Salivary IgA antigliadin antibody as a marker for coeliac disease.

Hakeem, Vaseem; Fifield, R.; al-Bayaty, H F; Aldred, Michael J.; Walker, DM; Williams, Joshua; Jenkins, Huw

doi:10.1136/adc.67.6.724

Cited by 32 publications

(20 citation statements)

References 23 publications

(12 reference statements)

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“…28-34 AGA detection had generally low sensitivity, and when used to screen children with CD, also a limited specificity. [28][29][30][31][32][33][34][35] IgA EMA were evaluated in saliva fluid in two studies performed with indirect immunofluorescence methods. 33,34 Lätheenoja et al 33 failed to detect a salivary EMA immune response in all the subjects with CD investigated at disease diagnosis; they postulated that salivary IgA EMA are not produced locally.…”

Section: Discussionmentioning

confidence: 99%

“…20,[25][26][27] The most sensitive assays to detect tTG-Abs were those using human recombinant tTG in a fluid-phase radioimmunoassay (RIA) format. 26,27 Attempts have been made in assaying CD-related Ab in saliva, [28][29][30][31][32][33][34][35] which are easily obtained by noninvasive techniques, bypassing blood sample collection. However, the proposed salivary assays were not accurate enough, suggesting that saliva is not suitable for CD screening…”

mentioning

confidence: 99%

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Tissue transglutaminase autoantibody detection in human saliva: a powerful method for celiac disease screening

Bonamico

Ferri

Nenna

et al. 2004

The Journal of Pediatrics

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Objective To test the possibility of detecting tissue transglutaminase autoantibodies (tTG-Abs) in saliva with a novel sensitive fluid-phase radioimmunoassay (RIA).Study design Paired saliva and serum samples from 39 patients with celiac disease (CD), at the first biopsy (Group 1: 28 females, mean age 11.5 ± 11.1 years); 32 controls with a normal duodenal mucosa (Group 2: 18 females, mean age 8.1 ± 3.6 years); and 32 healthy volunteers (Group 3: 21 females, mean age 31.7 ± 9.8 years) were studied for tTG-Ab presence. Limit of positivity for salivary assay was calculated according to the 99th percentiles of Group 2 control children and was expressed as an autoantibody (Ab) index.Results Salivary tTG-Abs were found in 97.4% of the patients with CD and in 100% of the corresponding serum samples. All Group 3 subjects were negative with both saliva and serum assays. A correlation between saliva and serum tTG-Ab titers was found (r = 0.826, P = .0014).Conclusions This study demonstrates that it is possible to detect salivary tTG-Abs in CD with a non-invasive, simple to perform, reproducible and sensitive method. (J Pediatr 2004;144:632-6) C eliac disease (CD) may appear in a classic presentation, with gastrointestinal complaints and growth failure or with extraintestinal manifestations and ''atypical forms'' 1 characterized by anemia and short stature, 2,3 or with a silent form, more frequent in first-degree relatives of patients with CD. 4 The prevalence of CD is increased in subjects with elevated aminotransferase levels, 5,6 autoimmune diseases, 7,8 and chromosomal aberrations. 9,10 Complications of long-standing CD may include osteopathy, 11 endocrinopathy, 12 infertility, low birth weight infants, 13,14 cancer, 15 and dilated cardiomyopathy and other forms of heart failure. 16 CD has a high prevalence in the general population (0.55% in Italy), often in an asymptomatic form. 17 To reduce the risks associated with prolonged gluten exposure, CD should be diagnosed early, on the basis of the result of one or more intestinal biopsies. 18 Patients with CD receiving a gluten-containing diet have increased levels of anti-gliadin (AGA), anti-endomysium (EMA), 19 and anti-tissue transglutaminase autoantibodies (anti-tTG-Ab). 20 Serum AGA have proved to be effective in the identification of children at risk for CD, but less so in adult screening. 21 EMA are more specific than AGA but are observer-dependent, and sometimes they are not found in children with CD younger than aged 2 years. 19 The recent identification of tTG as the main autoantigen recognized by EMA 22 has lead to the development of various studies that suggest an important role for this enzyme in the etiopathogenesis of CD. 23,24 Several methods have been proposed for the detection of humoral anti-tTG immunoreactivity in CD. 20,[25][26][27] The most sensitive assays to detect tTG-Abs were those using human recombinant tTG in a fluid-phase radioimmunoassay (RIA) format. 26,27 Attempts have been made in assaying CD-related Ab in saliva, [28][29][30][31][32][...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Tissue transglutaminase autoantibody detection in human saliva: a powerful method for celiac disease screening

Bonamico

Ferri

Nenna

et al. 2004

The Journal of Pediatrics

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“…3). In two studies employing samples of unstimulated whole saliva, the discrimination of confirmed celiac patients was quite satisfactory, 99 or even better than by measurement of IgA antibodies in serum. 100 However, comparable studies employing stimulated parotid secretion showed only little, 101 or virtually no 102 elevation of IgA antibody levels to gliadin in contrast to the results obtained with serum (FIG.…”

Section: Celiac Diseasementioning

confidence: 96%

Do Salivary Antibodies Reliably Reflect Both Mucosal and Systemic Immunity?

Brandtzæg

2007

Annals of the New York Academy of Sciences

223

230

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Two major antibody classes operate in saliva: secretory IgA (SIgA) and IgG. The former is synthesized as dimeric IgA by plasma cells (PCs) in salivary glands and is exported by the polymeric Ig receptor (pIgR). Most IgG in saliva is derived from serum (mainly via gingival crevices), although some is locally produced. Gut-associated lymphoid tissue (GALT) and nasopharynx-associated lymphoid tissue (NALT) do not contribute equally to mucosal PCs throughout the body. Thus, enteric immunostimulation is an inadequate mode of stimulating salivary IgA antibodies, which are poorly associated with the intestinal SIgA response, for instance after enteric cholera vaccination. Nevertheless, the IgA response in submandibular/sublingual glands is better related to B cell induction in GALT than the parotid response. Such disparity is suggested by the elevated levels of IgA in submandibular secretions of AIDS patients, paralleling their highly upregulated intestinal IgA system. Moreover, in patients with active celiac disease, IgA antibodies to disease-precipitating gliadin are reliably represented in whole saliva but not in parotid secretion. Parotid SIgA may be more consistently linked to immune induction in palatine tonsils and adenoids (human NALT), as supported by the homing molecule profile of NALT-derived B cell blasts. Also several other variables influence the levels of antibodies in oral secretions. These include difficulties with reproducibility and standardization of immunoassays, the impact of flow rate, acute or chronic stress, protein loss during sample handling, and uncontrolled admixture of serum-derived IgG and monomeric IgA. Despite such problems, saliva remains an interesting biological fluid with great scientific and clinical potentials.

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“…Thus, the production of IgA antibodies to gluten (gliadin) that is induced in the gut of patients with coeliac disease, is reflected as diagnostic IgA titers in whole saliva (86, 87). Nevertheless, in subjects immunized orally with a cholera toxin (CT) B subunit–whole-cell Vibrio cholerae vaccine, the specific IgA antibody detection sensitivity in whole saliva was not better than in serum and only approximately 50% of that in intestinal lavage (88).…”

Section: Homing Of Activated B Cells To Salivary Glandsmentioning

confidence: 99%

Secretory immunity with special reference to the oral cavity

Brandtzæg

2013

Journal of Oral Microbiology

258

268

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The two principal antibody classes present in saliva are secretory IgA (SIgA) and IgG; the former is produced as dimeric IgA by local plasma cells (PCs) in the stroma of salivary glands and is transported through secretory epithelia by the polymeric Ig receptor (pIgR), also named membrane secretory component (SC). Most IgG in saliva is derived from the blood circulation by passive leakage mainly via gingival crevicular epithelium, although some may be locally produced in the gingiva or salivary glands. Gut-associated lymphoid tissue (GALT) and nasopharynx-associated lymphoid tissue (NALT) do not contribute equally to the pool of memory/effector B cells differentiating to mucosal PCs throughout the body. Thus, enteric immunostimulation may not be the best way to activate the production of salivary IgA antibodies although the level of specific SIgA in saliva may still reflect an intestinal immune response after enteric immunization. It remains unknown whether the IgA response in submandibular/sublingual glands is better related to B-cell induction in GALT than the parotid response. Such disparity is suggested by the levels of IgA in submandibular secretions of AIDS patients, paralleling their highly upregulated intestinal IgA system, while the parotid IgA level is decreased. Parotid SIgA could more consistently be linked to immune induction in palatine tonsils/adenoids (human NALT) and cervical lymph nodes, as supported by the homing molecule profile observed after immune induction at these sites. Several other variables influence the levels of antibodies in salivary secretions. These include difficulties with reproducibility and standardization of immunoassays, the impact of flow rate, acute or chronic stress, protein loss during sample handling, and uncontrolled admixture of serum-derived IgG and monomeric IgA. Despite these problems, saliva is an easily accessible biological fluid with interesting scientific and clinical potentials.

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Salivary IgA antigliadin antibody as a marker for coeliac disease.

Cited by 32 publications

References 23 publications

Tissue transglutaminase autoantibody detection in human saliva: a powerful method for celiac disease screening

Tissue transglutaminase autoantibody detection in human saliva: a powerful method for celiac disease screening

Do Salivary Antibodies Reliably Reflect Both Mucosal and Systemic Immunity?

Secretory immunity with special reference to the oral cavity

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