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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To explore the potential contributions of gastroesophageal reflux disease, as opposed to Helicobacter pylori infection, to the development of gastric carditis, we evaluated gastric carditis (using the criteria of the updated Sydney system for the classification of gastritis), clinical and morphologic features of esophagitis, and H. pylori infection (evaluation of Steiner stains) in biopsy specimens from the gastroesophageal squamocolumnar junction. We correlated clinical, endoscopic, and histologic features in an unselected group of 116 patients. Some degree of carditis was found in 107 (92%) of the patients. The mean age of the patients increased with increasing severity of carditis (P < .05). The various groups of patients with different degrees of carditis did not differ significantly in sex ratio, ethnic background, presence of obesity, percentage having symptoms of gastroesophageal reflux disease (such as heartburn, regurgitation, dysphagia, or odynophagia), endoscopic evidence of esophagitis and columnar epithelium in the distal esophagus, or histologic evidence of active esophagitis. The presence, however, of active gastritis and H. pylori infection in the distal stomach and/or in the cardia was significantly associated with carditis. In patients without carditis, H. pylori was not detected in any cardiac or distal gastric biopsy specimen. In contrast, H. pylori was demonstrated in gastric tissue samples (either from the cardia or distally) of patients with carditis, with the prevalence rate increasing with greater degrees of cardiac inflammation. The H. pylori prevalence rate was 12% in the group with mild carditis, 40% in those with moderate carditis, and 57% in patients with marked carditis (P = .0001). In summary, carditis is commonly found in patients with symptoms related to upper gastrointestinal diseases. From analysis of our study cohort, we concluded that carditis was significantly associated with H. pylori infection and active gastritis but not with symptoms or signs of gastroesophageal reflux disease. These findings suggest that carditis with histologic features similar to those of gastritis in the distal stomach was a sequel of H. pylori infection and represented a part of an H. pylori--associated gastric inflammation.
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PMID:Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis. 979 21

The incidence of adenocarcinoma of the esophagus and esophagogastric junction (EGJ) has been increasing over the past 15 years in western countries. Surgical series and population-based studies show that, by 1994, adenocarcinomas of the esophagus accounted for half of all esophageal cancer among white men. The causes of this increase in incidence remain to be elucidated. Esophageal adenocarcinomas and a portion of EGJ adenocarcinomas arise from long and short segments of specialized intestinal metaplasia (Barrett's esophagus). The prevalence of long segments of Barrett's esophagus (> 3 cm) in patients having endoscopy for reflux symptoms is 3%, and 1% in those undergoing endoscopy for any clinical indication. However, a silent majority of patients with Barrett's esophagus remain unrecognized in the general population and may not be diagnosed unless adenocarcinoma develops. Recent studies document a rise in the diagnosis of specialized intestinal metaplasia of the cardia. Nearly all these patients have associated carditis, and Helicobacter pylori infection has been linked to this condition. The possible origin of EGJ adenocarcinomas in the sequence carditis--specialized intestinal metaplasia needs to be clarified. Smoking and obesity are additional risk factors for adenocarcinoma of the esophagus and EGJ. Current data does not confirm H. pylori as a risk factor for cancer of the EGJ.
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PMID:Epidemiology of esophageal cancer, especially adenocarcinoma of the esophagus and esophagogastric junction. 1069 34

The incidence and mortality related to esophageal adenocarcinoma (EAC) have been increasing in the United States, several European countries, and Oceania for the past 2 to 3 decades. Survival remains dismal, with little improvement during the same time period. Variations in the coding, classification, and detection of gastroesophageal malignancy may have contributed partially to the observed trends. Remarkable differences related to gender, ethnicity, and geography characterize the epidemiology of EAC. Gastroesophageal reflux disease (GERD) is the main risk factor for Barrett's esophagus, which is the only known precursor lesion for EAC. Several risk factors that promote the development of GERD and/or Barrett's esophagus have been proposed to explain these rising trends; these factors include the declining rates of Helicobacter pylori infection, obesity, dietary factors, and certain drugs.
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PMID:The epidemic of esophageal adenocarcinoma. 1213 11

There is increasing incidence of adenocarcinoma of the esophagastric junction (EGJ) especially in young white men (+35% in 30 years). The reasons for this are not yet well known, however one of the main causes is gastro-esophageal-reflux disease (GERD). The differentiation of a EGT carcinoma in three subtypes is important for therapy: adenocarcinoma of the distal esophagus (type I), cardia carcinoma (type II) and subcardial gastric carcinoma (type III). The most important risk-factor for type I-cancers is "barrett's metaplasia" resulting from GERD over years. The risks for the type II- and type III-carcinomas may be obesity and high caloric and fat intake. The role of Helicobacter pylori infection and adenocarcinoma of the subcardia is unproven. Preoperative tumor staging is difficult and tumor-stage is most often underestimated (esp. in the case of a high-grade dysplasia where in 43% carcinomas one already established). Therapy for all three types of EGJ tumors is surgical. Transhiatal (rarely transthoracic) esophagectomy with lymphadenectomy and proximal gastrectomy is performed for type-I-tumors, type-II and III-tumors are treated like a gastric cancer with total gastrectomy, lymphadenectomy and distal esophagectomy. Lymph-node metastases and advanced tumor-stage are bad prognostic factors, complete tumor resection (R0 resection) with extended lymphadenectomy will improve prognosis. The results of a preoperative combined-modality therapy are encouraging, but have not yet shown a definitive benefit. In case of distant metastases, radio-chemotherapy combined with gastroenterologic treatments (e.g. esophageal prostheses, PEG, etc.) will be used as a palliative treatment option.
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PMID:[Carcinomas of the esophago-gastric junction: surgical strategies]. 1281 32

Most available information on the epidemiology of Barrettacute;s esophagus (BE) relates to patients with long segments (> 3 cm) of specialized intestinal metaplasia (SIM). Its prevalence is 3% in patients undergoing endoscopy for reflux symptoms and 1% in those undergoing endoscopy for any clinical indication. The latter prevalence is similar to the 1% found in autopsy series. A "silent majority" with BE remain unrecognized in the general population. BE is more common in men, and the prevalence rises with age. Recent endoscopic series document a rise in the diagnosis of endoscopically apparent short segments (< 3 cm) of BE (SSBE). The prevalence of SSBE in both unselected and reflux patients is 8% to 12%. Specialized intestinal metaplasia at the cardia, below a normal-appearing squamocolumnar junction, has been reported to vary from 6% to 25% in patients presenting for upper endoscopy. Unlike patients with long segment Barrett's esophagus (LSBE), the role of gastroesophageal reflux disease in the pathogenesis of SSBE and SIM of the cardia is controversial. Recent data suggest that the etiology of SIM of the cardia might be secondary to Helicobacter pylori infection, although the role of other environmental factors cannot be ruled out. The incidence of adenocarcinoma of the esophagus and esophagogastric juction (EGJ) has been increasing over the past 15 years in Western countries. Surgical series and population-based studies show that by 1994 adenocarcinomas of the esophagus accounted for half of all esophageal cancer among white men. LSBE and SSBE predispose to the development of adenocarcinoma of the esophagus and EGJ. The role of SIM of the cardia as a precursor lesion for EGJ adenocarcinoma is still unclear. The prevalences of dysplasia in LSBE and SSBE are around 6% and 8%, respectively. The incidence of adenocarcinoma in patients with LSBE is about 1 in 100 patient-years. Cancer risk for SSBE and SIM at the cardia is unknown. Smoking and obesity increase the risk for esophageal and EGJ adenocarcinomas.
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PMID:Trends in incidence and prevalence of specialized intestinal metaplasia, barrett's esophagus, and adenocarcinoma of the gastroesophageal junction. 1291 64

The incidence of esophageal adenocarcinoma has risen rapidly over the past 3 decades. This increase had been most dramatic among white men. It has supplanted squamous cell carcinoma as the predominant histologic type of esophageal cancer in the United States. The reasons underlying this phenomenon are not readily apparent. Improvements in diagnostic techniques and changes in cancer classification may explain some of the rise in reported incidence rates, but detection bias and misclassification bias do not appear adequate to explain the increase entirely. Risk factors for esophageal adenocarcinoma are reviewed, with particular emphasis on their role in underlying the rising cancer incidence. The etiologic factors most likely to explain the current epidemic of esophageal adenocarcinoma are the parallel epidemic of obesity, rising use of lower esophageal sphincter-relaxing medications, decreasing Helicobacter pylori infection, changes in the Western diet, and distant smoking habits.
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PMID:The changing epidemiology of esophageal adenocarcinoma. 1465 11

Gastrointestinal cancer is a major medical and economic burden worldwide. Oesophageal and gastric cancers are most common in the non-industrialized countries, while colorectal cancer is the predominant gastrointestinal malignancy in westernized countries. Their aetiology is mainly related to correctable and preventable lifestyle habits; namely diet (including obesity), physical activity, alcohol and tobacco intake, and sanitation. Prevention and/or treatment of Helicobacter pylori infection would significantly reduce the prevalence of gastric cancer. Screening for cancer, its early detection and treatment requires medical facilities, endoscopic expertise and a major investment of national financial resources. This is only feasible in affluent industrialized countries such as Japan for gastric cancer, some western countries for oesophageal and colorectal cancer. Only population screening for colorectal cancer has been proven feasible and cost-beneficial.
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PMID:Cancer of the gastrointestinal tract: early detection or early prevention? 1507 91

The demographics of esophageal and gastric cancer have been changing dramatically in the United States over the past several decades. While incidence rates for esophageal squamous cell carcinoma and distal gastric carcinoma have been declining, the trends for adenocarcinoma of the esophagus and proximal stomach have been rising rapidly, particularly among white males. The incidence of these upper gastrointestinal (GI) malignancies varies widely based on geographic location, race, and socioeconomic status. The primary causes of squamous cell carcinoma of the esophagus are tobacco use and alcohol consumption, whereas the main risk factors for adenocarcinoma of the esophagus are gastroesophageal reflux disease and obesity. Dietary factors and Helicobacter pylori infection play an important role in the development of gastric cancer. Understanding the epidemiology and etiologies of esophageal and gastric carcinomas will lead to the development of interventions for screening and prevention in high-risk populations.
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PMID:Epidemiology of upper gastrointestinal malignancies. 1529 38

Gastric bypass is a clinical option for obesity surgery. An increased susceptibility to Helicobacter pylori infection in the bypassed stomach has been speculated. The aim of the present study was to examine the susceptibility of the bypassed stomach to H. pylori infection in rats and mice. Adult Sprague-Dawley and Wistar rats and NMRI mice were subjected to either gastric bypass or laparotomy only as control. The animals were inoculated with the CagA- and VacA- positive H. pylori strain 67/21 (not mouse-adapted) in the first experiment and with 9 additional isolates in the second, by injection into the bypassed stomach or the control stomach during surgery. The stomach of each animal was collected for H. pylori culture 2-3 weeks later. While all the rats were H. pylori negative, 54% of gastric bypassed mice and 75% of controls were positive (P = 0.4). We conclude that susceptibility to H. pylori infection in the stomach is not increased by gastric bypass surgery.
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PMID:Gastric bypass surgery does not increase susceptibility to Helicobacter pylori infection in the stomach of rat or mouse. 1625 42

The authors' aim in this study was to explore the prevalence, symptomatology, and risk factors for peptic ulcer in a general adult population. Between December 1998 and June 2001, the authors surveyed a random sample (n=3,000) of the adult population (n=21,610) in two communities in northern Sweden using a validated questionnaire, the Abdominal Symptom Questionnaire (response rate=74%). A subsample (n=1,001) of the responders was randomly invited to undergo esophagogastroduodenoscopy and symptom assessment (response rate=73%). The prevalence of peptic ulcer was 4.1% (20 gastric ulcers and 21 duodenal ulcers). Nausea and gastroesophageal reflux were significant predictors of peptic ulcer disease, but epigastric pain/discomfort was not. Six persons with gastric ulcer and two persons with duodenal ulcer were asymptomatic. Eight subjects with duodenal ulcer (38%) lacked evidence of current Helicobacter pylori infection. Five (25%) of the gastric ulcers and four (19%) of the duodenal ulcers were idiopathic (no use of aspirin or nonsteroidal antiinflammatory drugs, no H. pylori infection). Smoking, aspirin use, and obesity were risk factors for gastric ulcer; smoking, low-dose (<or=160 mg) aspirin use, and H. pylori infection were risk factors for duodenal ulcer. Peptic ulcer disease often coexists with atypical symptoms or no symptoms at all, and idiopathic duodenal ulcer may be more common than anticipated.
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PMID:Peptic ulcer disease in a general adult population: the Kalixanda study: a random population-based study. 1655 43


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