Can Consumption of Wheat Lead to Malabsorption?
By Avik Basu1 and Saikat Kumar Basu2
Guyana Journal, February 2012
Abbreviations: AIDS: Acquired Immunodeficiency Syndrome; IgA: Immunoglobulin A; MHC-I: Major histocompatibility complex I; HLA: Human Leukocyte Antigen; IL: Interleukin; APC: Antigen presenting cell; CD4: Cluster of Differentiation factor 4
Malabsorption may be defined as an impaired or defective absorption of food, be it carbohydrates, proteins, fats, vitamins or minerals (Asimov et al., 1966). It may occur in a variety of clinical conditions like AIDS, Biliary atresia, gastrinomas and Crohn's disease. Certain parasitic infestations like that caused by Diphyllobothrium latum and Giardia lamblia also predispose to malabsorption. However, consumption of wheat, barley and other related cereals containing a major storage protein called gluten has been found to cause severe malabsorption in susceptible individuals. This particular form of malabsorption is designated as the Celiac Disease or Gluten-induced Enteropathy (Kumar et al., 2010).
Pathogenesis of Celiac Disease
Environmental, immunological and genetic factors together play a role in the pathogenesis of Celiac Disease (Binder, 2008). The environmental factor includes gliadin, the alcohol-soluble fraction of gluten protein in wheat that upon interaction with the immune components of the human body, leads to the malabsorptive symptoms of this disease (Kumar et al., 2010). An immunological factor is suspected from the detection of IgA antigliadin, IgA antiendomysial and IgA anti-tTG antibodies in the patient's serum (Binder, 2008). The genetic factor involves the expression of a particular MHC-I allele in 0.5% to 1% of Europeans (Kumar et al., 2010). This gene resides on chromosome 6p (Stewart, 2007). It codes for a specific HLA molecule in these individuals, i.e., HLA-DQ2 or HLA-DQ8 (Kumar et al., 2010).
Gliadin proteins induce expression of IL-15 on the intestinal epithelial cells. These, in turn, activate the Natural Killer cells of the immune system which launch a lethal attack on the enterocytes having a specific marker molecule MIC-A resulting in their destruction. The damaged epithelia lead to an unabated entry of deamidated (by transglutaminase) gliadin peptides into the cells allowing their interaction with HLA-DQ molecules on surface of APCs and presentation to CD4+ T lymphocytes. The lymphocytes then elaborate cytokines that lead to complete blunting of the villi, thus adding fuel to fire (Kumar et al., 2010).
The spectrum of manifestations range from complete absence of any gastrointestinal symptoms but for signs of depletion of one particular nutrient (edema from protein loss or pallor from iron depletion) to significant malabsorptive events accompanied by diarrhea, steatorrhea, significant weight loss and secondary manifestations (Binder, 2008).
The frequent complications include Enteropathy-associated T cell lymphoma and small intestinal adenocarcinoma (Kumar et al., 2010).
Dietary modification with exclusion of the offending cereals and supplementation of rice, maize, vitamins and minerals stands the conventional procedure of management (Palmer et al., 2002). However, in refractory cases glucocorticoids need to be administered (Binder, 2008).
Asimov et al. (eds.) 1966. Stedman's Medical dictionary. The Williams & Wilkins Co, Baltimore, US., p. 941.
Binder, H. 2008. Disorders of absorption. In: Fauci et al. (eds.) Harrison's principles of internal medicine. 17th ed. McGraw-Hill Co. pp. 1872-1886.
Palmer et al. 2002. Alimentary tract and pancreatic disease. In: Haslett et al. (eds.) Davidson's principles and practice of medicine. 19th ed. Churchill Livingstone Elsevier. pp. 747-830.
Medline plus, 2010. Malabsorption. Available online at: http://www.nim.nih.gov/medlineplus/ency/article/000299.html [Accessed January 25, 2012].
Stewart, J. 2007. Immunological principles: antigens and antigen recognition. In: Greenwood et al. (eds.) Medical microbiology. 17th ed. Churchill Livingstone Elsevier. pp. 96-106.
Turner, J. 2010. The gastrointestinal tract. In: Kumar et al. (eds.) Robbins and Cotran's pathological basis of disease. 8th ed. Elsevier. pp. 763-831.
1Medical College Kolkata, WB India
2School of Agriculture & Life Sciences, CAAS, Lethbridge College, Lethbridge, AB, Canada; Email