Tissue transglutaminase antibodies in patients with end-stage heart failure

Peracchi, M.; Trovato, Cristina; Longhi, M. Paula; Gasparin, Maurizio; Conte, Dario; Tarantino, C.; Prati, Daniele; Bardella, Maria Teresa

doi:10.1111/j.1572-0241.2002.07033.x

Cited by 48 publications

(34 citation statements)

References 31 publications

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“…The first practical consequence of this age-related fluctuation in anti-transglutaminase autoantibodies was a change in IgA and IgG cutoff limits among the age groups studied. This enabled us to distinguish the pediatric population from the adult population with more precision and allowed us to potentially disregard unexpected positive sera with minor increases in anti-tTG titer, as reported recently in a nonceliac adult population (13,14 ).…”

Section: Anti-transglutaminase Antibodies and Age Valentinamentioning

confidence: 99%

Anti-Transglutaminase Antibodies and Age

et al. 2004

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Section: Anti-transglutaminase Antibodies and Age Valentinamentioning

confidence: 99%

Anti-Transglutaminase Antibodies and Age

et al. 2004

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“…The discovery that tTG was the main autoantigen for the EMA enzyme-linked immunosorbent assay (ELISA) [18] prompted the development of testing for tTGs. Anti-tTG antibodies are less specific, however, and have been reported to be positive in the presence of liver disease, diabetes and severe heart failure [94][95][96].…”

Section: Diagnosis Of CDmentioning

confidence: 99%

Mechanisms underlying celiac disease and its neurologic manifestations

Green

Alaedini

Sander

et al. 2005

CMLS, Cell. Mol. Life Sci.

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The extra-intestinal manifestations of celiac disease (CD), including ataxia and peripheral neuropathy, are increasingly being recognized as the presenting symptoms of this autoimmune disease. Although there is a greater understanding of the pathogenesis of the intestinal lesions in CD the mechanisms behind the neurologic manifestations of CD have not been elucidated. In this article, the authors review the cellular and molecular mechanisms behind the histopathologic changes in the intestine, discuss the presentation and characteristics of neurologic manifestations of CD, review the data on the mechanisms behind these manifestations, and discuss the diagnosis and treatment of CD. Molecular mimicry and intermolecular help may play a role in the development of neurologic complications.

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“…In a study of 288 patients with end stage heart failure awaiting cardiac transplantation, nearly half were found to have positive IgA and IgG antibodies directed at recombinant human TG2 (172). These patients had no clinical evidence of celiac disease.…”

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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Tissue transglutaminase antibodies in patients with end-stage heart failure

Abstract: IgA and IgG tTGA occur in a large number of EmA-negative patients with end-stage heart failure, and their presence is unlikely to be caused by concomitant CD.

Cited by 48 publications

References 31 publications

Anti-Transglutaminase Antibodies and Age

Anti-Transglutaminase Antibodies and Age

Mechanisms underlying celiac disease and its neurologic manifestations

Roles of transglutaminases in cardiac and vascular diseases

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