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)

It is known that Helicobacter pylori (H. pylori) plays an important role in gastritis and peptic ulcer disease in the general population. Although upper gastrointestinal mucosal lesions have been one of the most common complications in patients with chronic renal failure, quite few reports are available regarding the prevalence of H. pylori and its influence on the upper gastro-intestinal tract. The present study was conducted to examine whether H. pylori is involved in the pathogenesis of upper gastrointestinal mucosal lesions in dialysis patients. The subjects consisted of 43 dialysis patients with upper gastro-intestinal tract symptoms. Thirty-four patients without any known kidney disease were used as controls. Gastric mucosa and gastric juice were obtained endoscopically. For the determination of H. pylori, culture of biopsy specimens from the gastric mucosa and histopathological examination with hematoxylin-eosin stain were used. Concentrations of serum gastrin and gastric juice ammonia were also measured. H. pylori was observed in 53.5% of the dialysis group and 64.0% of the controls. Gastro-duodenal lesions in H. pylori-positive dialysis patients included atrophic gastritis, superficial gastritis, erosive gastritis, and gastric ulcer. In the dialysis group, ammonia concentrations in the gastric juice were higher in patients with H. pylori than in those without H. pylori (489.1 +/- 35.8 mu g/ml vs 67.0 +/- 19.2 mu g/ml, p < 0.001). The former value was also higher than that seen in the H. pylori-positive controls (152.4 +/- 18.7 mu g/ml, p < 0.01). Serum levels of gastrin were significantly higher in patients with H. pylori than in patients without H. pylori (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of Helicobacter pylori in gastro-duodenal mucosal lesions in patients with end-stage renal disease under dialysis treatment]. 747 17

Double pylorus is either a congenital abnormality or an acquired complication of peptic ulcer disease. We had followed two patients for 3 and 5 yr, respectively, to observe the processes of formation and the prognosis of double pylorus. Initially, duodenal ulcer was found in one patient with diabetes mellitus and chronic renal failure, and gastric ulcer was found in the other with chronic obstructive pulmonary disease. Both developed double pylorus with refractory courses. In spite of intensive medical treatment, both of them had persistent ulcers in the fistulous tract and failed to develop reepithelization. Helicobacter pylori was found in all of the specimens of gastroduodenal biopsies in both cases. Therefore, we believe that the refractory courses of double pylorus may be related to the underlying diseases and/or the presence of H. pylori. Antibacterial treatment of H. pylori or surgical intervention should be considered for patients with this condition.
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PMID:Double pylorus: report of a longitudinal follow-up in two refractory cases with underlying diseases. 773 94

Helicobacter pylori (Hp) infection is thought to play an important role in for the pathogenesis of atrophic gastritis and even gastric carcinoma. The ratio of Pepsinogen I/II (P I/II) also shows good correlation with atrophic gastritis and gastric ulcer. Since many hemodialysis (HD) and renal transplantation patients suffer from gastrointestinal problems, we investigated the importance of Hp infection and P I/II in these patients. Serum Hp IgG was measured by EIA. Pepsinogen titer was measured with antipepsinogen antibody-bearing beads and anti-pepsinogen antibody. Hp positive HD patients accounted for 50.7% of the subjects. Of the renal transplantation patients, 23.5% were positive with lower values than the HD patients. The value of P I/II in all patients with a high Hp positive titer also was low (under 3). In conclusion, serum IgG antibody to Hp and P I/II exhibit good correlation and both are useful for the diagnosis of atrophic gastritis in chronic renal failure.
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PMID:[Importance of Helicobacter pylori infection and pepsinogen titer in hemodialysis and renal transplantation patients in Japan]. 807 24

We have noticed calcium deposits (gastric mucosal calcinosis, or GMC) in the superficial gastric mucosa of 28 organ transplant patients (OTPs) (11 liver, seven bone marrow, four kidney, three kidney/pancreas, two heart, and one each of liver and kidney transplant) who underwent endoscopic biopsies. The deposits were tinctorially similar to cytomegalovirus inclusions, ranged from 40 to 250 mu in diameter, and were present just beneath the surface epithelium at the tips of the foveolae. An x-ray microanalysis showed that these mucosal deposits contained the elements aluminum, phosphorus, calcium, and chlorine. Clinical chart review showed that all OTPs with GMC were taking aluminum-containing antacids or sucralfate. Review of biopsies from gastric ulcer patients found GMC in a significantly smaller percentage than in transplant patients (32.7% vs. 5.1%, p < 0.0002). In addition, all three ulcer patients with calcified deposits were chronic renal failure patients on long-term aluminum-containing antacid therapy. Gastric mucosal calcinosis appears to be caused by aluminum phosphate accumulation secondary to antacid or sucralfate therapy in organ transplant patients. The presence of GMC in OTPs and chronic renal failure patients rather than other gastric ulcer patients is most likely due to the longer duration of therapy with aluminum-containing compounds in the former two patient groups. The clinical relevance of GMC remains to be seen. In theory, however, accelerated bone demineralization via loss of phosphates and absorption of aluminum in the gastrointestinal tract may be a consequence of long-term aluminum-containing antacid or sucralfate therapy.
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PMID:Gastric mucosal calcinosis. Calcified aluminum phosphate deposits secondary to aluminum-containing antacids or sucralfate therapy in organ transplant patients. 844 8

The role of specific pathological findings in the upper gastrointestinal tract in chronic renal failure remains uncertain. Most of the studies were conducted in the West, and the number of subjects was small. We have tried to look at that problem in Taiwan. Endoscopy to evaluate the source of upper gastrointestinal hemorrhage was performed in 698 patients over a 37-month period; that represents 4.4% of all patients undergoing upper gastrointestinal endoscopy for miscellaneous reasons in that time span. Fifty-eight patients (8.3%) who had been hemodialyzed for chronic renal failure were selected, as were 640 control patients who did not have renal failure. Patients with renal transplant were not included. Endoscopic diagnoses, contributing factors of bleeding, and the course and outcome of the hospitalization were analyzed. chi 2 Test with or without Yates' correction and Student's t test were used as appropriate. Erosive gastritis was the most frequent source of bleeding in patients with chronic renal failure. Erosive gastritis (p < 0.005), erosive esophagitis (p < 0.001), and esophageal ulcer (p < 0.005) were significantly more common causes of bleeding in the renal failure population than in the group without renal failure. The two groups did not differ significantly (p > 0.05) in smoking, heavy alcohol intake, or use of ulcerogenic medications. The age was older (64.1 +/- 11.4 vs. 55.7 +/- 16.2 years) and the mortality rate higher (13% vs. 2%) in patients with renal failure than in those without. The differential diagnoses of upper gastrointestinal bleeding sites differ in patients with and without chronic renal failure; they are diverse. However, erosive gastritis, rather than gastric ulcer or duodenal ulcer, is the most common cause in the patients with renal failure. The mortality rate is significantly higher in these patients than in the general population.
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PMID:Investigation of upper gastrointestinal hemorrhage in chronic renal failure. 877 85

Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
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PMID:Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use. 1040 Apr 1

Any type hemorrhagic manifestation may occur 12 hours to 5 weeks after the administration of beta-lactam antibiotics. The mechanisms of blood losses proved to be by: 1) immunologic thrombocytopenia (penicillins); 2) alteration of platelet functions (semisynthetic penicillins); 3) hypoprothrombinemia (cephalosporins). The risk factors for the occurrence of hemorrhage under beta-lactam antibiotics therapy are: concomitant administration of cytostatics for a neoplastic malignancy; b) acute or chronic renal failure; c) concomitant treatment for duodenal and gastric ulcer; d) malnutrition; e) dosage and duration of antibiotic administration. The frequency of bleeding under beta-lactams is not determined as yet. A severe case diagnosed at the IIIrd Medical Clinic of Iasi presenting spontaneous daily nasal bleedings that occurred 24 hours after the initiation of the treatment with cephalosporins (Kefurox) is presented. In this patient the risk factor was chronic renal failure.
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PMID:[Hemorrhagic risk factors during beta-lactam antibiotics therapy]. 1208 12

The patient was a 62-year-old female. Total gastrectomy was performed due to gastric ulcer in 1969. She was diagnosed as rheumatoid arthritis (RA) in 1985 and was developed to amyloidosis in 1991. She was started on hemodialysis (HD) for chronic renal failure in 1996. In 1998, her arthralgia was aggravated, and 100 mg/day of bucillamine was administered on the day of HD. Her arthralgia persisted, and switching to salazosulfapyridine (SASP) was considered. As there were no standards and no reports for the use of SASP in HD patients, we examined the pharmacokinetics of SASP and its metabolites, and compared our patient with the results of phase one study in normal subjects in Japan. In this case, the blood concentration of SASP was similar to that in healthy controls after single administration of 500 mg of SASP on the day of non-HD, while the concentration of sulfapyridine (SP) was higher than that in healthy donors. However, the blood concentrations of SASP, SP, and N4-acetyl-SP (AcSP) at 24 hours after administration were similar to those obtained in healthy men. SASP was not dialyzed, while about half of SP and AcSP, were dialyzed. In a five-day consecutive administration study also, the blood concentrations of these compounds on Day 5 were similar to those of phase one study, suggesting no accumulation. No adverse drug reaction was observed. As this case had the past history of total gastrectomy and amyloidosis, it is possible that this result is influenced by the factors. Therefore it is necessary to examine pharmacokinetics of SASP and its metabolites beforehand when administering this agent to other HD/RA patients.
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PMID:[Pharmacokinetics of salazosulfapyridine in a hemodialysis patient]. 1291 Sep 67

Gastroduodenal ulcers in renal transplant recipients are usually originated from excessive acid secretion or infection of Helicobacter pyroli. Herein, we report a case of cytomegalovirus (CMV)--induced gastric ulcer following cadaveric renal transplantation. The patient was a 48-year-old man with chronic renal failure and received cadaveric renal transplantation. A month later, he had epigastralgia without CMV-positive antigenemia and received gastrointestinal fiberscopy. Endoscopically, gastric ulcer was identified. Histological findings revealed conspicious nuclear enlargement of the non-epithelial cells in the ulcer bed, which indicated CMV infection. The patient was treated with ganciclovir for 2 weeks and the symptom was relieved. He discharged with a good renal function on day 75 posttransplant. CMV infection plays an important role in gastric ulcer after renal transplantation. Antigenemia assay dose not seem feasible for the detection of CMV-induced gastric ulcer.
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PMID:[Cytomegalovirus infection in peptic ulcer in renal transplant recipient: a case report]. 1550 3

A 12-year-old girl, who had been diagnosed as having Cockayne syndrome (CS), was admitted for emaciation and dehydration. On admission the patient had mild chronic renal failure (glomerular filtration rate: GFR 50 mL/min) and hyperuricemia. After rehydration, allopurinol was commenced for her hyperuricemia. Then, her renal function rapidly deteriorated (GFR 20 mL/min) with enhancement of proximal tubular dysfunction and hypertension. A renal biopsy showed that the patient had acute tubulointerstitial nephritis (ATIN). Based on this diagnosis, allopurinol was stopped and prednisolone was started (2 mg/kg per day), following which the renal tubular function improved. However, the proteinuria intensified to become nephrotic syndrome. After 1 month the patient developed a gastric ulcer. Famotidine was commenced but GFR deteriorated and renal proximal tubular dysfunction re-occurred. The renal pathology was evaluated by referring to the previous reports of renal pathology in CS. It is suggested that rapid deterioration of the renal function in CS patients might be the result of ATIN. In addition, the present nephrotic syndrome seemed to be accompanied by ATIN, as in other reports.
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PMID:Cockayne syndrome with recurrent acute tubulointerstitial nephritis. 1704 Feb 91


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