Clinical Studies
Association between abnormal gastric function risk and Helicobacter pylori infection assessed by ELISA and 14C-urea breath test

https://doi.org/10.1016/j.diagmicrobio.2014.09.009Get rights and content

Highlights

  • Helicobacter pylori infection leads to the change in the morphology and function of gastric mucosa.

  • What kind of H. pylori detecting assay represents gastric function change is unclear.

  • Both urea breath test (UBT) and IgG assay may map out abnormal gastric function.

  • IgG assay was more closely correlated with abnormal gastric function than UBT.

  • H. pylori infection related abnormal gastric function should be considered in clinical settings.

Abstract

Objective

Epidemiological studies found a significant correlation between Helicobacter pylori infection and elevated serum pepsinogen, especially pepsinogen II (PGII), and reduced pepsinogen I (PGI)/PGII ratio. The study aimed to evaluate the association between abnormal gastric function risk and H. pylori infection assessed by H. pylori IgG assay and 14C-urea breath test (UBT).

Methods

A total of 1555 subjects who underwent a health check were enrolled. Serum PGI, serum PGII, PGI/PGII ratio, gastrin 17 (G17), H. pylori IgG antibody titer, and UBT results were collected.

Results

Median PGII and G17 levels were higher, but PGI/PGII ratio was lower in H. pylori–seropositive compared with seronegative participants (P < 0.001, respectively). Similar effects were demonstrated by UBT. The consistency between H. pylori IgG assay, and UBT results were 86.9%, 82.29%, and 84.64% in individuals with normal gastric function, but only 73.4%, 67.98%, and 74.6% in those with abnormal gastric function. The correlation coefficients for H. pylori infection and abnormal gastric function diagnosed by PGI/PGII <7 were 0.336 (P < 0.001) by H. pylori IgG assay and 0.231 (P < 0.001) by UBT, diagnosed by PGII ≥8.25 µg/L were 0.594(P < 0.001) by H. pylori IgG assay and 0.493 (P < 0.001) by UBT, diagnosed by G17 >3 pmol/L was 0.469 (P < 0.001) by H. pylori IgG assay and 0.394 (P < 0.001) by UBT. The odds ratios (ORs) (95% confidence intervals) of abnormal gastric function were 7.477 (5.278–10.594), 19.204 (14.526–25.387), and 7.921 (6.286–9.982) comparing positive versus negative by H. pylori IgG assay and 4.084 (2.98–5.598), 9.552 (7.494–12.174), and 5.402 (4.335–6.731) comparing positive versus negative by UBT.

Conclusions

H. pylori infection assessments by antibody-based or bacterial component–based detection are both related with abnormal gastric function. Moreover, serum H. pylori IgG assay was stronger associated with abnormal gastric function than UBT assay.

Introduction

Helicobacter pylori is one of the most common bacterial infections of humans. It is well known that H. pylori infection has been associated with the development of gastric diseases. The crucial role of H. pylori makes its detection necessary in various situations. So far, multiple methods have been introduced including invasive and noninvasive assays. Among the noninvasive assays, the methods most widely used are antibody-based detection and bacterial component–based detection (Koletzko et al., 2003, Leal et al., 2008, Shimizu et al., 2003). Common design of antibody-based detection test is the serum IgG assay, which has the advantages that many serum samples can be tested in parallel, the process can be completely automated and the test is less expensive. The sensitivity and specificity of serological H. pylori IgG assay are reported at 85% and 79%, respectively (Loy et al., 1996). Serological IgG is useful in diagnosis of H. pylori in patients taking proton pump inhibitors (PPIs) or other antireflux medications; those recently treated with antibiotics; and patients with upper gastrointestinal bleeding, gastric atrophy, or gastric malignancy. It is the only test that is not affected by localized changes in the stomach that affect H. pylori load. However, serologic testing is not suitable for the diagnosis of active H. pylori infection or as a follow-up test after H. pylori eradication therapy. Common design of bacterial component detection test is urease activity by urea breath test (UBT) (Kato et al., 2002). UBT exploits the ability of H. pylori to convert urea into carbon dioxide (Chey, 2000), which is simple, innocuous, easy to repeat, and easy to collect and can even be sent by mail to a central laboratory for analysis. The sensitivity and specificity of UBT commonly exceed 95% (Leodolter et al., 1999). Additionally, The UBT has been used to screen patients before endoscopy and to assess the success of therapies aimed at eradicating H. pylori (Gisbert and Pajares, 2004). However, UBT in patients on long-term PPI therapy may result in false-negative results because PPI use leads to a rise in gastric PH and a subsequent reduction in H. pylori load. Some previous study also compared serum IgG assay and UBT to each other for diagnosis with histology stain and/or a positive culture as gold standard. They found that the sensitivity, specificity, and accuracy rates for H. pylori diagnosis were higher by UBT than by H. pylori IgG assay (Cohen et al., 1999).

As we know, H. pylori can colonize in the gastric mucosa, leading to the changes in the morphology and function of gastric mucosa (Suerbaum and Michetti, 2002, Sun et al., 2007). Morphological changes usually can be observed by endoscopic biopsy, and functional changes often are judged by enzymes and hormones secreted by the gastric mucosa. Serum pepsinogen (sPG) and gastrin levels seem to be related to the functional changes in the stomach, and their use as “serological biopsy” has been reported for over 20 years (Samloff, 1982, Samloff and Taggart, 1987, Samloff et al., 1982). Recently in our group, we further defined the cut-off values to differentiate Chinese patients with healthy and diseased stomach mucosa by 8.25 μg/L for serum pepsinogen II (sPGII) or 3 pmol/L for serum gastrin 17 (sG17) (He et al., 2011, Liping Sun et al., 2014, Sun et al., 2007) or atrophic and nonatrophic stomach by 6.9 for the pepsinogen I (PGI)/pepsinogen II (PGII) ratio (Sun et al., 2007). Establishment of these cut-off values made it possible to compare healthy and diseased stomach with changes of gastric function.

Although epidemiological studies have shown significant correlations between H. pylori infection and elevated sPG, especially sPGII, gastrin 17 (G17), and reduced PGI/PGII ratio (Ohkusa et al., 2004). However, what kind of H. pylori detecting assay represents gastric function change is unclear, which has important value to guide antibiotic therapy. This study, therefore, compared antibodies detected by serum H. pylori IgG assay and bacterial component detected by UBT to assess the associations between H. pylori infection and risk of abnormal gastric function in a health check-up population.

Section snippets

Subjects

This retrospective study included 1555 asymptomatic subjects (930 men, 625 women, and median age 48 years [16–86]) who were selected into our present study as follows. First, a total of 6207 participants (3476 males and 2731 females) who underwent PGI, PGII, PGI/II ratio, G17 examination, and H. pylori IgG assay during a health check-up program from September 2011 to May 2012 were included. Among the 6207 that had undergone serologic testing, 1555 had also previously undergone 14C-UBT. We had no

General characteristics of the study population

Among the 1555 participants, 618 (39.74%) were H. pylori seropositive and 937 (60.26%) were H. pylori seronegative, while 650 (41.8%) were H. pylori positive and 905 (58.2%) were H. pylori negative by UBT. sPGI, sPGII, and sG17 levels were significantly skewed from the normal distribution in the whole study. The median values (ranges) of sPGI, sPGII, PGI/PGII, and sG17 were 94.8 (74–121.4) μg/L, 8.2 (5.5–13) μg/L, 11.43 (8.22–15.02), and 2.43 (0.85–6.11) pmol/L, respectively (Table 1).

Discussion

Among all the diagnostic methods of H. pylori, the detection target basically comprises 2 kinds: one is to detect the bacterial components itself, e.g., urease, to directly prove that whether the human body is infected with the bacterium; another is to detect human antibodies produced against bacterial infection, e.g., H. pylori IgG assay, to indicate whether there is a response against H. pylori infection in the human body. Unlike other invasive detection methods, such as biopsy-PCR method and

Statement

No companies provided any support in terms of kits or funds or advice regarding the manuscript.

Acknowledgments

This work was supported by grants from the National Basic Research Development Program of China (973 Program Award No. 2010CB529304) and Science Technology Project in Liaoning Province (Ref No. 2011225002).

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