Low molecular weight protein of Helicobacter pylori and its relation to gastroduodenal diseases

In Taiwan, CagA and VacA cannot be used as markers to evaluate the risk of developing serious gastroduodenal pathogenesis in the hosts. Recent research suggests that the low molecular weight proteins, 35kDa and 19kDa, in Helicobacter pylori may be related to duodenal ulcers and gastric MALToma (mucosa-associated lymphoid tissue lymphoma) respectively. The aims of this study were to examine the sero-prevalence of antibodies against specific Helicobacter pylori antigen in patients with different gastroduodenal diseases and further to find possible virulence factor(s) associated with the development of clinically relevant disease in Helicobacter pylori-infected subjects in Taiwan.

Sera were obtained from 108 patients, of which 22 had gastric adenocarcinoma, 31 had non-ulcer dyspepsia and 65 had peptic ulcer disease. The sera were analyzed for specific Helicobacter pylori antigen by using one commercial kit (HelicoBlot 2.0, Genelabs Diagnostic, Singapore, HB2.0). Helicobacter pylori infection was confirmed when the culture was positive or when any two of the other three tests (biopsy CLO test, histology and 13C-urea breath test) were positive.

The data showed a high prevalence of CagA and VacA proteins [CagA(+): gastric adenocarcinoma--88.1%, non-ulcer dyspepsia--87.1%, peptic ulcer disease--91%; VacA(+): gastric adenocarcinoma--78.6%, non-ulcer dyspepsia--58.1%, peptic ulcer disease--71.4%] in Taiwan. This is similar to the findings in other Chinese and Taiwanese studies. No significant difference was found among the three groups (P > 0.05) for any Helicobacter pylori protein. We found that antibody responses to the 26.5-kDa and 116-kDa (CagA) antigens were most prevalent in the peptic ulcer disease group. Consequently, we analyzed two special phenotypes, which have simultaneous presence in bands at 116 and 26.5kDa. The phenotype [116-kDa (+) and 26.5kDa(+)] predicted the risk of peptic ulcer disease with 76.7% sensitivity and 62% specificity.

We confirm the universal prevalence of CagA and VacA-positive Helicobacter pylori infection in Taiwan independent of disease. Although we did not find any single specific Helicobacter pylori protein which could act as an indicator of clinical outcome, we found a possible marker of peptic ulcer disease which may be acceptable. This is the phenotype with simultaneous presence in bands at 116kDa and 26.5kDa protein. Our report differs from some previous reports from other regions. This may reflect differences of race and geography.