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)

Gastric juice from 15 normals, 20 patients with gastric ulcer and 14 patients with erosive haemorrhagic gastroduodenitis was investigated in respect of its activity on unheated and heated fibrin plates and its content of FDP and plasminogen or plasmin with immunochemical methods. Gastric juice from normals showed no activity on unheated and heated fibrin plates, and no FDP or plasminogen could be demonstrated. In the patients with gastric ulcer the gastric juice showed little or no fibrinolytic activity on fibrin plates except in 2, who had regurgitation of duodenal juice and neutral pH of the juice. These patients had equally high activity on heated as on unheated plates and no plasmin could be demonstrated. It was shown that this activity was not due to fibrinolysis, but to non-specific proteolytic activity (probably trypsin). The patients with erosive haemorrhage gastroduodenitis exhibited quite a different picture. The gastric juice from these patients showed extremely high activity on fibrin plates, the activity was higher on unheated than on heated plates. The activity was inhibited in vitro by addition of EACA and in vivo after administration of AMCA. The occurence of plasmic could be demonstrated directly immunologically in the gastric juice. By comparsion of plasmin and trypsin in various assays it could further be improved that the gastric juice in these cases contained plasminogen activator and plasmin. The patients with erosive haemorrhagic gastroduodenitis showed no increase in fibrinolysis in the blood, but low values for plasminogen and alpha2-M, and the serum contained FDP. These findings in the blood and gastric juice were interpreted as signs of local fibrinolysis in the stomach and duodenum. There is reason to assume that this gastric fibrinolysis contributes substantially to the bleeding tendency. The effect of administration of AMCA on fibrinolytic activity and the haemorrhage lends support to the assumption of such a mechanism.
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PMID:Gastric fibrinolysis. 0 Aug 7

Anti-ulcer effects of cetraxate, a new compound possessing anti-plasmin, anti-casein and anti-trypsin actions were investigated by using experimental gastric ulcer models in rats. Cetraxate, 300 mg/kg p.o. showed significant inhibitory effects of 65.3%, 70.0%, 30.2%, and 67.1% against aucte types of ulcers producing by aspirin, phenylbutazone, indomethacin, and pyloric ligature (Shay's ulcer), respectively. These effects were greater than those obtained by gefarnate and aluminum sucrose sulfate may be mainly attributed to the protecting action of this drug on gastric mucosa. Ctraxate further revealed remarkable inhibitory effects on chronic types of ulcers produced by acetic acid, clamping, and clamping-cortisone. In acetic acid ulcer in particular, cetraxate was found to have a dose-dependent inhibitory effect at doses over 50 mg/kg. Of test drugs including L-glutamine and methylmethionine sulfonium chloride, cetraxate showed the most remarkable inhibitory effect on beta-glucuronidase activity in ulcer tissue of these three types of ulcers. These findings suggest that cetraxate may prevent the connective tissue in the ulcer location from decomposition due to lysosomal enzymes such as beta-glucuronidase, thereby accelerating the recovery from ulcer.
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PMID:Anti-ulcer effects of 4'-(2-carboxyetyl) phenyl trans-4-aminomethyl cyclohexanecarboxylate hydrochloride (cetraxate) on various experimental gastric ulcers in rats. 100 3

Tryptase, a serine endoprotease, was determined in mucosal biopsies from fundus, corpus, antrum and corpus-fundus of the stomach and from the duodenum in 15 controls, 66 patients with duodenal ulcer, 22 with gastric ulcer and 9 with duodenitis. Intra- and inter-assay coefficients of variation ranged from 3.3% to 8.0% and from 3.5% to 8.6%, respectively. In controls, the highest values for tryptase were found in the fundus and progressively decreased in the corpus, antrum and duodenum. Analysis of variance of data from repeated measurements, performed in six subjects having multiple determinations, achieved statistical significance (F = 16.85, P less than 0.001). Data from the corpus-fundus area documented a significant difference among patient groups (F = 2.70, P less than 0.05). Patients with an active gastric ulcer had higher mean values when compared to controls and to patients with healed gastric ulcer. A similar trend was found in patients with active duodenal ulcer. Furthermore, corpus-fundus tryptase evaluated longitudinally in three patients with an active ulcer (point A) and after healing (point B), showed significant decrease from point A to point B. By contrast it remained elevated or showed only minor decrease in two patients with a persistent active ulcer.
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PMID:Measurement of tryptase in endoscopic gastroduodenal biopsies: distribution and relationship with ulcer disease. 157 72

Radioimmunoassay was used to determine trypsin, pepsinogen and gastrin content in the blood serum with the use of kits produced by the firm "Oris" (France). A total of 43 patients with peptic ulcer (25 with duodenal ulcer and 18 with gastric ulcer), 20 patients with chronic gastritis and 10 normal subjects were investigated. The study was conducted on an empty stomach and after a test breakfast consisting of 2 boiled eggs, 100 g of cheese, 100 g of white bread, 25 g of butter, 50 g of sugar and 200 g of tea (57 g of proteins, 63 g of fats, 103 g of carbohydrates; calorie value comprised 1212 kcal). It has been shown that food intake is a regulator of gastrin, pepsinogen and trypsin production that permits evaluating functional possibilities of gastrin-producing cells, the main gastric cells and acinar cells of the pancreas. The investigation conducted has evidenced that compensatory shifts in the levels of gastrin, pepsinogen and trypsin taking place in gastroduodenal disease are directed to the improvement of digestive processes.
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PMID:[The effect of food intake on the content of proteolytic enzymes and gastrin in the blood of patients with peptic ulcer and chronic atrophic gastritis]. 179 41

Blood serum insulin, glucagon, pepsinogen, trypsin was studied by radioimmunological methods in 95 patients with ulcer disease. Fasting values and values 1 and 2 hours after a standard breakfast (1212 kcal) were evaluated. It was established that all patients showed a statistically valid increase of the basal level of glucagon while patients with gastric ulcer showed an increase of the basal insulin level. Use of a test breakfast showed reserve and compensatory capacities of the hormonal pancreatic function. Patients with gastric and duodenal ulcer revealed an increase of the pepsinogen level under conditions of basal secretion and after a test breakfast.
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PMID:[Pancreatic hormonal function and proteolytic activity in peptic ulcer]. 208 6

We here ascertain whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (CD, a lysosomal hydrolase that seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori (Hp) infection. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer, and 11 with duodenitis. Tryptase and CD were measured in mucosal biopsies (body and antrum of the stomach and duodenum) using IRMA methods. Hp infection was histologically evaluated (Giemsa). Tryptase and CD levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. In Hp-positive patients the CD mucosal content was higher while tryptase mucosal levels were lower than in Hp-negative patients. Tryptase was correlated with gastrin content. CD seems to be mainly related to the phlogistic reaction of the mucosa to Hp infection; tryptase may reflect an indirect link between Hp infection, gastrin release, and the function of mast cells.
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PMID:Influence of Helicobacter pylori on tryptase and cathepsin D in peptic ulcer. 758 35

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others, Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method. Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated with Helicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa to Helicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.
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PMID:Are tryptase and cathepsin D related to Helicobacter pylori infection and mucosal gastrin in peptic ulcer? 820 35

Numerous studies have shown that alcohol causes both acute and chronic damage to gastroduodenal mucosa. The methods of damage differ however, and experimental studies in animals have shown that the degranulation of mast cells in gastric mucosa causes acute hemorrhagic lesions after the consumption of alcohol. It is not known whether this mechanism also operates in man. The aim of the present study was therefore to evaluate whether there is a correlation between mast-cell activation, determined by assaying tryptase levels in gastric mucosa, and the consumption of alcohol in patients with ulcerative diseases. Thirty-one patients with cicatrized ulcerative lesions (13 gastric ulcers, 18 duodenal ulcers) were included in the study. Biopsies at the level of the gastric fundus and antrum and the duodenal bulb were performed in all patients to determine tryptase levels. Biopsy material was frozen and subsequently homogenized; the enzyme was assayed in the supernatant using a radioimmunometric method. The mean daily alcohol consumption was calculated in clinical terms for each patient over the past 5 years and patients were subdivided into non-drinkers and moderate (< 60 g alcohol/day) and excessive (> 60 g alcohol/day) drinkers. It was found that tryptase concentrations were higher in the fundus compared to the gastric antrum and duodenal bulb, irrespective of alcohol consumption both in patients with gastric ulcer and duodenal ulcer. The importance of mast cells in provoking alcohol-dependent damage was studied at a gastric level. Alcohol leads to their degranulation and therefore contributes to the formation of gastric lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Alcohol-dependent mast cell activation in ulcer]. 835 86