H. pylori infection.

It has to be emphasized that H. pylori infection was diagnosed by histology and urease test in all patients. The results were concordant with those obtained by the evaluation of H. pylori specific ureA gene in the paraffin imbedded gastric tissue from a subgroup of patients (data not shown) and both HIV-positive and -negative patients belong to the same low-income population. As above mentioned, the prevalence of H. pylori infection in a similar population from Fortaleza in respect to the socio-economical level is high [17]. It is well known that H. pylori infection is mainly acquired during childhood and that once acquired it is life-long lasting [1]. There- fore, we may hypothesize that the HIV-infected patients we studied had been exposed to the bacterium early in life and most of them became infected, but loose the infection after acquired HIV infection. Alternatively, the H. pylori gastric load might be decreased in the HIV-positive patients leading to H. pylori infection mis- diagnosis. Explanations include decreased gastric acid secretion predisposing to gastric colonization by other microorganisms that might compete with H. pylori, the use of either antibiotics or PPI and, as suggested in other studies, the low count of T CD4 cells in AIDS patients [6,21,23,24].

Furthermore, the incidence of H. pylori is very different from one region to another [26]. In our area this incidence is very high, as we have shown previously [13]. Such a high incidence could mask a potential, weak, effect of H. pylori on the risk of Barrett's esophagus, but, on the other hand, it could be also expected that a real effect of H. pylori infection or virulent H. pylori strains on the devel- opment of Barrett's esophagus could be more easily shown in areas with high incidence of the infection in the general population. On the contrary, we found that H. pylori infection was more frequent in patients with Bar- rett's esophagus than in our control population, and that infection with the more virulent strains of H. pylori infec- tion was not associated with a decreased risk for the devel- opment of Barrett's esophagus. In fact, the prevalence of CagA+ strains was similar in H. pylori positive patients and controls, although a trend toward a greater prevalence of virulent strains was seen in patients with Barrett's esophagus. In general, the prevalence of CagA+ strains obtained in different studies are lower than that found in our study, however a great variability is observed, with prevalences ranging from 13.3% to 82% [12,26,30]. In some way, it is surprising that H. pylori infection was greater in patients than in controls, indicating that there was a trend towards an increased frequency of non viru- lent strains (CagA negative) in controls that in cases. In any case, all these data indicate that CagA+ H. pylori strains do not seem to play an important role in this con- dition among our population and that other factors may be more important for the development of Barrett's esophagus. These additional factors could be intrinsic to the host (i.e. genetic factors) and extrinsic. In fact, it has been suggested that there may be a genetic predisposition to the development of reflux in families of patients with Barrett's esophagus, although a specific genetic defect has not been found [31,3].

The percentage of blood group O in the infected patients was higher than other blood groups and higher percentage of blood group A in the uninfected patients is high significant (P< 0.01) as shown in table (5) & figure (2). These finding was similar to that previously reported by Mattos et al.(2002); who demonstrated a higher prevalence of blood group A among the uninfected and blood group O in infected PUD patients in Brazil population. [28] A recent study of Ryberg et al. (2013), who found positive associations between the presence of blood group O and H. pylori infection in PUD in Swedish population. [29] Furthermore, these results may be reinforced by data obtained from other researchers showing a greater susceptibility of blood group O patients to H. pylori infection. [30-32,2] Pervious study by Lin et al. (1998), demonstrated a high frequency of infection with this bacteria in 90.3% of blood group O patients suffering from gastroduodenal diseases. [33]

There are also non-conventional methods to de- tect H. pylori. For example, H. pylori stool antigen (HpSA) immunochromatography has been used to detect the microorganism in fecal samples (19). An enzyme-linked immunosorbent assay (ELISA) has also been developed for the detection of H. pylori in saliva (20) and serum (21) samples. Unlike endosco- py and the urea-breath test, which are observer-based assessments, these techniques rely on laboratory tools to detect the microorganism. However, compar- ative data between these non-conventional methods and endoscopic biopsy are lacking. Therefore, the aim of the present study was to compare the sensitiv- ity and specificity of HpSA, salivary immunoglobu- lin (Ig) G, serum IgG, and IgM, to those of endoscop- ic-biopsy as the gold standard for the diagnosis of H. pylori infection.

individuals using nested RT-PCR. Thirteen of the non-infected individuals were without inflammation. The results suggest that inflammation alone does not change CD44 expression. There was a significant correlation between the expression of CD44 variant exons V8, V9 and V10 and H. pylori infection. Further investigations will be necessary to address the possibility that infection and inflammation have synergistic roles in the increased expression of V8, V9 and V10. These exons code for parts of the extracellular portion of the protein and changes in their expression may affect oncogenic processes because of changed affinities for the extracellular matrix.

Objective: The purpose of this study was to deter- mine the risk factors associated with having H. pylori infection as proven by endoscopic biopsy at Maricopa Medical Center (MMC), a safety-net hospital in phoe- nix, Arizona which serves primarily patients with limited financial and insurance resources. Methods: A total of 1116 biopsies were identified in a Depart- ment of Pathology database searched from Novem- ber 2004 to March 2013. To be included, the subjects had to have an endoscopy with gastric biopsy. After the inclusion criteria were applied, 282 control sub- jects without histological evidence of H. pylori infec- tion and 256 cases with histological evidence of H. pylori infection were identified. Patient charts were reviewed to extract information on variables collected for this study. Results: The mean age of cases and controls was 50.5 and 52.3 years respectively. The BMI of the cases and controls was 28.1 and 28.0 res- pectively. The mean number of upper endoscopic exams performed was 1.3 in cases and 1.4 in controls respectively. Potential predictors examined were gen- der, history of drug abuse, history of alcohol abuse, chronic pain medication use, smoking, employment status, outpatient vs. inpatient upper endoscopy exam, language spoken (English, Spanish, or bilingual), race/ ethnicity, type of insurance, heart burn, dysphagia, abdominal pain, gastroduodenal ulcers, intestinal me- taplasia, and having vs. not having a primary care physician. Based on univariate analyses, having a gastroduodenal ulcer, having a history of abdominal pain, Hispanic race, government insurance status, self-pay insurance status, and speaking Spanish only were found to be significantly related to having H. pylori infection. These variables were next entered into a multivariate analysis. The multivariate analysis

The dynamic of infection in 1987 seems to be similar with that seen in the developing countries. Ten years later, in 1997, the picture changed toward what was found in the developed countries. Thus, the crude seroprevalence was reduced about 10% units; multiple regression analysis showed that a person of the O-87 group had a significant higher risk of seropositivity than a comparable person of the O-97 group (OR:1.73, 95% CI: 1.14–2.65, p = 0.010). As we did not found paired serum samples of the same pa- tient in groups O-87 and O-97 we could not know the rate of serocorversion in our population. But, in both develop- ing and developed countries, there are many studies sug- gesting that, during adulthood, the rate of seroconversion and seroreversion is almost the same[9,14,15]. Thus, though our data showed that increasing age does increase the risk of H pylori infection, the fact that patients from group O-87 had higher rates of infection than comparable patients from group O-97, supports the "birth cohort phe- nomenon" as the main cause for the increasing occurrence of the infection seen with age.

In developing countries, H.pylori is an infection acquired early in childhood causing chronic diarrhea and malnutrition. (Tafiar et al., 2006) All malnourished patients admitted to NRC were assessed for H. pylori infection by H. pylori stool Ag (HpSA). HpSA is non invasive test with high sensitivity and specificity for detection of H.pylori infection as proved by many studies as in study in Tehran (100%, 83.4%) (Falsafi et al., 2005) and in Istanbul (98%, 100%) (Gulcan et al., 2005) respectively. Higher frequency of malnourished females admitted to NRC (58.2%) because probably female numbers more than males in the society. This result is similar to study carried out by Firas et alt in Basra, (Fadhil and Issa 2011) in contrast to a study done by Sunguya et al. (2006) in Tanzania which shows admitted malnourished males more than females. (Sunguya et al., 2006) Regarding age of malnourished patients: more than 60% of patients were younger than 12months. This result was similar to a study carried in Babylon by Muder et al. (Noor et al., 2009) this may be caused by absence of breast feeding, early weaning and in proper food preparation. Moderately malnourished children admitted to nutritional rehabilitation ward were more than severe malnourished patients because number of moderate malnourished children in the society is more than severe malnutrition. This result is similar to study done in Basra by Firas et al. (2011)

Genetic instability plays a key role in neoplastic trans- formation and progression [17, 18]. A previous study by our group showed that in gastric carcinomas, such gen- etic instability may be classified into two different forms, in which hypermutability occurs by means of either chromosomal instability or microsatellite instability (MSI) [19, 20]. Although a wide spectrum of MSI alter- ations in the nuclear DNA (nMSI) of cancer cells has been established, little attention has been paid to MSI in the mitochondrial DNA (mtMSI) of H. pylori-infected gastric tissues. The mitochondrial genome is more vul- nerable to oxidative damage and experiences a higher rate of mutation than the nuclear genome [21]. The biol- ogy of the mitochondrion suggests that its genome may be an attractive target for ROS, which could drive tumorigenesis. Tumor formation is often associated with mtDNA mutations and alterations in mitochondrial gen- ome function. Our previous studies have identified se- quential accumulation of mtMSI in the histological progression from chronic gastritis to gastric cancer, sug- gesting that mtMSI may play an early and important role in the gastric carcinogenesis pathway, especially in intestinal-type cancer and distal gastric cancer [22]. However, the role of mtMSI following oxidative DNA damage in H. pylori-related gastric carcinoma is less clear. In the present study, we explored the associations between H. pylori infection, mtMSI and IL-8 to elucidate whether mtMSI triggers the progression from H. pylori- gastritis to intestinal metaplasia and dysplasia and, finally, to gastric cancer.

helminth infections [28]. The authors attributed differ- ences in Th1 or Th2-dominant responses across the low vs. mountainous regions to differences the prevalence of helminth infections and suggested that parasitic infection may modify H. Pylori-induced gastric cancer risk in Columbia. Thus, those studies and ours lend support to the hypothesis that Th1/2 immunity modulated by para- site infections may influence the risk of H. pylori-associ- ated gastric cancer in diverse environments [15,28,35,36]. Our study has some limitations. H. pylori infection was measured using serological assays, and some subjects may have been misclassified. The finding of almost universal seropositivity among adults is surprising because we would have expected a small proportion of individuals to be seronegative due to loss of bacterial colonization that occurs with age in chronically infected persons or with development of chronic gastric atrophy. We lacked endos- copy data on the state of gastric mucosa (presence of ulcer, gastric atrophy or not) and therefore are unable to draw conclusions about the relationship between Th2 domi- nance and severity of gastric mucosal inflammation. Direct measurement of pepsinogen levels could have also provided some information on the presence or not of gas- tric atrophy, but the volume of residual samples from the study population were inadequate for additional testing. Furthermore, our study was cross-sectional so we cannot infer temporality of associations demonstrated. We note that our "highland" area villages were in low hills, not mountainous areas, thus our study does not provide data for Th1 vs. Th2 responses in low vs. mountainous regions in Africa. The use of IgG subclasses assays as markers for type1/2-dominant immune response in a general popula- tion in Africa is novel, and our study provides valuable baseline data for sub-Saharan Africa. Finally, IgE measure- ments would strengthen our results on the role of para- sites, but we lacked a validated assay to perform IgE studies.

In general practice at Netherlands, 5% of childhood consultations were for abdomen pain [12] , while 2% to 4% consultation occurred in studies performed in Austria and the United States. [13] Label of Functional abdominal pain is given to undiagnosed medical cases. Poor physical and mental activity, as well as disturbed social life and school failure due to repeated return of abdomen pain found in 10% to 15% of school subjects, resulted in frequent health care visits [3,4] This problem is underestimated as one out of three children suffer from tummy pain for at least 5 years5. Irritable Bowel Syndrome in adults is considered to be continuation of functional gastrointestinal disorders in childhood. [6,14] Few factors have been identified to predict weather childhood functional abdominal pain, interferes with wellbeing of victims, as it persists for years. Recently, functional gastrointestinal disorders in young adulthood have been associated with higher level of no gastrointestinal symptoms. [4,14] Children with Functional abdominal pain having somatic symptoms in addition to abdominal pain can be used as clinical marker for prediction of poor outcome. Subjects with long term persistence of abdominal pain can be correlated to parents, if they also have gastrointestinal symptoms. In the light of these facts family physician can identify those subjects who are at risk for long term abdomen pain. They can plan more appropriate management strategies before any sequel, such as strict fallow up or consulting other health care colleagues if required. H. Pylori is the most common pathogen in children worldwide [16] , it is gram negative bacterium present in more than 50% of the world population, most of the infected children remain asymptomatic, although chronic gastritis and peptic ulcer occurred due to prolong exposure to H. Pylori infection. H. Pylori prevalence varies with age, region and race. Increase in age in associated with increase prevalence of H. Pylori infection. Socioeconomic status modifies its prevalence as its frequency is variable in developed and developing countries.

The objective of the present study was to evaluate in vivo anti H. pylori activity ethanolic extract of Psoralea corylifolia (called as PCE)in laboratory rats. Naproxen was administered orally to produce ulcers and then rats were orally inoculated with H. pylori. The animals were divided into following five treatment groups: Clarithromycin 30 mg/kg, PCE at 100, 200 and 400 mg/kg/day, p.o and vehicle (0.25 % Sodium CMC) for 10 weeks. On 4 th , 7th and 10 th week infection status was determined by polymerase chain reaction, rapid urease test and histopathology. The extent of neutrophil infiltration was estimated by myeloperoxidase assay. Clarithromycin treated animals demonstrated absence of infection at 4 th , 7 th and 10 th week whereas the control group of animals showed the presence of infection throughout the treatment regimen. Ethanolic extract of Psoralea eradicated the H. pylori infection in a dose and time dependent manner. The level of myeloperoxidase was elevated in the control group whereas significantly reduced in the clarithromycin and PCE treated groups when compared with the vehicle treated group of animals but decreased in the clarithromycin and PCE treated groups. It is concluded that PCE showed anti H. pylori activity in vivo.

In other hands, it is used to fail standard triple and sequential therapy, and levofloxacin therapy is shown that eradication rate is more than 95% for esomeprazole plus amoxicillin followed by esomeprazole plus levofloxacin plus metronidazole for 5 days (Ramesh et al., 2017). It has been postulated that eradication rate 93-96% for esomeprazole, amoxicillin and levofloxacin administration of 7 days (Schrauwen et al., 2009). It is revealed that the cure rate is 90-92% for esomeprazole plus amoxicillin plus a levofloxacin administration for 10 days and their eradication rate is87%, 91% and 96% study in Germany, Italian, and Netherlands (Skender et al., 2013). Choice of amoxicillin instead of metronidazole because the resistance rate of amoxicillin is minor than metronidazole; but the resistance rate is growing (9-13%) in Korea (Moon et al.,2013). Levofloxacin, esomeprazole and either amoxicillin or clarithromycin are highly effective and protective against H. pylori infection, but the combination with amoxicillin is better tolerated than the combination with clarithromycin. Levofloxacin therapy is fantastic bioavailability, higher eradication rate (more than 90%) and low side effects (Schrauwen et al., 2009).Another same drug group is established that sitafloxacin based therapy is used to eradicate H. pylori infection in Japan instead of triple therapy and eradication rate is 70-80% for a PPI, amoxicillin, sitafloxacin (Hirata et al., 2016).

patients responding to anti-H. pylori therapy, the dur- ability of platelet response is more than 7 years, indicat- ing the disease is cured [36]. Another meta-analysis by Arnold et al. performed a meta-analysis to determine the effect of H. pylori eradication therapy in patients with ITP by comparing the platelet response in ITP patients with and without H. pylori infection [37]. The odds of achieving a platelet count response following eradication therapy were 14.5 higher (95% CI: 4.2 to 83.0) in patients with H. pylori infection than in those without infection (response rate: 51.2% vs. 8.8%). These findings strengthen the causal association between H. pylori infection and ITP. Several mechanisms regarding H. pylori-associated ITP have been proposed [38]. One intriguing hypothesis concerning molecular mimicry is that cross-reactive antibodies are produced that react both H. pylori components and platelet surface antigens. Takahashi et al. showed that platelet elutes from H. pylori-infected ITP patients recognized CagA protein in immunoblots, but those from H. pylori-infected non-ITP patients did not [39]. Bai et al. also reported that mono- clonal antibodies generated against H. pylori urease B react with GP IIb/IIIa expressed on the platelet surface [40]. While these findings suggest molecular mimicry be- tween H. pylori components and platelet surface antigens, the exact pathogenic roles of these cross-reactive anti- bodies remain obscure. In another potential mechanism, H. pylori infection may alter Fcγ receptor balance of mon- cytes/macrophages and induce autoantibody formation. A recent study showed that the FcγR II B expression on cir- culating monocytes was down-regulated in H. pylori-in- fected ITP patients [41]. Therefore, H. pylori may alter Fcγ receptor balance of moncytes/macrophages through downregulation of the inhibitory receptor FcγR II B.

This cross-sectional study was performed at the Medica Sur Clinic & Foundation, Mexico City, from January 2011 to January 2012. Endoscopic images were collected from studies of patients with upper gastrointestinal symptoms who were .18 years. Endoscopic results were required to include images of the gastric antrum and a histopathological report of the presence or absence of H. pylori. Studies that included endoscopic images with a low definition of the gastric antrum and histopathological reports without a description of the pres- ence or absence of H. pylori were excluded from this study. Endoscopic studies were performed using a Q180 apparatus from Olympus Medical Systems (Center Valley, PA, USA). Biopsy sampling was performed using standard forceps according to the updated Sydney System classifica- tion and grading of gastritis. Biopsies were evaluated for H. pylori infection in the pathology department of the same insti- tution; pathologists were blinded to the endoscopy results.

Objective: The present study was aimed at developing Gastroretentive Bilayer drug delivery systems containing Amoxicillin Trihydrate and Ranitidine Hydrochloride for the treatment of H. pylori induced peptic ulcer to minimize the side effect, improve the prolongation of action, to reduce the frequency of drug administration. Materials and Method: The tablet is characterized by immediate release layer of Ranitidine Hydrochloride and Gastroretentive layer of Amoxicillin Trihydrate. The formulation containing Gastroretentive layer was designed using HPMC K15M and HPMC K4M as floating agents, sodium bicarbonate and citric acid as gas-generating agent. Crospovidone was used as superdisintegrant for the preparation of immediate release layer. The prepared Gastroretentive layer was evaluated for their precompression parameters, physical characteristics like hardness, friability, uniformity of weight, uniformity of drug content, swelling index, In-vitro floating studies and In-vitro drug release. For the estimation of Ranitidine Hydrochloride and Amoxicillin Trihydrate in a formulation, simultaneous estimation method was employed. Results: The release of the Ranitidine Hydrochloride from the immediate release layer was found to be 94.6% ± 0.02% in 30 minutes. The release of Amoxicillin Trihydrate for the sustained release floating layer was found to be 90.5 ± 0.06% in 12 hours. The data obtained from In-vitro release were fitted into the various kinetic models (Zero Order, Higuchi, First Order and Korsmeyer–Peppas Model). Conclusion: The best fitted model for Amoxicillin Trihydrate and Ranitidine Hydrochloride was found to be zero order release model and first order release model, respectively.

This case was a classical one of typical DH with Coeliac disease, in a female patient, 30 years old, What was of significance in this case was the association of H. Pylori in high IgA titer (3.8) which suggested to be considered as a possible antigen as DH is of known antibody, but of unknown antigen, as well as H. Pylori has a definite relation with autoimmune diseases; thyroiditis, Diabetes Mellitus, Sjögren's Rheumatoid Arthritis, and neoplastic conditions include GI lymphomas (MALT) and non-Hodgkin lymphoma, as well as all above mentioned are known to be also associated with DH (Gaspari et al., 1990). Detection of Helicobacter pylori antibodies with dyspeptic manifestations in this case could be related to possible underlying cause as has been observed. The case was received triple therapy with some response in the form of, Doxycyclin 100 mg bid for 8 days, Cefixime 400 mg for 5 days and Rabeprazole as proton pump inhibitor (PPI) 20 mg for 28 days, then H. Pylori – stool antigen (Ag) test was done to show that antigen is not detected.

The rationale of the present investigation is to develop a new oral drug delivery system utilizing both the concepts of controlled release and mucoadhesiveness, which could remain in stomach and control the drug release for longer period of time and thus to improve the bioavailability of the drug and reducing its dose related side effects. Gelatin/Acrypol 934P mucoadhesive microspheres of Levofloxacin were prepared by Emulsification cross- linking method. Drug and excipients interactions are tested using Fourier Transform-Infrared Spectroscopy indicated no interactions. The average particle size for optimized formulations of Gelatin/Acrypol 934P microspheres were found to be 41.5µm. Photomicrographs revealed that the microspheres were spherical in shape. The drug entrapment efficiency for Gelatin/ Acrypol 934P microspheres was found to be 85.43%. In vitro drug release from Gelatin/ Acrypol microspheres showed more than 75% of the drug was released within 8 Hr, while pure drug showed complete drug release within 3 hours. This suggested controlled delivery of Levofloxacin for a longer period. Regression analysis revealed that the drug release from the microspheres was followed zero order kinetics. SEM images suggested spherical shape with smooth surface of microspheres formulations. Optimized formulation of Gelatin/ Acrypol 934P microspheres showed excellent mucoadhesivity i.e., 86.5%. Thus, the proposed Gelatin/ Acrypol 934P mucoadhesive microspheres might make a contribution in complete eradication of Helicobacter pylori owing to prolonged stomach residence time and small particle size.

0.98; 95% confidence interval: 0.58 –1.66; P ⫽ .954). Twenty-one (61.7%) of 34 positive patients and 24 (55.8%; P not significant) of 43 positive controls re- sulted infected with the more virulent Cag-A-posi- tive strains. H pylori-positive children were older (16 ⫾ 5.6 years) than negative participants (14.3 ⫾ 5.5; P ⫽ .06). No difference in prevalence of infection was found between males and females both in pa- tients and in controls. The prevalence of H pylori infection proved to be related to socioeconomic sta- tus (annual family income and overcrowding) as already described (Table 2 and Table 3). Twenty-six of (83%) 35 H pylori-positive patients and 61 (72%; P not significant) of 86 negative participants had asso- ciated dyspeptic symptoms. No difference in the prevalence of the gastrointestinal symptoms studied was observed between positive and negative patients (Table 4), with the exclusion of halitosis. In fact, among the investigated gastrointestinal symptoms, a higher incidence of halitosis was observed in patients with DM1 than in negative participants (P ⫽ .033). However after correction for age by means of logistic regression analysis prevalence of halitosis differ be- tween group even if it was not significant (P ⫽ .08). Moreover, DM1 patients with halitosis did not show a different glycemic control when compared with patients without it. Interestingly, patients with hali- tosis and H pylori infection showed higher serum levels of HbA1c (8.6 ⫾ 1.5 vs 7.9 ⫾ 1; P ⬍ .05) and a longer history of disease (96.6 ⫾ 54.2 vs 64.2 ⫾ 49.1 month; P ⬍ .05) when compared with H pylori-neg- ative patients with halitosis. An increased prevalence of severe symptoms, even if not statistically signifi- cant, was found for dyspepsia (P ⫽ .132), bloating (P ⫽ .154), nausea (P ⫽ .060), and vomiting (P ⫽ .158). No significant correlation was found between

H. pylori infection can lead to a variety of diseases. Presently, the only reliable way to identify the illness associated with a H. pylori infection remains an endoscopic examination coupled with histologic examination of the gastric mucosa. Attempts have been made before to correlate the severity of the H. pylori-associated diseases to the antibody level, the specificity of the serum antibodies, or the isotypes of these antibodies (4, 6, 10, 17, 21, 22). The polymorphism of the antibody response to H. pylori has been suspected to reflect either an evolution of the immune response or an antigenic shift of the infecting strain (2, 30). Nevertheless, it has also been suspected to be correlated to a predisposition for severe diseases. The pres- ence of anti-CagA has been associated with the presence of ulcers; however, the relevance of this correlation remains con- troversial (10, 23, 24, 41, 48, 49). In any case, other serum antibodies may be better markers for predicting severe dis- eases. In the present work, we found that three single antigens (CagA, VacA, and p35) elicited antibodies more frequently in patients suffering from ulcers. The anti-VacA antibody is a more powerful marker of ulcers than anti-CagA. This is not surprising, because the vacuolating toxin has been suspected to be involved in the mechanism of ulcerous lesions of the mucosa (35, 38, 40, 41, 44). The anti-p35 antibody appears to be the best marker of ulcers, and the simultaneous presence of anti- VacA and anti-p35 antibodies predicts, with good sensitivity, a predisposition to ulcers. The poor specificity observed could be due to the fact that peptic ulcers may be intermittently present and certain patients may be nonulcerous at the time of endo- scopic examination but may later evolve to an ulcerous state. On the other hand, none of the serologic markers tested have been able to predict atrophic gastritis. It may be necessary to look for other antibodies, or the atrophy could be unrelated to serologic status. Other authors have attempted to establish correlations between certain antibody patterns and gastric can- cer (21).