Noninvasive evaluation of Helicobacter pylori therapy: role of fasting or postprandial gastrin, Pepsinogen I, Pepsinogen II, or serum IgG antibodies

1999 ◽  
Vol 94 (9) ◽  
pp. 2367-2372 ◽  
Author(s):  
M. Tarek Al-Assi ◽  
Kazumasa Miki ◽  
John H. Walsh ◽  
David P. Graham ◽  
Masahiro Asaka ◽  
...  
2019 ◽  
Vol 9 (3-4) ◽  
pp. 523-530
Author(s):  
L. B. Drygina ◽  
V. N. Ellenidi ◽  
N. A. Bardysheva ◽  
M. M. Bogoslovskiy

Effective eradication of Helicobacter pylori infection is an important means to reduce the risk of precancerous changes in the gastric mucosa and prevention of gastric cancer. A search for non-invasive diagnostic tools for Helicobacter pylori infection, evaluation of the effectiveness of eradication remains of high importance.The aim of the study was to assess an informative value of detecting pepsinogen I and II as well as serum antibodies to Helicobacter pylori while assessing an efficacy of treated chronic Helicobacter gastritis and identifying preneoplastic changes in the stomach mucosa. There enrolled 113 male patients with chronic gastritis aged 41 to 76, average age- (56.7±0.7) years. Examination of patients was carried out at admission to the clinic, as well as at 2 and 12 months after administering a standard eradication therapy. It was found that Helicobacter pylori infection was detected in 101 (89.4%) patients. Groups of patients with effective eradication therapy were noted. A time-dependent level of antibodies to Helicobacter pylori, as well as measured concentration of pepsinogen I and II after the onset of eradication treatment were determined. Which were analyzed in connection with the results of histology examination of gastric mucosa biopsy specimens and expression of oncoproteins Ki-67, Bcl-2, c-erbB-2, p16 in the gastric mucosa depending on efficacy of eradication therapy. It is shown that effective eradication therapy was characterized by significantly decreased serum level of IgG antibodies to Helicobacter pylori 2 months after the onset of treatment. Moreover, a significantly decreased pepsinogen II and serum IgG antibodies to Helicobacter pylori during eradication therapy were accompanied by a significant decrease in Ki-67 expression in the gastric epithelium. Decreased concentration of pepsinogen II within the first year after Helicobacter pylori eradication therapy was due to a greater decrease in activity of inflammatory changes in the gastric mucosa than to dynamic changes in gastric atrophy and metaplasia. An inverse relation between the serum level of pepsinogen I and atrophy as well as intestinal metaplasia within the gastric mucosa were found.


2004 ◽  
Vol 39 (5) ◽  
pp. 568-569 ◽  
Author(s):  
Nicolas Kalach ◽  
J. Legoedec ◽  
Abdul-Rahim Wann ◽  
Michel Bergeret ◽  
Christophe Dupont ◽  
...  

2001 ◽  
Vol 100 (3) ◽  
pp. 291-298 ◽  
Author(s):  
Byung Oh KIM ◽  
Sung Seup SHIN ◽  
Young Hyo YOO ◽  
Suhkneung PYO

Helicobacter pylori is a major cause of gastric-associated diseases. To evaluate the efficacy of a possible vaccine antigen against H. pylori infection, the chimaeric construct adhesin–CTXA2B, derived from H. pylori adhesin genetically coupled to cholera toxin (CTX) subunits A2 and B (CTXA2B), was expressed in Escherichia coli as an insoluble recombinant chimaeric protein. The protein was then purified by denaturation, renaturation and size-exclusion chromatography. The composition of purified adhesin–CTXA2B was verified by SDS/PAGE and Western blotting with antibodies to antigenic components of adhesin and CTXB, and confirmed as a chimaeric protein with GM1-ganglioside binding activity and adhesin epitopes by a GM1-ELISA developed using antibodies to adhesin. Oral immunization of mice with adhesin–CTXA2B induced higher levels of mucosal IgA and serum IgG antibodies to H. pylori adhesin and to CTXB than in mice immunized with adhesin or CTXA2B alone. Adhesin–CTXA2B was also demonstrated to be a potential protective antigen in a mouse model of H. pylori infection. The immunization of mice with adhesin–CTXA2B protected 62.5% of mice infected with H. pylori SS1 strain, whereas adhesin immunization was not able to confer protection to mice. This protection may be correlated with high levels of mucosal IgA and serum IgG antibodies against H. pylori adhesin. Taken together, the results indicate that the genetically linked CTXA2B acts as a useful mucosal adjuvant, and that the adhesin–CTXA2B chimaeric protein could be a potential component in future H. pylori vaccine development.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Khitam Muhsen ◽  
Samba O. Sow ◽  
Milagritos D. Tapia ◽  
Fadima C. Haidara ◽  
Mardi Reymann ◽  
...  

Abstract Accumulating evidence indicates that persistent Helicobacter pylori gastric infection influences immune responses to oral enteric vaccines. We studied the association between pre-existing H. pylori serum IgG and serum pepsinogens levels (PGs) as markers of gastric inflammation and the immune response to single-dose live oral cholera vaccine CVD 103-HgR in Malian adults. Baseline sera obtained during a phase 2 safety/immunogenicity clinical trial of cholera vaccine CVD 103-HgR among 93 healthy Malian adults were tested for H. pylori IgG antibodies and PGI and PGII levels using enzyme linked immunosorbent assays. Overall 74/93 (80%) vaccine recipients were H. pylori IgG seropositive at baseline. Vibriocidal antibody seroconversion (≥ fourfold increase 14 days following administration of CVD 103-HgR compared to baseline) among vaccine recipients was 56%. However, vibriocidal antibody seroconversion was markedly higher among H. pylori seropositives than seronegatives 64% vs. 26% (p = 0.004); adjusted relative risk: 2.20 (95% confidence intervals 1.00–4.80; p = 0.049). Among H. pylori seropositive vaccine recipients, there were no significant associations between PGI, PGII and PGI:PGII levels and vibriocidal seroconversion. The enhanced seroconversion to oral cholera vaccine CVD 103-HgR among H. pylori seropositive African adults provides further evidence of the immunomodulating impact of H. pylori on oral vaccine immunogenicity.


2005 ◽  
Vol 337 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Germán A. Messina ◽  
Angel A.J. Torriero ◽  
Irma E. De Vito ◽  
Roberto A. Olsina ◽  
Julio Raba

2004 ◽  
Vol 39 (5) ◽  
pp. 569-570
Author(s):  
Cristina Gonz??lez-Roiz ◽  
Maria Jos?? L??pez-Rodriguez ◽  
Luis F-Pereira ◽  
Juan-Diego Pedrera Zamorano

2012 ◽  
Vol 168 ◽  
pp. 297-302 ◽  
Author(s):  
Marco A. Seia ◽  
Sirley V. Pereira ◽  
Carlos A. Fontán ◽  
Irma E. De Vito ◽  
Germán A. Messina ◽  
...  

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