DIAGNOSTIC WORKUP

All patients with acute abdominal pain should have a stat, flat, and upright plate of the abdomen, a chest x-ray to rule out pneumonia, an electrocardiogram (EKG) to rule out myocardial infarction, and a complete blood count (CBC), urinalysis, amylase, and chemistry panel. Sometimes lateral decubitus films of the abdomen are necessary to show the step ladder pattern of intestinal obstruction. A pregnancy test is ordered when age and sex dictate it!

When these tests fail to confirm the clinical diagnosis, x-ray contrast studies or ultrasound may be necessary. For example, an intravenous pyelogram (IVP) can be done for a suspected renal calculus. Serial cardiac enzymes may confirm a myocardial infarction. Gallbladder ultrasound can be done to confirm cholecystitis and cholelithiasis. A nuclear scan of the gallbladder with iminodiacetic acid derivatives is very accurate in detecting acute cholecystitis. Ultrasonography may also help diagnose impending rupture of an abdominal aneurysm or ectopic pregnancy. A peritoneal tap may diagnose a ruptured ectopic pregnancy. Laparoscopy should also be considered. A urine porphobilinogen helps exclude porphyria. A double enema may help diagnose intestinal obstruction. A computed tomography (CT) scan of the abdomen is the next logical step.

If the diagnosis remains in doubt, an exploratory laparotomy must be done before the patient’s condition deteriorates. The only case where this might be risky is acute pancreatitis. If this is suspected and the serum amylase is repeatedly normal, a quantitative urine amylase or peritoneal tap may confirm the diagnosis. Endoscopy may need to be done to diagnose a peptic ulcer, gastritis, gastric tumor, or reflux esophagitis. In obscure cases of appendicitis and diverticulitis, a contrast barium enema may help confirm the diagnosis. Angiography can diagnose an aneurysm or mesenteric infarction.

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Smoking and the risk of gastric cancer

Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking.

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Cancer, stomach:

 Stomach is the main organ that holds food for digestion. Worldwide, stomach cancer is the second most frequent cancer and the second leading cause of death from cancer. It can develop in any part of the stomach and spread to other organs. It is also known as gastric cancer.

Duodenal ulcers (peptic ulcers) are not associated with stomach cancer. However, infection with a bacterium called Helicobacter pylori is associated with gastric cancer. In one study, gastric cancer developed in about 3% of the infected patients and none of the uninfected patients. Eradication of the bacterium prevents or delays the development of gastric cancer. The risk of gastric cancer is also increased in Down syndrome.

Symptoms of stomach cancer are often vague, such as loss of appetite and weight, so diagnosis is often delayed. The cancer is diagnosed definitively with a biopsy of stomach tissue.

Cancer of the stomach is difficult to cure unless it is found early. Treatment may include surgery, chemotherapy and radiotherapy. Surgery is the most common treatment. It involves removal of part  or all of the stomach.

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Background Germ-line truncating mutations in the E-cadherin (CDH1) gene have been found in families with hereditary diffuse gastric cancer. These families are characterized by a highly penetrant susceptibility to diffuse gastric cancer with an autosomal dominant pattern of inheritance, predominantly in young persons. We describe genetic screening, surgical management, and pathological findings in young persons with truncating mutations in CDH1 from two unrelated families with hereditary diffuse gastric cancer.

Methods Mutation-specific predictive genetic testing was performed by polymerase-chain-reaction amplification, followed by restriction-enzyme digestion and DNA sequencing in Family 1 and by heteroduplex analysis in Family 2. A total gastrectomy was performed prophylactically in five carriers of mutations who were between 22 and 40 years old. In each case, the entire mucosa of the stomach was extensively sampled for microscopical analysis.

Results Superficial infiltrates of malignant signet-ring cells were identified in the surgical samples from all five persons who underwent gastrectomy. These early diffuse gastric cancers were multifocal in three of the five cases, and in one person infiltrates of malignant signet-ring cells were present in 65 of the 140 tissue blocks analyzed, representing in aggregate less than 2 percent of the gastric mucosa.

Conclusions We recommend genetic counseling and consideration of prophylactic gastrectomy in young, asymptomatic carriers of germ-line truncating CDH1 mutations who belong to families with highly penetrant hereditary diffuse gastric cancer.

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We assessed the trends in the proportion of articles on gastric cancer published in major cancer journals, the research fields of interest, and the first author’s affiliation. Articles in PubMed, addressing cancer in general and stomach cancer in particular, were quantified. Abstracts of gastric cancer articles were hand-searched. The British Journal of Cancer, Cancer, Cancer Research, the International Journal of Cancer, and the Journal of the National Cancer Institute were included in the journal survey. Stomach cancer was addressed in 2.9% of the articles in 1982–1984 and 3.3% in 2000–2002. The proportion of articles from Asia increased (32.2% vs 50.2%) and that for the United States decreased (34.4% vs 15.1%) in 2000–2002. Articles addressing etiologic genetic factors were more frequent in 2000–2002 (11.5% vs 61.6%). The proportion of stomach cancer articles was largely below the expected share considering the frequency of malignancies, and did not reflect the geography of biomedical publications. A trend was observed favoring the evaluation of genetic factors.

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There are several major factors that seem to increase one’s risk of gastric cancer. Men are twice as likely to get gastric cancer as women, and it is more common in people of Asian and Pacific Island descent. One’s diet probably plays a major role. Smoked foods, salted meat and fish and pickled vegetables increase one’s risk of gastric cancer, while eating whole grains and fresh fruits and vegetables seems to lower the risk. Obesity, too, increases one’s risk. Other factors that increase one’s risk of stomach cancer include:

—      Smoking

—      Excessive intake of alcohol

—      A bacterial, H. pylori, ,stomach infection

—      Stomach surgery

—      Stomach polyps

—      Increased age

—      Type A blood

—      Family history of cancer

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Purpose: The small GTPase RhoA has been implicated in the regulation of cell morphology, motility, and transformation, but the role of RhoA protein in the carcinogenesis of gastric cancer remains unclear. In the present study, we have analyzed the expression status of the RhoA protein in human gastric cancer cells and tissues and investigated the possible involvement of RhoA in regulating the malignant phenotype of gastric cancer cells.

Experimental Design: RhoA expression was analyzed by immunohistochemistry and Western blot in gastric cancer tissues and cell lines. The RhoA-specific small interfering RNA (siRNA) vector was designed and constructed. We examined the role of RhoA in the malignant phenotype of gastric cancer cells by using siRNA knockdown and dominant-negative RhoA mutant suppression of endogenous RhoA activity.

Results: RhoA was found frequently overexpressed in gastric cancer tissues and cells compared with normal tissues or gastric epithelial cells. RhoA-specific siRNA could specifically and stably reduce RhoA expression up to 90% in AGS cells. Both RhoA-specific siRNA and dominant-negative RhoA expressions could significantly inhibit the proliferation and tumorigenicity of AGS cells and enhance chemosensitivity of the cancer cells to Adriamycin and 5-fluorouracil.

Conclusion: RhoA may play a critical role in the carcinogenesis of gastric cancer, and the interference of RhoA expression and/or activity could provide a novel avenue in reversing the malignant phenotype of gastric cancer cells.

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Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow–derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.

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Background: Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. Methods: A total of 521 457 men and women aged 35–70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric noncardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case–control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. Results: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric noncardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52; 95% CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric noncardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non–statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. Conclusion: Total, red, and processed meat intakes were associated with an increased risk of gastric noncardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer.

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Gastric Cancer, a joint official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, publishes significant studies related to stomach neoplasms. The journal welcomes original articles, case reports, short communications, and technical notes, which will be peer-reviewed by the editorial board. Letters to the Editor commenting on articles published in the journal or expressing views on topics concerning gastric cancer are also welcomed. Review articles are in principle solicited by the Editor. Meeting reports will include summaries of symposia or consensus achieved in the congresses of related associations.

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