Celiac disease or celiac sprue is predominantly a disease of the small intestine characterized by chronic malabsorption in genetically susceptible individuals who ingest grains containing gluten, such as wheat, barley, and rye.
Heart failure occurs when the heart muscle weakens and is unable to circulate enough blood to meet the body’s needs, often causing shortness of breath, fatigue and leg swelling. The definition of a cardiomyopathy by the World Health Organization recognizes that ventricular dysfunction can result from a failure to correct volume or pressure overload in valve disease or to control hypertension.
One study of 52 patients reported an increased prevalence of celiac disease (5.8%) in patients with dilated cardiomyopathy (Curione M, Barbato M, De Biase L, Viola F, Lo Russo L, Cardi E. Prevalence of coeliac disease in idiopathic dilated cardiomyopathy. Lancet. 1999;354:222-223).
Several pathogenic mechanisms have been proposed for the development of cardiomyopathy in the course of celiac disease. Chronic malabsorption, common in celiac disease, may lead to cardiomyopathy secondary to nutritional deficiencies.
Hypoxia which is responsible for the change in the intestinal permeability may decrease absorption of important micronutrients for myocardial contraction, one of them being carnitine. Carnitine deficiency in celiac disease has been shown in some studies and this can be one of the parameters explaining this co-morbidity.
Abnormalities of intestinal permeability in patients with celiac disease may lead to increased systemic absorption of various luminal antigens or infectious agents that may cause myocardial damage through immune-mediated mechanisms.
Myocardial injury may be secondary to an immune response directed against an antigen present in both the myocardium and the small intestine.
Celiac disease and heart failure
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