Celiac Disease and Coronary Artery Disease

Celiac disease (celiac sprue) is a malabsorptive syndrome that results from gluten dependent inflammation of the small bowel. Although the disease is typically characterized by diarrhea, flatulence and weight loss, more subtle symptoms such as non-specific bloating and malaise can be characteristic. Subgroups of patients can present with iron deficiency alone. A variety of pathological entities are associated with celiac disease. Folate, iron, vitamin K and vitamin D deficiencies are often present and can be explained by the malabsorptive process itself. Other conditions such as peripheral neuropathy, cerebellar ataxia and dermatitis herpetiformis are also associated but the pathogenesis is not as well understood. Autoimmune diseases including type 1 diabetes mellitus and autoimmune thyroiditis are also seen with increased frequency in patients with celiac sprue. Much work has been done on the epidemiology of celiac disease. Although commonly thought of as a pediatric disease, the condition often first presents in adulthood. Many earlier studies underestimated the frequency of celiac disease because only cases with typical presenting symptoms were identified. However, with an increased awareness that celiac disease can present with much more subtle and varied symptoms, more cases are being recognized. Coupled with new serologic tests including antigliadin and antiendomysial antibodies, the prevalence has been found to range from 1:100 to 1:600 (1). The pathogenesis of celiac disease involves an autoimmune reaction triggered by the ingestion of gluten (2). This phenomenon typically occurs in susceptible patients who possess the HLA-DQ2 cell surface antigen. Gluten derived gliaden proteins are expressed in conjunction with these antigens to T cells in the lamina propria of the small bowel. Tissue transglutaminase facilitates this process by deaminating gliadin peptides, thus evoking a stronger T-cell response. A localized inflammatory state ensues characterized by the generation of various cytokines. Tissue transglutaminase also acts as an autoanitgen itself, inducing the formation of autoantibodies that perpetuate the inflammatory response.