep 2, 2009

Treatment

Medical Care

Total lifelong avoidance of gluten ingestion is the cornerstone treatment for patients with celiac disease (CD). Wheat, rye, and barley are the grains that contain toxic peptides. They should be eliminated as completely as possible, although daily intake doses larger than 10 mg are likely needed to cause mucosal reaction.21 GI symptoms in patients with symptomatic celiac disease who adhere to a gluten-free diet typically resolve within a few weeks; these patients experience the normalization of nutritional measures, improved growth in height and weight (with resultant normal stature), and normalization of hematological and biochemical parameters.

Furthermore, treatment with a gluten-free diet reverses the decrease in bone mineralization and the risk for fractures . Symptomatic children treated with a gluten-free also improve their sense of physical and psychological well being.

For a long time, oats were considered toxic as well, and their elimination from the diet had been recommended. However, over the past decade, a growing body of scientific evidence obtained from in vitro studies as well as from clinical investigations (particularly in adults but also, more recently, in children) suggests that oats are totally safe. Because of uncontrolled harvesting and milling procedures, as well as the possibility that lines of manufacturing used for wheat-based flours are also used in the preparation of oat-based foods, cross-contamination of oats with gluten is still a concern.

Lactose is often eliminated in the initial phases of dietary treatment as well. This is because lactase deficiency is thought to accompany the flat mucosa. However, most newly diagnosed patients with celiac disease are diagnosed in the absence of overt malabsorptive symptoms; in these circumstances, clinically significant lactose malabsorption or intolerance is rarely seen. Furthermore, even in cases with obvious malabsorption, the recovery of lactase activity is typically fast; thus, a lactose-free diet must be used on a short-term basis only, even in these individuals.

The American Dietetic Association (ADA) publishes guidelines for the dietary treatment of celiac disease. They are a reliable source of information for a gluten-free. However, because of the dynamics of this field, the diet requires ongoing collaboration between patients, health care providers, and dietitians.

Consultations

Because of the protean nature of celiac disease, multiple consultations may be necessary. For example, consultations with an endocrine specialist should be arranged for patients who also have Hashimoto thyroiditis or type I diabetes mellitus, and a rheumatologist must be consulted for patients who have arthritis.

Diet

See Medical Care.

Activity

No additional restriction is necessary beyond that imposed by the patient's fatigue. However, if a completely gluten-free diet is followed, celiac disease completely regresses, and individuals have a completely normal quality of life.

Medication

Glucocorticoids

Corticosteroids can rapidly control severe symptoms of celiac disease (CD). They may also have a role in rare cases in which the patient has no response to diet; this condition is known as refractory celiac disease and occurs exclusively in adults (1-3% of total).

For celiac disease in children, steroids are almost never needed.


Hydrocortisone (A-Hydrocort, Solu-Cortef)

Some cases of refractory celiac disease (with all other forms of colitis and enteritis excluded) respond to parenteral corticosteroids, for reasons unknown. Exclude other etiologies of failure to thrive, especially in children, because systemic steroids can pose risk to growth. Sodium succinate salt formulation may be administered IV or IM.

Adult

100-500 mg IV q12h

Pediatric

20-120 mg/m2 IV/IM q12h or 0.67-4 mg/kg IV/IM q12h

CYP450 2D6 and 3A3/4 substrate; corticosteroid clearance may increase with phenytoin, barbiturates, or rifampin treatment or decrease with estrogens; cholestyramine may decrease AUC; corticosteroids may increase digitalis toxicity secondary to hypokalemia; coadministration with potassium depleting agents (eg, diuretics) may increase risk of hypokalemia; corticosteroids may decrease growth-promoting effect of GH; decreases effects of salicylates and vaccines used for immunization; monitor for hypokalemia with coadministration of diuretics or amphotericin B; antagonizes effects of anticholinergics; may increase anticoagulant effects of warfarin; decreases hypoglycemic effects of sulfonylureas and insulin; increases toxicity of cyclosporine

Active bacterial infection, chickenpox, measles or concurrent immunosuppressant therapy; avoid in patients with HIV, tubercular infection, congestive heart failure, renal disease, diabetes, or myasthenia gravis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Compare dose for surface area to dose for weight to avoid overdose in overweight child (good rule is use former if weight dose higher); typical child with sprue is severely malnourished and underweight, so mg/kg should present no problem; avoid prolonged use (ie, >1 wk) in children without checking growth parameters and adrenal function; caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis

More on Celiac Disease

Overview: Celiac Disease
Differential Diagnoses & Workup: Celiac Disease
Treatment & Medication: Celiac Disease
Follow-up: Celiac Disease
Multimedia: Celiac Disease
References

References

  1. Guandalini S, Setty M. Celiac disease. Curr Opin Gastroenterol. Nov 2008;24(6):707-12. [Medline].

  2. [Best Evidence] Rubio-Tapia A, Kyle RA, Kaplan EL, et al. Increased prevalence and mortality in undiagnosed celiac disease. Gastroenterology. Jul 2009;137(1):88-93. [Medline].

  3. Tang F, Chen Z, Ciszewski C, et al. Cytosolic PLA2 is required for CTL-mediated immunopathology of celiac disease via NKG2D and IL-15. J Exp Med. Feb 23 2009;[Medline].

  4. Marsh MN, Hinde J. Inflammatory component of celiac sprue mucosa. I. Mast cells, basophils, and eosinophils. Gastroenterology. Jul 1985;89(1):92-101. [Medline].

  5. Catassi C, Kryszak D, Louis-Jacques O, et al. Detection of Celiac disease in primary care: a multicenter case-finding study in North America. Am J Gastroenterol. Jul 2007;102(7):1454-60. [Medline].

  6. Lohi S, Mustalahti K, Kaukinen K, Laurila K, Collin P, Rissanen H, et al. Increasing prevalence of coeliac disease over time. Aliment Pharmacol Ther. Nov 1 2007;26(9):1217-25. [Medline].

  7. Kondrashova A, Mustalahti K, Kaukinen K, Viskari H, Volodicheva V, Haapala AM, et al. Lower economic status and inferior hygienic environment may protect against celiac disease. Ann Med. 2008;40(3):223-31. [Medline].

  8. Catassi C, Cobellis G. Coeliac disease epidemiology is alive and kicking, especially in the developing world. Dig Liver Dis. Oct 2007;39(10):908-10. [Medline].

  9. Silano M, Volta U, Vincenzi AD, Dessì M, Vincenzi MD. Effect of a gluten-free diet on the risk of enteropathy-associated T-cell lymphoma in celiac disease. Dig Dis Sci. Apr 2008;53(4):972-6. [Medline].

  10. Metzger MH, Heier M, Maki M, et al. Mortality excess in individuals with elevated IgA anti-transglutaminase antibodies: the KORA/MONICA Augsburg cohort study 1989-1998. Eur J Epidemiol. 2006;21(5):359-65. [Medline].

  11. Guandalini S, ed. Celiac Disease. In. Textbook of Pediatric Gastroenterology and Nutrition. London: Taylor & Francis;. 2004: 435-50.

  12. Pope R, Sheiner E. Celiac disease during pregnancy: to screen or not to screen?. Arch Gynecol Obstet. Jan 2009;279(1):1-3. [Medline].

  13. Akobeng AK, Ramanan AV, Buchan I, Heller RF. Effect of breast feeding on risk of coeliac disease: a systematic review and meta-analysis of observational studies. Arch Dis Child. Jan 2006;91(1):39-43. [Medline].

  14. Olsson C, Hernell O, Hornell A, Lonnberg G, Ivarsson A. Difference in celiac disease risk between Swedish birth cohorts suggests an opportunity for primary prevention. Pediatrics. Sep 2008;122(3):528-34. [Medline].

  15. Troncone R, Auricchio S. Rotavirus and celiac disease: clues to the pathogenesis and perspectives on prevention. J Pediatr Gastroenterol Nutr. May 2007;44(5):527-8. [Medline].

  16. Bonamico M, Mariani P, Thanasi E, et al. Patchy villous atrophy of the duodenum in childhood celiac disease. J Pediatr Gastroenterol Nutr. Feb 2004;38(2):204-7. [Medline].

  17. Rostom A, Murray JA, Kagnoff MF. American Gastroenterological Association (AGA) Institute technical review on the diagnosis and management of celiac disease. Gastroenterology. Dec 2006;131(6):1981-2002. [Medline].

  18. [Guideline] Hill ID, Dirks MH, Liptak GS, et al. Guideline for the diagnosis and treatment of celiac disease in children: recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr. Jan 2005;40(1):1-19. [Medline].

  19. Walker-Smith JA, Guandalini S, Schmitz J, Shmerling DH, Visakorpi JK. Revised criteria for diagnosis of coeliac disease. Report of Working Group of European Society of Paediatric Gastroenterology and Nutrition. Arch Dis Child. 1990;65:909-911. [Medline].

  20. Kurppa K, Collin P, Viljamaa M, et al. Diagnosing mild enteropathy celiac disease: a randomized, controlled clinical study. Gastroenterology. Mar 2009;136(3):816-23. [Medline].

  21. [Best Evidence] Akobeng AK, Thomas AG. Systematic review: tolerable amount of gluten for people with coeliac disease. Aliment Pharmacol Ther. Jun 1 2008;27(11):1044-52. [Medline].

  22. Leffler DA, Dennis M, Edwards GJ, et al. A Simple Validated Gluten-Free Diet Adherence Survey for Adults With Celiac Disease. Clin Gastroenterol Hepatol. Jan 11 2009;[Medline].

  23. University of Chicago Celiac Disease Center. Available at www.celiacdisease.net.

  24. Isselbacher KJ, Braunwald E, Wilson JD. Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw Hill; 1994:1398-400.

  25. McCance KL, Huether SE. Pathophysiology: The Biologic Basis for Disease in Adults and Children. St Louis, MO: Mosby; 1990:1277-80.

  26. Saltzman JR, Russell RM. The aging gut. Nutritional issues. Gastroenterol Clin North Am. Jun 1998;27(2):309-24. [Medline].

  27. USP. United States Pharmacopeial Convention: Drug Information (USP DI) for the Health Care Professional. 16th ed. Rockville, MD: United States Pharmacopeial Convention; 1996:978-95.

Further Reading

Keywords

celiac sprue, celiac disease, gluten-sensitive enteropathy, nontropical sprue, wheat, potbelly, rye, barley, osteopenia, osteoporosis, short stature, delayed puberty, anemia, intestinal T-cell lymphoma, diarrhea, abdominal distension, malnutrition, celiac crisis, explosive watery diarrhea, dehydration, hypotension, hypokalemia, constipation, failure to thrive, dermatitis herpetiformis, dental enamel hypoplasia, iron-deficiency anemia, chronic hepatitis, hypertransaminasemia, arthritis, arthralgia, Down syndrome, Williams syndrome, Turner syndrome, diabetes mellitus type 1, alopecia, thyroiditis, rotavirus

Contributor Information and Disclosures

Author

Stefano Guandalini, MD, Director, University of Chicago Celiac Disease Program, Section Chief of Gastroenterology, Hepatology and Nutrition; Professor, Department of Pediatrics, University of Chicago Comer Children's Hospital
Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Coauthor(s)

Phyllis A Vallee, MD, Associate Program Director, Department of Emergency Medicine, Henry Ford Hospital
Phyllis A Vallee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Jorge H Vargas, MD, Professor of Pediatrics and Clinical Professor of Pediatric Gastroenterology, David Geffen School of Medicine, University of California at Los Angeles; Consulting Physician, Department of Pediatrics, University of California at Los Angeles Health System
Jorge H Vargas, MD is a member of the following medical societies: American Liver Foundation, American Society for Gastrointestinal Endoscopy, American Society for Parenteral and Enteral Nutrition, Latin American Society of Pediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

 
 
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