Celiac Sprue, also known as gluten-sensitive enteropathy or nontropical sprue is a disease primarily affecting the small bowel caused by a reaction to gluten, a protein found in wheat, barley and rye. Over the past several decades, it has become apparent that celiac sprue is often underdiagnosed due to minimal or no clinical symptoms. Studies suggest that celiac sprue is present in 1:250 to 1:500 persons in most countries (1,2). Celiac sprue is particularly common in populations from Northern Europe and Western Ireland. Affected individuals poorly absorb fat, iron, vitamin D, calcium and other nutrients, resulting in symptoms of abdominal bloating, malaise, easy fatigability, abdominal cramps, diarrhea, osteoparosis (thin bones) and skin rashes. It is also possible, that those with celiac sprue will have minimal or no symptoms (3).

We recommend testing for celiac sprue in cases of unexplained malabsorbtion, weight loss or bloating. Testing for celiac sprue should also be done in those with iron deficiency anemia, folate or B-12 deficiency, short stature, delayed puberty or a chronic elevation in liver enzymes.

The diagnosis is made by a combination of blood testing for anti-tissue transglutaminase antibody (anti-tTG), antiendomysial or less commonly antigliadin antibodies, as well as a biopsy of the small bowel obtained during endoscopy. This blood testing should be done while ingesting a diet that DOES contain gluten (4,5). It is recommended that patients with blood tests consistent with celiac sprue have confirmation of the disease by small bowel biopsy with the only exception being those with biopsy proven dermatitis herpetiformis (classically associated rash). The benefit of diagnosing celiac sprue lies primarily in the recognition and treatment of nutritional deficiencies, treatment of bone loss and the potential reduction in risk of some malignancies (6-9). A small bowel follow through or capsule endoscopy may provide information about the extent of disease.

Treatment consists of a life-long gluten free diet with close monitoring by your gastroenterologist for malabsorption. This diet can be difficult to follow and in most cases it is recommended that a registered dietitian provide education on which foods are acceptable. Resolution or improvement of symptoms typically occurs in a few weeks to months. In cases where there is a failure to improve with a gluten free diet, the most likely explanation is continued ingestion of gluten. Also possible is that the diagnosis is incorrect…for example irritable bowel syndrome and lactose intolerance can present with similar symptoms to celiac sprue. Less commonly there are sprue associated lymphomas of the small bowel or structural colon abnormalities (microscopic colitis) that can produce malabsorption, diarrhea, bloating etc. Life-long follow up is needed to monitor for potential complications of celiac sprue such as osteoporosis, anemia, and cancers particularly lymphoma (10,11).

It is typical for celiac sprue to remain undiagnosed for years. If you have symptoms as described above, consider making an appointment with a Borland-Groover gastroenterologist for specialized testing. 

The National Celiac Sprue Association is an excellent resource available to all. Their website can be found at: http://www.csaceliacs.org

References

1.    Fasano, A. Where have all the American celiacs gone?. Acta Paediatr Suppl 1996; 412:20.
2.    Not, T, Horvath, K, Hill, ID, et al. Celiac disease risk in the USA: High prevalence of antiendomysium antibodies in healthy blood donors. Scand J Gastroenterol 1998; 33:494.
3.    Rampertab, SD, Pooran, N, Brar, P, et al. Trends in the presentation of celiac disease. Am J Med 2006; 119:355.
4.    Jansson, UH, Gudjonsdottir, AH, Ryd, W, Kristiansson, B. Two different doses of gluten show a dose-dependent response of enteropathy but not of serological markers during gluten challenge in children with coeliac disease. Acta Paediatr 2001; 90:255.
5.    Laurin, P, Wolving, M, Falth-Magnusson, K. Even small amounts of gluten cause relapse in children with celiac disease. J Pediatr Gastroenterol Nutr 2002; 34:26.
6.    Holmes, GK, Prior, P, Lane, MR, et al. Malignancy in coeliac disease: Effect of a gluten free diet. Gut 1989; 30:333.
7.    Corrao, G, Corazza, GR, Bagnardi, V, et al. Mortality in patients with coeliac disease and their relatives: a cohort study. Lancet 2001; 358:356.
8.    Askling, J, Linet, M, Gridley, G, et al. Cancer incidence in a population-based cohort of individuals hospitalized with celiac disease or dermatitis herpetiformis. Gastroenterology 2002; 123:1428.
9.    Collin, P, Reunala, T, Pukkala, E, et al. Coeliac disease—associated disorders and survival. Gut 1994; 35:1215.
10.    Green, PH, Fleischauer, AT, Bhagat, G, et al. Risk of malignancy in patients with celiac disease. Am J Med 2003; 115:191.
11.    Card, TR, West, J, Holmes, GK. Risk of malignancy in diagnosed coeliac disease: a 24-year prospective, population-based, cohort study. Aliment Pharmacol Ther 2004; 20:769.