Prevalence of coeliac disease in idiopathic dilated cardiomyopathy

Curione, Mario; Barbato, M.; Biase, Luciano De; Viola, Franca; Russo, L. Lo; Cardi, E

doi:10.1016/s0140-6736(99)01501-9

Cited by 102 publications

(74 citation statements)

References 4 publications

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“…Thus, DQ8 might be able to positively select T cells with specificity to cardiac antigens that are able to present self-peptides in heart of NOD.DQ8 mice. In human myocarditis, cardiac myosin heavy chain is the major target of autoantibodies, however few patients with myocarditis also produce anti-tissue transglutaminase (Ttg) antibodies [7,8]. We also observed an increased level of anti-Ttg antibodies in mice with myocarditis suggesting similarity with human disease.…”

Section: Discussionmentioning

confidence: 62%

“…Familial aggregation, presence of antibodies to cardiac antigens, association of HLA with DCM and antibodies, and abnormal expression of HLA class II on cardiac endothelium underscore the influence of genetic factors in development of autoimmune processes [4][5][6]. Several recent studies demonstrated an immunological basis of other systemic autoimmune disorder, celiac disease and anti-tissue transglutaminase antibodies, in patients with myocarditis [7,8].…”

Section: Introductionmentioning

confidence: 99%

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Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice

Taneja

Behrens

Cooper

et al. 2007

Journal of Molecular and Cellular Cardiology

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Most individuals have viral infections at some point in their life, however, only few develop autoreactivity to cardiac myosin following infection resulting in myocarditis suggesting a genetic predisposition. Most mouse models of myocarditis are induced by viral infection or by immunization with cardiac myosin. We generated HLA-DR3.Aβo and HLA-DQ8.Aβo transgenic mice in NOD and HLA-DQ8.Aβo in B10 background to study spontaneous autoimmunity. A high mortality was observed in NOD.DQ8 female mice 16 weeks or older. Echocardiography showed marked systolic dysfunction. Histopathology of various organs revealed an enlarged heart with mononuclear infiltrate consisting of CD4 and Mac-1+ cells and myocyte necrosis. The autoimmunity was associated with the presence of spontaneous autoreactive T cells and antibodies to cardiac myosin. Serologically, mice were negative for all known mouse viruses. NOD.DR3.Aβo, the transgene negative littermates, NOD, and B10.DQ8 Aβo mice had no gross or microscopic cardiac pathology. Spontaneous cellular and humoral response to cardiac myosin suggest that NOD.DQ8 may harbor autoreative cells that can lead to spontaneous myocarditis and dilated cardiomyopathy. HLA-DQ8 is required for predisposition to the spontaneous autoreactivity while NOD background influences onset and progression of disease. This model of myocarditis occurs predominantly in female mice and may provide insight into the pathogenesis of heart disease in women.

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Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice

Taneja

Behrens

Cooper

et al. 2007

Journal of Molecular and Cellular Cardiology

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“…Celiac Disease has been described in 4.4% of patients with myocarditis, a prevalence that is 14-fold higher than in control subjects (167). Similarly, CD occurs in up to 5.7% of patients with idiopathic dilated cardiomyopathy (168,169). A common auto-antigen in celiac disease and its associated autoimmune cardiomyopathy is TG2 (167,170).…”

Section: Lvh and Heart Failurementioning

confidence: 99%

Roles of transglutaminases in cardiac and vascular diseases

Sane

Kontos²,

Greenberg³

2007

Front Biosci

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All transglutaminases share the common enzymatic activity of transamidation, or the cross-linking of glutamine and lysine residues to form N epsilon (gamma-glutamyl) lysyl isopeptide bonds. The plasma proenzyme factor XIII is responsible for stabilizing the fibrin clot against physical and fibrinolytic disruption. Another member of the transglutaminase family, tissue transglutaminase or TG2 is abundantly expressed in cardiomyocytes, vascular cells and macrophages. The transglutaminases have a variety of functions independent of their transamidating activity. For example, TG2 binds and hydrolyzes GTP, thereby fostering signal transduction by several G protein coupled receptors. Accumulating evidence points to novel roles for factor XIII and TG2 in cardiovascular biology including: (a) modulating platelet activity, (b) regulating glucose control, (c) contributing to the development of hypertension, (d) influencing the progression of atherosclerosis, (e) regulating vascular permeability and angiogenesis (f) and contributing to myocardial signaling, contractile activity and ischemia/reperfusion injury. In this review, we summarize the cardiovascular biology of two members of the family of transglutaminases, Factor XIII and TG2.

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“…The withdrawal of gluten reverses not only the intestinal, but also the skin lesions in most dermatitis herpetiformis patients. Many other pathological conditions, such as autoimmune disorders (insulin-dependent diabetes mellitus type 1, thyroid disorders, autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, alopecia, vitiligo, Addison's disease, Sjögren's syndrome, IgA nephropathy and IgA deficiency), [55][56][57][58][59][60][61][62][63][64][65] idiopathic disorders (primitive dilated cardiomyopathy, atopy and inflammatory bowel disease) [66][67][68] and chromosome disorders (Down, Turner and Williams syndromes), [69][70][71] display a strong association with CD. The importance of diagnosing the subclinical form of CD associated with these disorders is twofold because a gluten-free diet not only prevents the clinical manifestations and complications of CD but also sometimes improves clinical symptoms of the associated disorders (Table 3).…”

Section: Introductionmentioning

confidence: 99%

Celiac disease: diagnostic criteria in progress

2011

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Until a few years ago, celiac disease (CD) was thought to be a rare food intolerance that was confined to childhood and characterized by severe malabsorption and flat intestinal mucosa. Currently, CD is regarded as an autoimmune disorder that is common in the general population (affecting 1 in 100 individuals), with possible onset at any age and with many possible presentations. The identification of CD is challenging because it can begin not only with diarrhea and weight loss but also with atypical gastrointestinal (constipation and recurrent abdominal pain) and extra-intestinal symptoms (anemia, raised transaminases, osteoporosis, recurrent miscarriages, aphthous stomatitis and associated autoimmune disorders), or it could be completely symptomless. Over the last 20 years, the diagnostic accuracy of serology for CD has progressively increased with the development of highly reliable tests, such as the detection of IgA tissue transglutaminase and antiendomysial and IgG antideamidated gliadin peptide antibodies. The routine use of antibody markers has allowed researchers to discover a very high number of 'borderline' cases, characterized by positive serology and mild intestinal lesions or normal small intestine architecture, which can be classified as potential CD. Therefore, it is evident that the 'old celiac disease' with flat mucosa is only a part of the spectrum of CD. It is possible that serology could identify CD in its early stages, before the appearance of severe intestinal damage. In cases with a positive serology but with mild or absent intestinal lesions, the detection of HLA-DQ2 and HLA-DQ8 can help reinforce or exclude the diagnosis of gluten sensitivity.

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Prevalence of coeliac disease in idiopathic dilated cardiomyopathy

Cited by 102 publications

References 4 publications

Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice

Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice

Roles of transglutaminases in cardiac and vascular diseases

Celiac disease: diagnostic criteria in progress

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