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

The role of tissue-type plasminogen activator (t-PA) was investigated in the gastric ulcer formation induced by microvascular derangement. The rat stomach was exposed and repeated electrical stimuli (irritation) were applied on the small arterial wall close to the lesser curvature to induce mucosal ischemia followed by hyperemia. The t-PA activity in the regional blood of the stomach was significantly elevated as early as 5 min after the irritation. Immunohistochemical study using anti-t-PA monoclonal antibody revealed that t-PA was detectable in the endothelial cells of capillaries and collecting venules, suggesting the involvement of endothelium-mediated fibrinolytic activity in the irritation-induced ulcer formation. Pretreatment of SOD or allopurinol significantly attenuated the irritation-induced t-PA activation, suggesting that the t-PA activity was modulated by xanthine oxidase-associated superoxide anions. CV-6209, a selective antagonist of platelet-activating factor (PAF), also prevented the activation of t-PA as well as ulcer formation, providing a concept that PAF may be associated with the local fibrinolytic activation which may cause hemorrhagic changes in the gastric mucosal microvasculature. The present study supports the hypothesis that increased t-PA activity may reflect the microvascular endothelial damages caused by vasomotor derangement and suggests that oxygen-derived free radicals may participate in the regulation of endothelium-derived fibrinolytic activities in the mucosal microvasculature.
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PMID:Involvement of superoxide anion and platelet-activating factor in increased tissue-type plasminogen activator during rat gastric microvascular damages. 165 Sep 66

The mucosal fibrinolytic activity was estimated in 24 patients with duodenal ulcer and in 11 patients with gastric ulcer. The fibrinolytic activity was estimated in biopsy specimens taken during gastroscopy. Specimens were taken in the corpus, in the antrum, and in the duodenal mucosa. In patients with duodenal ulcer the fibrinolytic activity was significantly higher in the corpus and antrum mucosa, whereas no difference was observed in the duodenal mucosa compared with controls. Gastric ulcer patients had, compared with controls, significantly higher activity in the corpus mucosa only. Fourteen patients with duodenal ulcer and five with gastric ulcer were treated with 1 g cimetidine daily for 4 weeks. The mucosal fibrinolytic activity was estimated before and after treatment in the above-mentioned regions. A significant reduction was observed after treatment in patients with duodenal ulcer, both in the corpus and in the duodenal mucosa, whereas no difference was seen in the duodenum. In patients with gastric ulcer a reduction was observed in the corpus mucosa only. The fibrinolytic activity estimated was plasminogen activator, and not other proteases, in all estimations.
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PMID:The antifibrinolytic properties of cimetidine. 346 84

The roles for the fibrinolytic activation and disorder of coagulation in formation of gastric ulcer induced by microvascular derangement were investigated. The rat stomach was exposed and repeated electrical stimuli (RES) were applied on the small arterial wall close to the lesser curvature to induce mucosal microcirculatory disturbances. The level of tissue-type plasminogen activator (t-PA), a key enzyme for fibrinolytic activity, in the regional blood of the stomach was significantly elevated immediately after RES. At 5 min after RES, the leakage of FITC-labeled albumin and thrombus formation in the mucosal microvasculature were visually demonstrated by using an intravital microscopic system. At 30 min, hemorrhagic erosions and linear ulcers were observed in the gastric mucosa. Pretreatment with human antithrombin-III (AT-III) in the range of 0.1-10 U/kg dose-dependently attenuated both the fibrinolytic activation and microvascular alteration promoted by RES. Human AT-III also prevented RES-induced gastric mucosal injury. Thrombin inhibitory activity in the gastric vein decreased (69.0 +/- 2.1%) just after RES, and further reduced at 30 min (47.7 +/- 5.3%). The present study suggests a hypothesis that human AT-III has a preventive effect on the gastric mucosal hemorrhagic changes via attenuating the fibrinolytic activation and subsequent microcirculatory disturbances.
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PMID:Attenuating effect of antithrombin III on the fibrinolytic activation and microvascular derangement in rat gastric mucosa. 816 29

The gastroduodenal mucosa has a rich blood supply. An active fibrinolytic system is presumably required to maintain vascular patency, and impairment may result in reduced blood flow, focal tissue necrosis, and peptic ulcerogenesis. Tissue type and urokinase type plasminogen activator activity (expressed as mIU/mg protein) and plasminogen activator inhibitor type-1 antigen were assayed in homogenates of gastric and duodenal biopsy specimens taken from patients with: normal endoscopy (controls) (n = 14); active duodenal ulcer (n = 21); healed duodenal ulcer (n = 12); and active benign gastric ulcer (n = 15). In controls mean duodenal tissue type plasminogen activator activity was 4110 and urokinase type plasminogen activator activity 150; gastric tissue type plasminogen activator was 2760 and urokinase type plasminogen activator 170; plasminogen activator inhibitor type-1 was generally undetectable. At the edge of active duodenal ulcers tissue type plasminogen activator was considerably reduced, 2220 (p < 0.001) whereas urokinase type plasminogen activator was raised, 290 (p < 0.01). At the edge of active benign gastric ulcers tissue type plasminogen activator was substantially reduced, 1160 (p < 0.001) but urokinase type plasminogen activator was unchanged. At the scar of healed duodenal ulcers tissue type plasminogen activator was slightly reduced, 3290, but urokinase type plasminogen activator was increased, 308 (p < 0.05). H2 receptor antagonist treatment had little effect on tissue type or urokinase type plasminogen activator activity. Plasminogen activator inhibitor type-1 was increased at the edge of active ulcers (p < 0.05) especially when tissue type plasminogen activity was low (r = -0.61, p < 0.05). These findings are consistent with the hypothesis that impaired fibrinolytic activity may be implicated in peptic ulcerogenesis.
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PMID:Reduced tissue type plasminogen activator activity of the gastroduodenal mucosa in peptic ulcer disease. 824 93

In the present study, we determined the plasma and tissue concentrations of tissue-type plasminogen activator, urokinase-type plasminogen activator, plasminogen activator inhibitor-1, plasminogen activator inhibitor-2 and urokinase-type plasminogen activator receptor in 32 patients with pathology-proved gastric cancer. The plasma levels of the same markers were compared in 37 patients with benign gastric ulcer in order to find out if these plasma levels could be used to evaluate the prognostic value in patients with gastric cancer. Plasma plasminogen activator inhibitor-1 was significantly higher in gastric cancer than in benign gastric disease (p < 0.0005), whereas plasma urokinase-type plasminogen activator was significantly lower in patients with gastric cancer than in those with benign ulcer (p = 0.003). There was no significant correlation between tissue and plasma concentrations of the same parameters. The plasma and tissue levels of fibrinolytic parameters were not affected by tumor size or distant metastasis, whereas tumor tissue concentration of urokinase-type plasminogen activator receptor and plasminogen activator inhibitor-2 were significantly higher in N0 than in N1 and N2, and tissue plasminogen activator inhibitor-1 was significantly higher in N0 than in N1. Plasma levels of the five fibrinolytic parameters could not take the place of the corresponding tissue concentrations on the diagnosis and prediction of prognosis in patients with gastric cancer. Tissue concentrations of urokinase-type plasminogen activator receptor and plasminogen activator inhibitor-2, especially the latter, can be used to predict lymph node involvement in patients with gastric cancer.
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PMID:Diagnostic and prognostic values of plasma levels of fibrinolytic markers in gastric cancer. 970 Aug 49

A 69-year-old male presented with symptoms of fulminant lung embolism and, despite immediate therapy with plasminogen activator, died of acute right heart failure. At autopsy multiple tumor cell emboli were detected in small pulmonary vessels in addition to widespread liver metastases from an urothelial carcinoma. - In a 23-year-old female a malignant gastric ulcer and multiple liver metastases were diagnosed at initial presentation. She too died from pulmonary hypertension due to a series of lung embolisms which occurred despite heparin therapy. At autopsy, many small pulmonary arteries were filled with adenocarcinoma cells; the primary gastric tumor and liver metastases were confirmed. These cases demonstrate that the shedding of tumor cells from hepatic metastases can obstruct the pulmonary vessels and lead to acute cor pulmonale. Tumor cell emboli should be considered in the differential diagnosis of acute pulmonary hypertension, especially in patients with a known tumor. They may, however, also represent the first clinical signs of previously unrecognized malignancy.
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PMID:[Tumor cell embolism to pulmonary arteries]. 1155 62

Extract: When we are wounded, either externally (for instance, when we cut ourselves) or internally (for instance, due to gastric ulcer or brain hemorrhage), blood clots -- sponge-like plugs that are rapidly formed in response to the injury by activated blood platelets and fibrin in a process called coagulation -- prevent profound bleeding. Thus, good or hemostatic clots save our lives. However, under pathological conditions blood clots can also form inside vessels. Such bad or thrombotic clots occlude blood vessels and cause oxygen starvation of vital organs including the brain (stroke), heart (acute myocardial infarction) or lungs (pulmonary embolism). Thrombosis is one of the leading causes of morbidity and mortality from cardiovascular and other disease conditions. Diverse anti-thrombotic means are being developed. For instance, anticoagulants (such as heparin) and platelet inhibitors (such as aspirin) help to prevent formation of clots (blood thinners). Fibrinolytics, known as plasminogen activators (such as tissue-type plasminogen activator, or tPA) dissolve formed clots by degrading the fibrin meshwork. Both types of therapeutics are widely used in medical practice, e.g., for treatment of two forms of ischemic heart disease caused by thrombi in coronary vessels -- acute myocardial infarction and unstable angina.
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PMID:Coupling of anti-thrombotic agents to red blood cells offers safer and more effective management of thrombosis. 2070 55

We discuss the case of a 55-year-old woman with a history of gastric ulcer, mechanical tricuspid and mitral valve replacement and a pacemaker for post-operative total heart block. The patient underwent elective pacemaker replacement. She developed a large infra-umbilical rectal sheath haematoma during bridging therapy with low-molecular-weight heparins (LMWH), for which she was treated with angiographic embolisation of the epigastric artery. Subsequently, an intravenous unfractionated heparin (UFH) drip was started. Shortly thereafter, the patient developed severe upper gastrointestinal bleeding, caused by a gastric ulcer with a visible vessel. Anticoagulant therapy was interrupted. On the third day after cessation of the UFH drip, the patient developed thrombosis of the prosthetic tricuspid valve, confirmed by transthoracic echocardiography and cinefluoroscopy. Due to the risk of bleeding (from gastric ulcer and rectus sheath), both thrombolytic therapy and redo surgery were deemed to pose an unacceptable risk. We decided to treat the patient with intravenous heparin and postpone thrombolytic therapy until after healing of the gastric ulcer. At 5 weeks after the bleeding event, alteplase was administered, with dissolution of the thrombus and restoration of valve disc motion. No embolic or bleeding complications occurred thereafter and six months after the event, the patient is in excellent general condition.
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PMID:Success of delayed thrombolysis for metallic tricuspid valve thrombosis. 2264 81