Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conventional transcutaneous ultrasound examinations are often compromised by intervening pulmonary or bowel gas and have limited resolution. Ultrasonic probes of frequencies greater than 5 MHz, which enhance resolution, cannot be used successfully on the skin surface, because they do not penetrate deeply enough to view intraabdominal organs in most adults. To overcome these problems, we tested an ultrasonic endoscope which had a 10-MHz, 64-element linear assay, generated real-time images at resolutions of less than 1 mm, and was an integral part of a 35-mm-long and 13-mm-wide endoscopic rigid tip. Thirty-two studies were performed in 15 healthy subjects, 4 patients with pancreatic cancer and 6 patients with chronic pancreatitis, and 1 patient each with a gastric ulcer and a suspected pancreatic abscess. We demonstrated that this procedure is safe, provides high resolution real-time ultrasound visualization of the heart, aorta, spleen, pancreas, liver, gallbladder, kidneys, and gastrointestinal mucosa and can detect moderate-sized pancreatic tumors and hepatic metastases less than 1 cm in diameter. Because endoscopic visualization of gastrointestinal mucosa and ultrasound examination of extraluminal organs can be obtained during a single procedure, rapid differentiation among mucosal and intramural disease of the hollow gut and disease of extraluminal organs should be possible with this diagnostic technique.
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PMID:Human endoscopic ultrasonography. 710 13

A proportional mortality analysis of jewelry workers as identified on death certificates is presented. The study group consisted of 931 males who died in Attleboro, Mass., between 1956 and 1975. An excess proportion of pancreas cancer was found in the entire group (16/9; p < 0.05) and was not explained by ethnic or other non-occupational factors. Job titles were specific enough to identify a subset of polishers and findings for this job category were compared to those for all other categories. Excesses of stomach cancer (odds ratio 4.4; p < 0.01) and stomach ulcer (odds ratio 5.0, p < 0.01) were found, but for each the observed number of deaths is small. Possible important exposures in the jewelry industry are reviewed.
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PMID:Cause of death among jewelry workers. 744 92

We described gene analysis of acid proteinases, cathepsin E (CTSE), pepsinogen A (PGA), and pepsinogen C (PGC), and demonstrated the clinical significance of these genes. CTSE was highly expressed in pancreatic cancer and can be a tumor marker for pancreatic cancer. PGC gene polymorphism was associated with gastric ulcer and can be a subclinical marker of the genetic predisposition to gastric ulcer.
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PMID:[Gene analysis of acid proteases]. 892 Jun 89

In a population-based case-control study of pancreatic cancer conducted in three areas of the USA, 484 cases and 2099 controls were interviewed to evaluate the aetiologic role of several medical conditions/interventions, including diabetes mellitus, cholecystectomy, ulcer/gastrectomy and allergic states. We also evaluated risk associated with family history of cancer. Our findings support previous studies indicating that diabetes is a risk factor for pancreatic cancer, as well as a possible complication of the tumour. A significant positive trend in risk with increasing years prior to diagnosis of pancreatic cancer was apparent (P-value for test of trend = 0.016), with diabetics diagnosed at least 10 years prior to diagnosis having a significant 50% increased risk. Those treated with insulin had risks similar to those not treated with insulin (odds ratio (OR) = 1.6 and 1.5 respectively), and no trend in risk was associated with increasing duration of insulin treatment. Cholecystectomy also appeared to be a risk factor, as well as a consequence of the malignancy. Subjects with a cholecystectomy at least 20 years prior to the diagnosis of pancreatic cancer experienced a 70% increased risk, which was marginally significant. In contrast, subjects with a history of duodenal or gastric ulcer had little or no elevated risk (OR = 1.2; confidence interval = 0.9-1.6). Those treated by gastrectomy had the same risk as those not receiving surgery, providing little support for the hypothesis that gastrectomy is a risk factor for pancreatic cancer. A significant 40% reduced risk was associated with hay fever, a non-significant 50% decreased risk with allergies to animals, and a non-significant 40% reduced risk with allergies to dust/moulds. These associations, however, may be due to chance since no risk reductions were apparent for asthma or several other types of allergies. In addition, we observed significantly increased risks for subjects reporting a first-degree relative with cancers of the pancreas (OR = 3.2), colon (OR = 1.7) or ovary (OR = 5.3) and non-significantly increased risks for cancers of the endometrium (OR = 1.5) or breast (OR = 1.3). The pattern is consistent with the familial predisposition reported for pancreatic cancer and with the array of tumours associated with hereditary non-polyposis colon cancer.
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PMID:Diabetes mellitus, other medical conditions and familial history of cancer as risk factors for pancreatic cancer. 1046 6

We studied accelerated death benefit (ADB) claims at the Dai-ichi Mutual Life Insurance Company (Dai-ichi Life). The ADB provision is designed to pay all or a portion of the death benefit if the insured is expected to die within 6 months. Dai-ichi Life paid 243 ADB claims and did not pay 17 ADB claims between December 1994 and March 1998. Of the 260 ADB claims, 253 (97.3%) were caused by malignant neoplasm, 2 by intracranial hemorrhage, 2 by angina pectoris, 1 by dilated cardiomyopathy, 1 by hepatic cirrhosis, and 1 by bleeding gastric ulcer. The age range of the 243 paid claims at the time when the attendant physician predicted a life expectancy below 6 months was 21.6-72.6 years (48.7 +/- 8.7 years [Mean +/- SD]). By the end of March 2000, 236 cases were followed up among the above 243 paid ADB claims. Of the 236 followed-up cases, 149 (63.1%) died within 6 months and 203 (86.0%) died within 1 year. The range of survival periods of these 236 cases was 6-1516 days (210 +/- 237 days). Of the 217 dead cases due to malignant neoplasm, 45 (20.7%) died of gastric cancer, 44 (20.3%) of lung cancer, 24 (11.1%) of liver cancer, 16 (7.4%) of colon cancer, 13 (6.0%) of rectum cancer, and 12 (5.5%) of pancreatic cancer.
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PMID:Analysis of accelerated death benefit claims at a Japanese life insurance company. 1530 85

Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N-nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.
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PMID:The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease. 1704 24

Thirty years of research with animal models has shown that pancreatic adenocarcinoma is induced by N-nitrosamine carcinogens, which damage DNA through adduct formation. Human risk factors for pancreatic cancer include gastric colonization by Helicobacter pylori, as well as dietary intake of those same N-nitrosamines or of nitrite which forms those N-nitrosamines in the stomach, and cigarette smoking which also contains those N-nitrosamines. Physiologic actions of H. pylori colonization enhance the carcinogenic effect of N-nitrosamines delivered by smoking or dietary sources. This effect is modulated by host inflammatory response to the organism, by various virulence and other properties of the Helicobacter itself, and by host-organism interactions. A recent genome-wide association study identified SNPs within the ABO 9q34 locus as statistically significantly associated with risk of pancreatic cancer. A number of recent and older studies going back 40 yr also support the ABO association. ABO-product antigens are expressed on gastrointestinal epithelium on which H. pylori binds, and ABO genotype is known to be associated with risks of duodenal and gastric ulcer and with risk of gastric cancer, conditions definitively related to Helicobacter colonization. We suspect that ABO genotype/phenotype status influences the behavior of H. pylori which in turn affects gastric and pancreatic secretory function, and these ultimately influence the pancreatic carcinogenicity of dietary- and smoking-related N-nitrosamine exposures, and thus risk of pancreatic cancer. Our study results on the interaction of ABO and H. pylori significantly confirm this hypothesis and together with other existing studies strongly implicate this organism in the disease etiology.
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PMID:Pancreatic cancer: Helicobacter pylori colonization, N-nitrosamine exposures, and ABO blood group. 2216 35

A 60-year-old woman presented to our department with severe tongue pain. On initial examination, the mucosal surface of the tongue was intact but a hard submucosal mass on the dorsum of the tongue was detected on palpation. Magnetic resonance imaging demonstrated an ill-defined tumor in the intrinsic tongue muscles. Sequential whole-body positron emission tomography/computed tomography revealed a tumor of the pancreas apart from the tongue lesion, and upper gastrointestinal endoscopy revealed gastric mucosa ulceration. On biopsy, the tongue lesion was confirmed to be metastatic gastric adenocarcinoma, and the gastric ulcer was simultaneously diagnosed as poorly differentiated gastric adenocarcinoma. The definitive diagnosis was thus gastric adenocarcinoma and synchronous pancreatic cancer, with gastric carcinoma metastases to the tongue. We administered FOLFIRINOX treatment for pancreatic cancer and FLTAX treatment for gastric cancer. Because of difficulty with oral intake due to the growth of the tongue lesion, we administered palliative radiation therapy at a dose of 30 Gy in 10 fractions following which the patient was able to resume oral intake and was satisfied with this outcome. She died 8 months after her first visit to our department.
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PMID:Metastatic gastric adenocarcinoma of the tongue with initial symptoms of glossodynia. 3114 58

Incretin contains two peptides named glucagon-like peptide-1(GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Drug therapy using incretin has become a new strategy for diabetic treatments due to its significant effects on improving insulin receptors and promoting insulinotropic secretion. Considering the fact that diabetes millitus is a key risk factor for almost all age-related diseases, the extensive protective roles of incretin in chronic diseases have received great attention. Based on the evidence from animal experiments, where incretin can protect against the pathophysiological processes of neurodegenerative diseases, clinical trials for the treatments of Alzheimer's disease (AD) and Parkinson's disease (PD) patients are currently ongoing. Moreover, the protective effect of incretin on heart has been observed in cardiac myocytes, smooth muscle cells and endothelial cells of vessels. Meanwhile, incretin can also inhibit the proliferation of aortic vascular smooth muscle cells, which can induce atherosclerogenesis. Incretin is also beneficial for diabetic microvascular complications, including nephropathy, retinopathy and gastric ulcer, as well as the hepatic-related diseases such as NAFLD and NASH. Besides, the anti-tumor properties of incretin have been proven in diverse cancers including ovarian cancer, pancreas cancer, prostate cancer and breast cancer.
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PMID:Protective Effects of Incretin Against Age-Related Diseases. 3162 2