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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of a 5-year follow-up of 289 consecutive, peptic ulcer patients treated by antrectomy and gastroduodenostomy, with or without vagotomy, are presented. Patients with a preoperative gastric acid secretory capacity (PAO) below 40 mmol/h were treated by antrectomy alone, while subjects with a higher PAO had a vagotomy in addition. The antrectomy was defined by lithmus indication of the corpus-antrum border and by histologic verification, including gastrin cell counting. The over all incidence of gastroscopically verified recurrent ulceration was 8.5%. In patients with ulcer location in the bulb or the pyloric/prepyloric region (juxtapyloric ulcer) and treated by antrectomy alone, the recurrence rate was 18% (n = 102), and in gastric ulcer patients it was 4% (n = 47). Altogether 14 patients with recurrent ulcer were subsequently reoperated on by vagotomy showing no further recurrence. Antrectomy combined with vagotomy was primarily performed almost exclusively in patients with juxtapyloric ulceration, in whom the recurrence rate was 2% (n = 106). According to a postoperative insulin test, the patients with recurrence after antrectomy and vagotomy were incompletely vagotomized. In patients who remained free of symptoms or signs of recurrent disease, the median reduction in gastric acid secretory capacity was about 60% after antrectomy alone and 80% after antrectomy and vagotomy. In juxtapyloric ulcer patients with recurrence after antrectomy alone there was a small median reduction in PAO one month after operation (26%) and then an increase close to the preoperative level (6% reduction). In patients with a postoperative reduction in PAO of less than 35%, there was a high probability of recurrent ulcer, about 70%. In spite of selection of patients with a comparatively low preoperative PAO (less than 40 mmol/h) for antrectomy alone, the recurrence rate was 18% in patients with juxtapyloric ulcer location. In this selected group of patients the preoperative PAO was not higher in patients with ulcer recurrence than in patients who were asymptomatic after the operation. Selecting patients with juxtapyloric ulcer for antrectomy, with or without vagotomy, on the basis of gastric acid secretory capacity therefore seems unjustified. When vagotomy was added to antrectomy and gastroduodenostomy it seemed to increase the risk of developing serious (Visick 3u and 4) postgastrectomy syndromes; 12% after antrectomy and vagotomy versus 3% after antrectomy alone. Vagotomy appeared to be associated with an increased risk of bile reflux gastritis, gastric mycosis, and milk intolerance. Dumping and diarrhoea after vagotomy often coincided with milk intolerance. Antrectomy, with or without vagotomy, did not markedly impair recorded nutritional parameters.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Antrectomy and gastroduodenostomy with or without vagotomy in peptic ulcer disease. A prospective study with a 5-year follow-up. 657 6

In patients with peptic ulceration, both vagal stimulation by insulin hypoglycaemia and stimulation by pentagastrin cause pepsin 1 to be secreted into gastric juice. There is a secretory threshold for pepsin 1, below which only pepsins 3 and 5 are secreted. Pepsin 1 accounts for an increasing proportion of the total peptic activity/ml of gastric juice as the total activity increases. Higher concentrations of pepsin 1 in the basal gastric secretion occurred significantly more frequently in patients with duodenal ulcer than with gastric ulcer. In these patients there may be an increased 'background' secretory drive.
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PMID:Pepsin 1 secretion in chronic peptic ulceration. 677 16

Among an initial series of 103 patients with selective vagotomy plus pyloroplasty for duodenal ulcer, 9 patients died of causes unrelated to ulcer and 7 were lost to follow-up without signs or symptoms of ulcer 8 to 15 years after operation; the remaining 87 patients were followed up for 12 to 17 years. Insulin testing revealed only one inadequate vagotomy in a patient who had a recurrence in the short term. Insulin tests were negative in 61 and negative or adequate in 6 other patients. Complete vagotomy reduced basal secretion effectively in the great majority of patients but not in a small minority. Three patients had antral hyperfunction with persistent hypersecretion despite complete vagotomy as indicated by two negative insulin tests in each patient. Inexplicably, only one of these patients had a stomal ulcer recurrence. Long-term follow-up revealed the development of gastric ulcer in one patient wit stasis from a pyloroplasty stenosed by angulation from adhesions. Three other patients, one with ulcer and two with hemorrhagic gastritis, developed gastric ulceration in the long term despite low acid output and negative insulin tests. Biliary reflux was demonstrated in two of these three patients and was probably the cause of gastric ulcer in the third. Pre- and postoperative cholecystograms in 66 patients showed the formation of gallstones in 4 patients after vagotomy. Another patient who did not undergo cholecystography developed acute cholecystitis from stone. This rate of gallstone formation was the normal expected rate and was not increased as in some series of total vagotomy. Dumping with and without associated diarrhea was the most frequent and troublesome sequela. Postvagotomy diarrhea did not occur. To prevent dumping, and also to decrease acid secretion more effectively, pyloroplasty was abandoned in favor of Maki's pyloruspreserving antrectomy to complement selective vagotomy in 1968.
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PMID:Long-term results of selective vagotomy plus pyloroplasty. 12 to 17 year follow-up. 746 6

A 58-year-old woman was admitted to our hospital for impaired consciousness, hyperglycemia and bitemporal hemianopsia. She was diagnosed as having NIDDM one year ago and was treated with diet and glibenclamide (1.25 mg/day) for 6 months. However, she stopped her medical treatment one month ago and then polydipsia and general fatigue were manifested. She was admitted to a hospital five days ago at which time hyperglycemia (405 mg/dl) and anemia (Hb8.0g/dl) were detected. She was transferred to our hospital for control of blood glucose and further examination of bitemporal hemianopsia. She showed typical acromegalic features including enlargement of the nose, lips and tongue, increased heel pad and acral growth. Conscious disturbance was cured by the infusion of saline and the administration of insulin. Endoscopy revealed an active gastric ulcer (A1). Endocrine data disclosed increased GH levels in plasma and urine, whereas plasma IGF-1 levels were low. Plasma GH paradoxically increased following the administration of TRH. A water deprivation test showed an impaired increase in urinary osmolarity, indicating partial central diabetes insipidus (DI). MRI with Gd-contrast revealed a macroadenoma which progressed toward suprasella. She was diagnosed as having acromegaly, partial DI and probable hyperosmolar hyperglycemic nonketotic diabetic pre-coma. Polyuria (5-101/day) due to partial DI was controlled by the administration of DDAVP (10 micrograms/day). The constant subcutaneous administration of octreotide (240 micrograms/day) resulted in normal plasma GH levels and a marked shrinkage of the pituitary tumor. The pituitary tumor was finally removed by the transsphenoidal approach following treatment with octreotide for 4 months. HE staining of the pituitary tumor showed atrophic and acidophilic cells surrounded by hyaloid connective tissue. After the surgery, plasma GH levels were normalized and complications were cured. In conclusion, this is a very rare case of acromegaly associated with diabetic pre-coma and partial DI, and effectively treated with constant subcutaneous infusion of octreotide.
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PMID:[Effective treatment with constant subcutaneous infusion of octreotide in a patient with acromegaly associated with diabetic pre-coma and diabetes insipidus]. 785 21

Between 1975 and 1980, 30 patients with type I corporeal gastric ulcer were randomly allocated to undergo selective proximal vagotomy with ulcer excision or partial gastrectomy with gastroduodenostomy. Sixteen patients underwent selective proximal vagotomy (1 was excluded from the follow-up since microscopic examination of the excised ulcer revealed an early gastric cancer) and 14 underwent partial gastrectomy. No significant differences in the clinical results were found 3 years after surgery. During a median follow-up of 10 years, ulcer recurred in 3 patients after selective proximal vagotomy and in 2 after partial gastrectomy. One patient in each group had recurrent ulcer without symptoms and received no treatment. Two selective proximal vagotomy patients and three partial gastrectomy patients had epigastric pain with or without ulcer. One patient with selective proximal vagotomy underwent a second operation because of epigastric pain and recurrent ulcer. Bowel habits remained unchanged in all but one patient in each group, and mild or moderate dumping was recorded for two patients in each group. Very good or good results (modified Visick scale) were recorded for 11 of 15 patients after selective proximal vagotomy and for 10 of 14 patients after partial gastrectomy. Except for one patient in each group who had moderate dumping, patients classified as Visick III or IV had no symptoms during treatment with antacids or H2-blockers, or had asymptomatic ulcers and needed no treatment. Selective proximal vagotomy reduced the median acid response to insulin hypoglycemia and to pentagastrin by 100% and 80%, respectively, for at least 3 to 5 years, and partial gastrectomy reduced the median acid response to pentagastrin by 97%. In our opinion, selective proximal vagotomy with ulcer excision is an alternative to partial gastrectomy for surgically treating type I gastric ulcer.
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PMID:Ten-year follow-up of a prospective, randomized trial of selective proximal vagotomy with ulcer excision and partial gastrectomy with gastroduodenostomy for treating corporeal gastric ulcer. 820 35

A 57-year-old man was admitted to our hospital for hepatic encephalopathy. He previously had undergone a partial gastrectomy for gastric ulcer, and also had been on maintenance hemodialysis because of diabetic nephropathy. Despite treatment with branched-chain amino acids and lactulose, encephalopathy occurred repeatedly. The findings of his laboratory examinations, computed tomography, and liver biopsy were not suggestive of chronic liver damage. Angiography revealed a portal-systemic shunt from the superior mesenteric vein via the left gastric vein to the left renal vein. A ligation of the gastrorenal shunt was performed. After the shunt ligation, hepatic encephalopathy no longer recurred, and no medication was required to prevent it. The insulin requirements also decreased, the plasma ammonia concentration then decreased, and serum concentration of several amino acids related to the ammonia metabolism also decreased. The molar ratio of branched-chain amino acids to aromatic amino acids increased. The ligation of the portal-systemic shunt was thus considered to be the key to the successful treatment of hepatic encephalopathy in this unusual case.
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PMID:Recurring encephalopathy abolished by gastrorenal shunt ligation in a diabetic hemodialysis patient. 946 59

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

In this review article we discuss the role of growth factors in gastric ulcer healing using an in vitro wound repair model with gastric epithelial and mesenchymal cells. Several growth factors accelerate gastric epithelial and mesenchymal wound healing in vitro with acceleration of cell migration and proliferation. Epidermal growth factor, transforming growth factor-alpha (TGFalpha), hepatocyte growth factor, and insulin accelerate predominantly gastric epithelial wound healing; and TGFbeta and basic fibroblast growth factor predominantly accelerate gastric mesenchymal wound healing. Platelet-derived growth factor-betabeta and insulin-like growth factor-1 (IGF-1) accelerate both significantly. Among these growth factors, IGF-1 produced from fibroblasts plays a key role in the gastric epithelial-mesenchymal interaction during the process of gastric wound healing.
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PMID:Epithelial-mesenchymal interaction in gastric mucosal restoration. 1077 21

These three papers present studies on gastrin. The first paper describes a method of biological assay using the rat. The second paper demonstrates that the highest concentration of gastrin-like activity occurs in the antral mucosa, with a clear gradient of concentration of activity down the gut. However, it is to be noted that the total amount of extractable activity is greatest in the duodenum, although the concentration there is less than in the antrum. No activity was detected in the pancreas. The third paper studies the contents of gastrin-like activity in patients with duodenal ulcer and demonstrates higher figures when stenosis is present. Patients with benign gastric ulcer and carcinomata showed results equal to or greater than in those with the average uncomplicated duodenal ulcer. It was noted that two patients with dilated antra both had very low total gastrin-like activity. There was no correlation between total activity and maximal histamine-stimulated output of acid. There was, however, a positive correlation between the insulin-stimulated acid secretion and the total gastrin-like activity in the cases of uncomplicated duodenal ulcers. The clinical studies are still tentative in view of the several variables present, but it seems likely that they will in due course clarify the role of gastrin in the ulcer problem.
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PMID:STUDIES ON GASTRIN. 1420 16

Gastric mucosa of diabetic rats is highly vulnerable to acute injury, but little is known about the influence of diabetic conditions on the healing of gastric ulcers. In this study, streptozotocin (70 mg/kg injected intraperitoneally) was used to induce diabetes mellitus in rats. Four weeks after streptozotocin injection, gastric ulcers were induced using the acetic acid method, and 10 days later, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively. Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNF alpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. In the diabetic rats, a significant delay in ulcer healing ( approximately by 300%), accompanied by a decrease in the gastric mucosal blood flow was observed. The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1 beta (IL-1 beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1 beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. Pentoxifylline, an inhibitor of TNF-alpha, which by itself accelerated ulcer healing in non-diabetic rats, counteracted the increase in the area of gastric ulcer induced by streptozotocin, raised significantly gastric blood flow and suppressed the plasma TNF-alpha levels. Aspirin and rofecoxib, that significantly suppressed the mucosal prostaglandin E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin in non-diabetic rats, and these changes were significantly augmented in diabetic animals. We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes.
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PMID:Impaired gastric ulcer healing in diabetic rats: role of heat shock protein, growth factors, prostaglandins and proinflammatory cytokines. 1464 93


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