Family History Of Gastric Carcinoma Research Articles

Clinical characteristics of distal gastric cancer in young adults from Northeastern Brazil

BackgroundIt has been suggested that distal gastric carcinoma (GC) in younger patients has a more aggressive outcome than in older patients, however this is a controversial issue. The aim of this study was to compare clinicopathological features between younger and older patients with GC in Northeastern Brazil.MethodsA total of 207 patients with distal GC (41 patients ≤45 years, considered younger group, and 166 > 45 years, considered older group) were evaluated prospectively during a 6 year period.ResultsThe mean patient age in the young group was 37.41 years old and 64.43 years in the older group. No significant difference was found regarding gender, area of residence, history of alcohol consumption, chronic tobacco smoking. Prevalence of first-degree GC history was 12.5% (7.3% in younger group vs. 13.9% in older; p < 0.46). The most frequent symptom was gastric pain and weight loss. Diffuse infiltrative cancer was more frequently seen in younger patients (70.70% vs. 33.70%, respectively; p < 0.01), as was histologically less differentiated tumors (63.40% vs. 33.10%; p < 0.01) and stage IV of GC (48.80% vs. 30.70%; p < 0.015). Five-year survival, evaluated in 82 patients, was lower in younger patients (p = 0.045); however, after adjusting for stage of GC in the multivariate analysis, this association did not remain significant. Family history of GC and gender had no impact on survival.ConclusionsYounger patients showed higher prevalence of diffuse type of Lauren and lower survival that was attributed to higher rate of advanced stage of GC. Gastric cancer screening strategies should also be considered in younger individuals, especially in areas of high prevalence. Further studies are warranted to determine risk factors associated with gastric cancer in young adults.

Gastric Intestinal Metaplasia: Defining the Natural History

Introduction: The management of intestinal metaplasia (IM), a pre-malignant condition and precursor to dysplasia and gastric carcinoma (GCa), is problematic because of paucity of data on its natural history, especially for the United States (US) population, and because of variance in guidelines. We aim to study the natural history of IM in the US and to identify potential risk factors for progression to GCa. Methods: A cohort of 9,000 consecutive patients with histologically confirmed IM were identified, and a subset from 2003-2004 was selected for this pilot study. Clinical, endoscopic, and histologic data was extracted, including demographics, BMI, symptoms, tobacco pack years, alcohol use, NSAID use, H. pylori, Barrett's esophagus, GERD symptoms, PPI use, anemia, blood group, and family history of GCa. Fisher's Exact Test (2-Tail) and the non-parametric Wilcoxon 2-Sample Test were used for analysis. Results: We identified 200 patients, with statistically equal distribution between genders. The majority were Caucasian (81.4%), with average age of 68, and mean BMI of 26.5. The majority of patients were symptomatic (82%) leading to endoscopy, including symptoms of: pain (43%), reflux (30%), GI bleeding (11%), and concern for GCa (8%). Sixty-one percent of patients were smokers, 18.6% of patients had H. pylori and 80.8% demonstrated eradication after treatment. Of the patients with documented blood type the majority, 54% had type A. Eleven percent of patients had a family history of GCa. Patients were followed for a mean of 4.1 years, and of those with clinical follow-up, 7%, (14) developed GCa. Those that lived (6), had a mean age of 67.5, while eight passed away from GCa with mean age of 75.6, and all were men. Conclusion: We found no association with H. pylori, obesity, or alcohol consumption and IM, and all other studied parameters did not appear to correlate. Of patients followed, 4% passed away from GCa, in contrast to SEER database prediction of 2% of deaths in US in 2014 due to GCa. This represents a significant, increase in risk of GCa death development in IM. The difference in gender and age was statistically significant for those with mortality. The progression from IM to GCa occurred in the US population and it appears the patients with IM were at higher risk than the general population. More frequent and rigorous endoscopic surveillance may be necessary, especially in elderly men if the increased risk is confirmed in the remainder of our cohort and by other studies.

Gastric arteriovenous malformation: a rare cause of upper GI bleed

A 72-year-old Asian man presented with abdominal pain and melena. Medical history included spinal tuberculosis, and there was a family history of gastric carcinoma. The patient did not drink any alcohol. On admission, he was hypotensive and tachycardic. The abdomen was soft, but with generalized tenderness. No mass was palpable. Blood tests revealed the following: hemoglobin 5.2 g/dL (normal 13-18 g/dL), urea nitrogen 22.4 mg/dL (7-18 mg/dL), normal clotting, and normal results on liver biochemical tests.

The Association Between the Interleukin-1 Polymorphisms and Gastric Cancer Risk Depends on the Family History of Gastric Carcinoma in the Study Population

The association between interleukin-1 polymorphisms, H. pylori and increased gastric cancer risk remains controversial. To compare the prevalence of these polymorphisms in individuals with two mutually exclusive diseases connected with infection, gastric cancer, and duodenal ulcer. 121 gastric cancer and 119 duodenal ulcer patients. Genomic DNA was typed for polymorphisms at position -511, -31 in the interleukin-1beta gene (IL-1 beta) using primer extension and mass-spectrometry. Analysis of the variable number of tandem repeats in intron 2, in its receptor antagonist gene (IL-1RN) was performed by PCR and agarose gel electrophoresis. All subjects were successfully genotyped for the three gene loci. IL-1 beta-511 was found to be in reverse linkage disequilibrium with IL-1 beta-31. The differences between gastric cancer and duodenal ulcer patients concerned only heterozygous variant of IL-1beta and were related to family history of gastric cancer, tumor stage, histology, site. Thus, CT carriers were found to have a higher risk of sporadic [OR 2.21 (95% CI, 1.22-3.99)], early [OR 2.81 (95% CI, 1.14-6.93)], diffuse [OR 2.48, (95% CI 1.21-5.09)] or non-cardia gastric cancer [OR 1.88 (95% CI 1.06-3.33)]. Furthermore, CT genotype was significantly more prevalent in gastric cancer patients with negative than in those with a positive family history (p = 0.039). The association between the interleukin-1 polymorphisms and gastric cancer risk depends on the family history of gastric carcinoma in the study population. This phenomenon may be in part responsible for differences in results of interleukin-1 studies performed on populations with low and high gastric cancer prevalence.

Loss ofFHITexpression in gastric mucosa of patients with family histories of gastric cancer andHelicobacter pyloriinfection

To answer the question whether FHIT gene expression is affected by the family history of gastric carcinoma and the presence of Helicobacter pylori (H pylori) in the gastric mucosa of patients with dyspepsia. FHIT gene expression in two different topographic sites of the gastric mucosa of twenty-one patients with dyspepsia and with or without familial gastric carcinoma, infected or not infected with H pylori, was evaluated by reverse transcription-PCR (RT-PCR) and IMAGE QUANT methods. A rapid urease test and histopathological examination were used to determine H pylori colonization. In the gastric mucosa of patients with family histories of gastric carcinoma, the amount of FHIT protein mRNA was reduced down to 32%, and for patients with H pylori colonization, to 24% in comparison to controls with dyspepsia and without cancer in the family. FHIT expression was independent of the topography of specimens (corpus vs antrum), and for the control patients it was less sensitive to infection with H pylori. A considerable statistical difference in FHIT levels was observed in the gastric mucosa from the corpus of patients with family histories of gastric carcinoma in respect to H pylori colonization (P = 0.06). Macroscopic evaluation of the gastric mucosa demonstrated that pathologic changes classified according to the Sydney system had no significant influence on FHIT expression within each tested group of patients. Loss of FHIT expression was observed in patients with dyspepsia and family histories of gastric carcinoma, especially those infected with H pylori. Such results may constitute an early indication of the development of gastric carcinoma, which is associated with family factors including heredity and H pylori infection. The loss of the FHIT gene may serve as a marker for early diagnosis and prevention of gastric carcinoma, especially in context of early monitoring of H pylori infection in individuals with a record of familial stomach cancer.

The death of Napoleon

It was with fascination that I read the paper ‘Channelling the Emperor: what really killed Napoleon?’(August 2004 JRSM1), but I must emphasize that despite its title it is only concerned with the immediate cause of Napoleon’s death. As indicated in my 1996 paper on Napoleon’s health,2 the Emperor first complained of nausea and upper abdominal discomfort after food in July 1820. The dyspepsia worsened to give loss of appetite, constant nausea, frequent vomiting, upper abdominal pain and constipation. There were periods of remission but the pain and vomiting became increasingly insistent. He lost weight and by the end of January 1821 could only manage fluid nourishment, finally taking to his bed on 17 March. On 27 April he vomited blood and his condition deteriorated with further bleeding and lapses into unconsciousness before death on 5 May. At necropsy in front of sixteen observers including seven British doctors, of whom five signed the official report, the external surface of the stomach appeared healthy. On opening, however, it contained altered blood and almost its entire lining was cancerous: a scirrhous cancer had converted the stomach into a leather-bottle stomach with spread to the adjacent lymph nodes and with a perforation that had become sealed off. There was a family history of gastric carcinoma, and Napoleon realized he was dying of the same disease as his father and grandfather, remarking on 15 April, ‘I know the truth and I am resigned’. Clinically the cause of death was clearly gastric carcinoma, but on the publication of my paper in 1996, I received abusive letters with accusations that Napoleon had died from deliberate arsenical poisoning. This theory had received encouragement in 1961 when some, though not all, samples of his hair were found to contain abnormal amounts of arsenic. Arsenic was used in medicaments such as Fowler’s and Donovan’s solutions, and liquor arsenicalis was still in use as a general tonic and for loss of appetite when I qualified. The drawing room at Longwood House in St Helena was redecorated in 1819, but a specimen of the wallpaper applied at that time contained only low levels of arsenic when analysed in 1982. As the immediate cause of death from, say, carcinoma of the prostate may be cardiac failure, so the immediate cause of Napoleon’s death has now been explained to those who still believe he died from arsenic toxicity and not from a carcinoma of the stomach.

Histological patterns of gastritis in H. pylori-infected individuals with a family history of gastric cancer

OBJECTIVE: Different types of chronic gastritis, including antral predominant, corpus predominant, and multifocal pangastritis, are associated with Helicobacter pylori infection. Specific patterns of H. pylori gastritis that might characterize individuals with family histories of noncardia gastric cancer (GC) were investigated. METHODS: Histopathological changes associated with H. pylori gastritis were assessed in 111 individuals with family histories of GC and in 77 without from a region with high prevalence of H. pylori infection and GC. Gastric biopsies were taken from 12 sites (antrum, five; corpus, six; and cardia, one). RESULTS: Individuals (age < 36 yr) with family histories of GC developed pangastritis and had higher H. pylori bacterial scores ( p < 0.05) in the gastric corpus, whereas those without family histories of GC typically had antral predominant gastritis. The correlation between density of polymorphonuclear leukocytes and density of H. pylori at each biopsy site was statistically significant ( p < 0.01). Pangastritis was associated with a higher density of lymphoid aggregates and follicles ( p < 0.05) in the corpus of younger individuals (age < 36) and in the antrum of older individuals (age ≥ 48) with positive family histories of GC. CONCLUSIONS: Pangastritis and high lymphoid follicle density associated with H. pylori infection were found in patients with family histories of GC. Because a family history of gastric carcinoma is associated with increased risk of gastric cancer development, characterization of histological patterns of gastritis may be applicable to gastric cancer screening and surveillance, especially in relatively young at-risk populations.

Histological patterns of gastritis in H. pylori-infected individuals with a family history of gastric cancer.

Different types of chronic gastritis, including antral predominant, corpus predominant, and multifocal pangastritis, are associated with Helicobacter pylori infection. Specific patterns of H. pylori gastritis that might characterize individuals with family histories of noncardia gastric cancer (GC) were investigated. Histopathological changes associated with H. pylori gastritis were assessed in 111 individuals with family histories of GC and in 77 without from a region with high prevalence of H. pylori infection and GC. Gastric biopsies were taken from 12 sites (antrum, five; corpus, six; and cardia, one). Individuals (age < 36 yr) with family histories of GC developed pangastritis and had higher H. pylori bacterial scores (p < 0.05) in the gastric corpus, whereas those without family histories of GC typically had antral predominant gastritis. The correlation between density of polymorphonuclear leukocytes and density of H. pylori at each biopsy site was statistically significant (p < 0.01). Pangastritis was associated with a higher density of lymphoid aggregates and follicles (p < 0.05) in the corpus of younger individuals (age < 36) and in the antrum of older individuals (age > or = 48) with positive family histories of GC. Pangastritis and high lymphoid follicle density associated with H. pylori infection were found in patients with family histories of GC. Because a family history of gastric carcinoma is associated with increased risk of gastric cancer development, characterization of histological patterns of gastritis may be applicable to gastric cancer screening and surveillance, especially in relatively young at-risk populations.

Family history and gastric carcinoma: the role of glutathione peroxidase

Background: The risk of gastric carcinoma is increased in persons with a positive family history of the disease. Previous findings suggest that free radicals are involved in both the initiation and promotion of carcinogenesis. Objective: The aim of this study was to assess whether alterations in the antioxidant defense system of gastric mucosal cells in patients with gastric carcinoma are related to a positive family history. Methods: Glutathione peroxidase activity, oxidized glutathione, total glutathione, and malondialdehyde levels were assayed in patients with gastric carcinoma with and without a family history of the disease. A control group consisted of healthy volunteers. Results: The study enrolled 65 patients with gastric carcinoma: 35 with and 30 without a family history of the disease, as well as 30 control subjects. The level of glutathione peroxidase activity in tumor-free tissue samples from patients with a family history of gastric carcinoma was higher than in samples from those without such family history. Glutathione peroxidase activity was also significantly higher in neoplastic than in tumor-free tissue. There was no significant difference in glutathione peroxidase activity between neoplastic tissue samples taken from patients with and without a positive family history. Conclusions: The results appear to support the existence of an enzymatic imbalance caused by cellular initiation in patients with a family history of gastric carcinoma. This imbalance may lead to an altered response to free radical oxygen species and a consequent progressive increase in biologic damage.

Vitamins, carotenoids, dietary fiber, and the risk of gastric carcinoma

BACKGROUND Numerous components of fruit and vegetables are considered to decrease the risk of gastric carcinoma. In the current prospective study, the authors examined the association between the intake of vitamins, carotenoids, and dietary fiber and vitamin supplement use and the incidence rate of gastric carcinoma. METHODS The Netherlands Cohort Study began in 1986 with 120,852 men and women ages 55–69 years. Data regarding diet and other covariates were collected by means of a self-administered questionnaire. After 6.3 years of follow-up, data regarding 282 incident cases of gastric carcinoma and 3123 subcohort members were available for case-cohort analyses. RESULTS In analyses adjusted for age, gender, smoking history, education, stomach disorders, and family history of gastric carcinoma, an inverse association with vitamin C intake (relative risk [RR] for highest vs. lowest intake category, 0.7; 95% confidence interval [95% CI], 0.5–1.0) was observed, with a borderline significant trend across three intake categories (P = 0.06). After the exclusion of cases diagnosed in the first and second follow-up years, the RR was 0.9 (95% CI, 0.6–1.2; P trend = 0.44). Intake of retinol and β-carotene were associated positively with gastric carcinoma risk with highest versus lowest quintile RRs of 1.6 (95% CI, 1.0–2.5; P trend = 0.02) and 1.6 (95% CI, 1.0–2.6; P trend = 0.13), respectively, after the exclusion of first-year and second-year cases. Intake of folate, vitamin E, α-carotene, lutein plus zeaxanthin, β-cryptoxanthin, lycopene, and dietary fiber was not associated with gastric carcinoma. Patients who used vitamin A-containing supplements had a lower risk of gastric carcinoma than nonusers (RR = 0.4; 95% CI, 0.2–0.9). CONCLUSIONS No clear inverse associations were found between the intake of vitamins, carotenoids, and dietary fiber and the risk of gastric carcinoma after adjustment for confounding variables and the exclusion of first-year and second-year cases. Cancer 2000;88:737–48. © 2000 American Cancer Society.

Vitamins, carotenoids, dietary fiber, and the risk of gastric carcinoma

Numerous components of fruit and vegetables are considered to decrease the risk of gastric carcinoma. In the current prospective study, the authors examined the association between the intake of vitamins, carotenoids, and dietary fiber and vitamin supplement use and the incidence rate of gastric carcinoma. The Netherlands Cohort Study began in 1986 with 120,852 men and women ages 55-69 years. Data regarding diet and other covariates were collected by means of a self-administered questionnaire. After 6.3 years of follow-up, data regarding 282 incident cases of gastric carcinoma and 3123 subcohort members were available for case-cohort analyses. In analyses adjusted for age, gender, smoking history, education, stomach disorders, and family history of gastric carcinoma, an inverse association with vitamin C intake (relative risk [RR] for highest vs. lowest intake category, 0.7; 95% confidence interval [95% CI], 0.5-1.0) was observed, with a borderline significant trend across three intake categories (P = 0. 06). After the exclusion of cases diagnosed in the first and second follow-up years, the RR was 0.9 (95% CI, 0.6-1.2; P trend = 0.44). Intake of retinol and beta-carotene were associated positively with gastric carcinoma risk with highest versus lowest quintile RRs of 1. 6 (95% CI, 1.0-2.5; P trend = 0.02) and 1.6 (95% CI, 1.0-2.6; P trend = 0.13), respectively, after the exclusion of first-year and second-year cases. Intake of folate, vitamin E, alpha-carotene, lutein plus zeaxanthin, beta-cryptoxanthin, lycopene, and dietary fiber was not associated with gastric carcinoma. Patients who used vitamin A-containing supplements had a lower risk of gastric carcinoma than nonusers (RR = 0.4; 95% CI, 0.2-0.9). No clear inverse associations were found between the intake of vitamins, carotenoids, and dietary fiber and the risk of gastric carcinoma after adjustment for confounding variables and the exclusion of first-year and second-year cases.

Individual and joint contribution of family history and Helicobacter pylori infection to the risk of gastric carcinoma.

Helicobacter pylori infection and a positive family history of gastric carcinoma have been identified as risk factors for the disease. It is unclear, however, to what degree their impact on the risk of gastric carcinoma is independent, because H. pylori also clusters within families. The authors carried out a population-based, statewide case-control study in Saarland, Germany, to assess the individual and joint contributions of family history and H. pylori infection to the risk of gastric carcinoma. Cases included 68 patients with histologically verified gastric carcinoma. Controls included 239 patients with colorectal carcinoma who were matched to the cases by age and gender. Information on family history (defined as gastric carcinoma in at least one first-degree relative) and potential confounders was collected by standardized interviews. Immunoglobulin G antibodies against H. pylori were measured by enzyme-linked immunosorbent assay. In addition, antibodies against the CagA antigen were determined by Western blot analysis. H. pylori infection and family history were positively related, and both risk factors were more common among cases than among controls. Although the association between family history and gastric carcinoma was somewhat reduced by control for H. pylori infection, both risk factors still showed strong independent relations with gastric carcinoma after control for each other. Compared with uninfected subjects who had no family history, subjects with both a positive family history and infection with a CagA positive H. pylori strain had a more than 8-fold total risk of gastric carcinoma (adjusted odds ratio [OR], 8.2; 95% confidence interval [CI], 2.2-30.4) and a 16-fold risk of noncardia gastric carcinoma (OR, 16.0; 95% CI, 3.9-66.4). Infection with CagA positive H. pylori strains and a positive family history appear to be strong independent risk factors for gastric carcinoma. They may be useful markers for identifying subjects at high risk for the disease and for targeting efforts of prevention and early detection.

Multifocal occurrence of gastric carcinoma in patients with a family history of gastric carcinoma

Smoking and alcoholic beverage drinking habits as well as a family history of cancer are well known risk factors for the multifocal occurrence of squamous cell carcinoma of the esophagus and the head and neck region. However, the role of these risk factors in multiple gastric carcinoma remains to be clarified. The purpose of this study was to examine the risk factors for multiple gastric carcinoma. The smoking and drinking habits as well as the family history of 157 patients with synchronous multiple gastric carcinoma and 157 patients with solitary gastric carcinoma who were similar with regard to gender, age, stage of the tumor, and year of admission were investigated. The risk of a multiple occurrence of gastric carcinoma also was elevated using the odds ratio (OR). The ORs of a multifocal occurrence of gastric carcinoma in patients who currently smoked and drank alcoholic beverages were 1.1 and 0.8, respectively, although the ORs were not related to the quantity of smoking or drinking. In patients with a close relative with gastric carcinoma the OR was 2.1 (95% confidence interval [CI], 1.3-3.7). In those patients with > or =2 close relatives with gastric carcinoma, the OR increased to 5.1 (95% CI, 1.2-21.1). Conversely, no significant elevation in the ORs was recognized regarding a family history of other cancers. In this study, a family history of gastric carcinoma was found to be clearly associated with the multifocal occurrence of gastric carcinoma; however, no significant correlation between the multifocal occurrence of gastric carcinoma in these patients and their smoking and drinking habits was recognized.

Multifocal occurrence of gastric carcinoma in patients with a family history of gastric carcinoma

Multifocal occurrence of gastric carcinoma in patients with a family history of gastric carcinoma

Increased cell proliferation of the gastric mucosa in first‐degree relatives of gastric carcinoma patients

BACKGROUND Studies not considering Helicobacter pylori infection have suggested the presence of a hereditary risk for gastric carcinoma. However, other studies have identified intrafamilial clustering of H. pylori infection as a causal factor in gastric carcinogenesis. This prompted the authors to study the effect of H. pylori and hereditary factors on the proliferation of gastric mucosa because hyperproliferation appears to be an early step in carcinogenesis. METHODS In a total of 39 patients (19 first-degree relatives of patients with gastric carcinoma and 20 dyspeptic controls), 2 biopsy specimens each from the antrum and corpus were examined histologically. In addition, crude nuclei fractions were prepared from other biopsy specimens obtained in the same manner. Nuclei were fixed in 70% ethanol and stained with propidium iodine prior to measurement. A cell cycle analysis was performed using a flow cytometer. For analysis a proliferative index (PI) (percentage of nuclei in the S- and G2/M-phases) was calculated. RESULTS In comparison with control patients, first-degree relatives of gastric carcinoma patients had increased mucosal proliferation of the antrum (Student's t test, P = 0.017). After excluding patients with H. pylori infection (12 in each group), relatives of gastric carcinoma patients had significantly increased proliferation not only in the antrum (PI: 16.5 vs. 12.1; P = 0.043), but also in the corpus (PI: 17.2 vs. 13.0; P = 0.024). CONCLUSIONS A family history of gastric carcinoma may increase the risk for developing gastric carcinoma via mucosal hyperproliferation, irrespective of H. pylori infection. Cancer 1998;83:876-881. © 1998 American Cancer Society.

Increased cell proliferation of the gastric mucosa in first-degree relatives of gastric carcinoma patients

Studies not considering Helicobacter pylori infection have suggested the presence of a hereditary risk for gastric carcinoma. However, other studies have identified intrafamilial clustering of H. pylori infection as a causal factor in gastric carcinogenesis. This prompted the authors to study the effect of H. pylori and hereditary factors on the proliferation of gastric mucosa because hyperproliferation appears to be an early step in carcinogenesis. In a total of 39 patients (19 first-degree relatives of patients with gastric carcinoma and 20 dyspeptic controls), 2 biopsy specimens each from the antrum and corpus were examined histologically. In addition, crude nuclei fractions were prepared from other biopsy specimens obtained in the same manner. Nuclei were fixed in 70% ethanol and stained with propidium iodine prior to measurement. A cell cycle analysis was performed using a flow cytometer. For analysis a proliferative index (PI) (percentage of nuclei in the S- and G2/M-phases) was calculated. In comparison with control patients, first-degree relatives of gastric carcinoma patients had increased mucosal proliferation of the antrum (Student's t test, P = 0.017). After excluding patients with H. pylori infection (12 in each group), relatives of gastric carcinoma patients had significantly increased proliferation not only in the antrum (PI: 16.5 vs. 12.1; P = 0.043), but also in the corpus (PI: 17.2 vs. 13.0; P = 0.024). A family history of gastric carcinoma may increase the risk for developing gastric carcinoma via mucosal hyperproliferation, irrespective of H. pylori infection.

Association between Family History and Gastric Carcinoma among Young Adults

The relationship between family history of gastric carcinoma and gastric carcinoma in Japanese under 40 years of age was analyzed. The subjects were 108 gastric carcinoma patients (86% were diffuse type) at 9 hospitals in the Kanto area of Japan. Firstly, incidence of gastric carcinoma among the parents of the subjects were compared with that in the general population. Observed/expected (O/E) ratios (P‐value) were 1.8 (0.06) for all subjects, 1.3 (0.62) for male subjects, 2.1 (0.04) for female subjects, 0.5 (0.41) for early carcinoma, 2.6 (P<0.01) for advanced carcinoma, 2.3 (0.22) for intestinal‐type carcinoma and 1.7 (0.13) for diffuse‐type carcinoma. Association between gastric carcinoma and parents’ history of gastric carcinoma was strong among women and regarding advanced carcinoma, and the difference in O/E ratios between early and advanced carcinoma was remarkable. Secondly, factors related to advanced‐stage gastric carcinoma were analyzed. Histological type (diffuse and intestinal types) was not related, but family history of gastric carcinoma among parents and grandparents was related to advanced stage, and the relationship was independent of other factors. The odds ratio (95% confidence interval) was 3.3 (1.1–9.9). Family history may be related to stage of gastric carcinoma through its relationship to the manner or speed of the tumor's progression. We hypothesis that some genetic factor exists which is involved both in progression from early to advanced stage and in occurrence of gastric carcinoma.

Treatment of Helicobacter pylori infections

The available literature on the relationship between several diseases and Helicobacter pylori (H. pylori) is reviewed. Duodenal ulcer, gastric ulcer, complicated peptic ulcer, abdominal symptoms and gastroduodenal mucosal damage during the use of non-steroid anti-inflammatory drugs (NSAIDs), non-ulcer dyspepsia (NUD) and gastric malignancy are discussed. The case for and against eradication is critically discussed. Eradication of H. pylori should be pursued in all patients with peptic ulcer disease, whether they are using NSAIDs or not. Eradication of H. pylori in the treatment of NUD should be considered experimental. Treatment aimed at the eradication of H. pylori should be considered in all patients with low-grade malignant mucosa-associated lymphoid tissue (MALT) lymphoma and in all patients with Ménétrier's disease. Finally, this treatment should be considered in a subset of H. pylori-infected patients who possibly are at an increased risk of gastric cancer: patients with a strong family history of gastric carcinoma and patients in need of long-term treatment with a proton-pump inhibitor. In view of the importance of patient compliance, the risk of side-effects and the possibility of inducing metronidazole resistance when treatment with a metronidazole-containing regimen is used, treatment aimed at the eradication of H. pylori should be carefully implemented and monitored.