9%. They found a lower level in alcohol consumers with normal liver function tests (27%) [9]. The highest prevalence among the studies published this year was found in 516 asymptomatic individuals from Pakistan

(74.4%) [10]. Using a combination of diagnostic tests (histology, serology, UBT, and rapid urease test (RUT)), Matsuo T et al. showed among 3161 gastric cancer cases diagnosed from 1996 to 2010 in Japan, only 21 were truly H. pylori negative. This low prevalence of H. pylori-negative gastric cancer cases was also correlated with pathological characteristics different from common gastric cancer cases [11]. H. pylori serology alone usually does not show a strong association between the presence of H. pylori antibodies and gastric cancer. For this reason, some authors looked at CagA antibodies that are supposed to persist for longer periods of time after curing the infection by antibiotic treatment, or spontaneous Mdm2 antagonist clearance during the progression of atrophy. In a nested European case–control study from the Eurogast-EPIC project, Gonzalez et al. [12] showed by using immunoblot

detecting CagA antibodies that nearly, all noncardia-gastric cancer cases were indeed H. pylori positive, with an odds ratio three times higher than that obtained by ELISA. Detection of anti-CagA antibodies combined with H. pylori ELISA, urease test, and histology was also used to determine H. pylori infection in Russian and eastern Siberian populations carrying a different risk of selleck chemicals gastric cancer. Tsukanov et al. [13] showed that H. pylori infection is high in these populations, but ethnic groups with a similar prevalence of CagA antibodies had a different prevalence of intestinal metaplasia (IM) and incidence of gastric cancer, indicating other host-related and/or environmental factors. Several

surveys have been carried out in children. They are presented in Table 2. To obtain insight into the natural history of H. pylori infection, Queiroz et al. followed Thalidomide up a cohort of 133 Brazilian children from a low-income community using UBT. The prevalence of H. pylori infection was 53.4% at baseline and 64.7% 8 years later. Among them, 6.0% had lost the infection, while 17.3% became infected [14]. Risk factors for H. pylori infection were a high number of children in the household and male gender. 575 Arabs 584 Jews 45.6 25.2 There is now evidence that H. pylori infection is declining in both developed and developing countries. This was clearly shown using UBT in a retrospective study (2002–2009) performed on 1030 children from Buenos Aires. The authors found a prevalence of 41.2% for the period of 2002–2004, dropping to 26.0% in the triennium 2007–2009 [15]. H. pylori antigen detection using monoclonal SAT was also used in a prospective study conducted among 231 Israeli Arab children. The incidence of H. pylori infection was 33.3%, and the mean age of acquisition was 14 months.