Enhanced systemic matrix metalloproteinase response in Helicobacter pylori gastritis.

BACKGROUND: Helicobacter pylori causes chronic gastritis, peptic ulcer disease, and is the most important risk factor for non-cardia gastric cancer, and has been shown to upregulate matrix metalloproteinases (MMPs) in infected gastric mucosa. MMPs are proteolytic enzymes regulated by tissue inhibitors of metalloproteinases (TIMPs). AIMS: We set up this study to find out whether H. pylori gastritis induces systemic MMP response. METHODS: Serum samples were collected from patients undergoing gastroscopy; 26 patients had H. pylori gastritis and 18 were H. pylori-negative controls with normal gastric mucosa. Serum MMP levels were analysed by enzyme-linked immunosorbent assay. RESULTS: Significantly elevated serum levels of collagenase-2 (MMP-8), gelatinase B (MMP-9), neutrophil elastase (NE), and myeloperoxidase (MPO), and reduced serum levels of gelatinase A (MMP-2) and TIMP-1 were demonstrated in patients with H. pylori gastritis as compared to H. pylori-negative controls. No significant differences were shown in serum matrilysin-1 (MMP-7) levels. CONCLUSIONS: For the first time, we show enhanced MMP-8 response in H. pylori infection together with other neutrophil degranulation products (MMP-9, MPO, NE). Elevated circulating neutrophil degranulation product levels in serum of H. pylori-positive patients reflect accelerated proteolysis and oxidative stress, and may contribute to extraintestinal sequelae, such as cardiovascular diseases.

Faecal antigen tests in the confirmation of the effect of Helicobacter eradication therapy.

BACKGROUND: The frequent occurrence of Helicobacter pylori infection requires significant health care resources after eradication therapy. Therefore the non-invasive testing methods are required to alleviate the increased work-load of health care personnel and to allow an easy control of eradication therapy. Conventionally, the effect of eradication therapy has been confirmed with 13C-urea breath test 4-6 weeks after a completed eradication. AIM: To assess the applicability of Helicobacter pylori stool antigen tests as alternatives to the breath test in the control of the effect of eradication therapy. METHODS: Fifty patients were diagnosed Helicobacter-positive by endoscopy and histology as well as by rapid urease test from mucosal specimen. Four weeks after an eradication therapy the patients were subjected to 13C-urea breath test as well as to faecal Helicobacter pylori antigen tests with mono- and polyclonal primary antibodies. RESULTS: The monoclonal and polyclonal stool tests had 94% and 88% sensitivity, and 100% and 97% specificity, respectively, in the detection of Helicobacter pylori infection as compared to the 13C-urea breath test. The non-invasive test results were completely parallel in patients with various grades of mucosal atrophy or intestinal metaplasia. CONCLUSIONS: Monoclonal faecal Helicobacter pylori antigen test is slightly superior to the polyclonal test regarding the sensitivity in the detection of stool Helicobacter antigens. Due to their sufficient sensitivity and specificity, and to their practicability and cost-effectiveness, they can be recommended for non-invasive testing of Helicobacter pylori infection as alternatives to the 13C-urea breath test.

Oesophageal histology in gastro-oesophageal reflux disease is of minor pre- and postoperative diagnostic value.

BACKGROUND AND AIM: The clinical value of oesophageal histology in non-complicated gastro-oesophageal reflux disease (GORD) is controversial. Our aim was to explore the role of histology in preoperative diagnosis and postoperative follow-up in GORD. METHODS: From 40 patients 2 histopathologists graded and scored 191 oesophageal biopsies in a blinded manner to evaluate inter- and intraobserver variation pre- and postoperatively. Correlation between preoperative histology and objective clinical findings (endoscopy, esophageal 24-hour pH monitoring, and manometry) was calculated as well. RESULTS: Pathologist I interpreted 16 (50%) preoperative biopsies as normal, 5 (16%) with mild, 4 (12.5%) moderate, and 7 (21.9%) severe reflux changes. Pathologist II interpreted 11 (35.5%) preoperative biopsies as normal, 11 (35.5%) with mild, 6 (19.4%) moderate, and 3 (9.7%) severe reflux changes. In preoperative biopsies, interobserver variation was 33.8% and intraobserver variation 9.7%. A positive correlation was detectable between preoperative endoscopic and morphologic findings; no correlation existed between either acid reflux or LES pressure and oesophageal morphology. Normal pH monitoring and fundic wrap were noted postoperatively in all cases. In postoperative histology no significant differences according to pathologist I existed when compared with preoperative changes: 22 normal (69%), 7 mild (22%), 1 moderate (3.1%), and 2 severe (6.3%). Compared to preoperative analysis, pathologist II interpreted 24 (77%, p = 0.001) of the postoperative findings as normal, 1 (3%, p = 0.003) as mild, 4 (12.9%, n.s.) as moderate, and 2 (6.5% n.s.) as severe reflux changes. In postoperative biopsies interobserver variation was 21.1% and intraobserver variation 5.6%. CONCLUSION: The role of oesophageal histology in preoperative diagnosis and postoperative follow-up of GORD may be considered limited.