Diagnostic performance of three serologic tests in childhood celiac disease.

BACKGROUND: IgA- and IgG-antibodies against deamidated gliadin peptides (DGP) specifically bind the disease-inducing antigen and might be superior to transglutaminase type 2 (TG2) IgA in monitoring patients on a gluten-free diet (GFD). The aim of this study was to compare the performance of DGP-IgG and DGP-IgA with TG2-IgA of four manufacturers in pediatric celiac patients at diagnosis and during follow-up under a GFD. PATIENTS AND METHODS: In total 411 sera of 91 IgA competent children with biopsy proven celiac disease were analyzed at diagnosis and during follow-up on a GFD. Ninety-eight children with normal duodenal histology served as controls. The tests (TheBindingSite, Euroimmun, Phadia, part of Thermo Fisher Scientific, INOVA) for detection of TG2-IgA, DGP-IgG and DGP-IgA were used according to the manufacturers' instructions. RESULTS: Sensitivity to diagnose CD was high for TG2-IgA (100 %) and DGP-IgG (90 - 100 %), but lower for DGP-IgA (67 - 86 %). Specificity was high for all tests (97 - 100 %). The frequency of TG2-IgA titers > 10â€Š× upper limit of normal at diagnosis ranged from 47 - 90 %. Under a GFD DGP-IgA became negative more rapidly than DGP-IgG and TG2-IgA. Non-adherence to GFD was best indicated by positive TG2-IgA. CONCLUSIONS: Combined testing for TG2-IgA and DGP-IgG does not increase the detection rate of CD in IgA competent children compared to TG2-IgA only. There are significant differences with respect to proportions of celiac children with titers > 10â€Š× ULN between the manufacturers. This calls for harmonization of tests. TG2-IgA showed the highest titer rise with non-adherence to the GFD, independent of the manufacturer.

Improved performance of a rapid office-based stool test for detection of Helicobacter pylori in children before and after therapy.

A modified version of a rapid office based one-step monoclonal immunoassay for detection of Helicobacter pylori antigen in stool samples from children was evaluated against biopsy specimen-based methods and compared to a monoclonal enzyme immunoassay using the same antigen. Blinded stool samples from 185 children (0.3 to 18.2 years) were investigated at the time of upper endoscopy prior to anti-H. pylori therapy; 62 children were H. pylori infected and 123 noninfected according to predefined reference standards. Samples obtained 6 to 8 weeks after anti-H. pylori therapy were available from 58 children (3.8 to 17.7 years) and were compared to results of the [(13)C]urea breath test (14/58 were positive). The rapid stool tests were performed by two independent readers. Of 243 rapid tests performed, 1 (0.4%) was invalid for technical reasons. Equivocal results (very weak line) were reported 16 times by reader 1 and 27 times by reader 2. When equivocal results were considered positive, the two observers agreed on 76 positive and 160 negative results and disagreed on 7 samples (2.9%). The sensitivity was 90.8% for reader 1 and 85.5% for reader 2, and the specificity was 91.0% and 93.4%, respectively. The monoclonal enzyme immunoassay revealed a sensitivity and specificity of 94.7% and 97.6%, respectively. The modified chromatographic immunoassay is a good alternative in settings or situations when the monoclonal enzyme immunoassay or the [(13)C]urea breath test are not available or feasible. In order to improve sensitivity, very weak lines should be considered positive test results.

Evaluation of a novel rapid one-step monoclonal chromatographic immunoassay for detection of Helicobacter pylori in stool from children.

A new rapid office-based one-step monoclonal immunoassay (RAPID Hp StAR, DakoCytomation, Cambridge, UK) for detection of Helicobacter pylori antigen in stool was evaluated in children against invasive diagnostic methods and compared to the results of a monoclonal EIA targeting the same antigen (Amplified IDEIA Hp StAR, DakoCytomation, Cambridge, UK). Coded stool samples from 118 symptomatic children (0.3-18.8 years) were investigated prior to any anti-H. pylori therapy. Fifty-four children were H. pylori infected defined by positive culture and/or two other positive tests ((13)C-urea breath test, histology, rapid urea test), the remaining 64 children showed concordant negative results. Thirty-four infected children (4.8-17.8 years) were monitored with (13)C-urea breath test (five remained positive) and stool test 6-8 weeks after anti-H. pylori therapy. The immunoassays were independently read by two investigators. The monoclonal EIA showed excellent sensitivity and specificity before (98% and 100%, respectively) and after therapy (100%; 96.2%). The rapid immunoassay was invalid for technical reasons in nine samples (5.9%). The two observers agreed in 31 positive and 93 negative results, but had discordant results in 17 samples (11.2%). Overall, the rapid test showed a poor sensitivity (63.8%-71.1%), but a good specificity (91.1%-96.2%) before treatment. We conclude that the new office based monoclonal enzyme immunoassay for diagnosis of H. pylori should be modified to improve sensitivity, inter-observer-variability and some technical problems. In contrast, the monoclonal EIA stool test is highly reliable, both pre- and post therapy, and equivalent to the (13)C-urea breath test.