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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present review concentrates on environmental factors which influence the outcome of peptic ulcer disease by acting from the outside. Endogenous risk factors, such as acid output, pepsin secretion and serum pepsinogen, gastritis and mucosal defense, blood group, and secretor status, are only dealt with when they help to explain the mechanism by which exogenous risk factors affect the upper gastrointestinal mucosa. After outlining the wax and wane of peptic ulcer, it is concluded that these changes resulted from similar temporal patterns of occupational workload in the general population. Cross sectional studies also support the contention of occupational workload being a risk factor in peptic ulcer, explaining several characteristic features of peptic ulcer, such as its sex, race, and social class distribution, increased incidence in immigrant workers, seasonal variation, healing by bed rest, and urban versus rural distribution. Susceptible subjects may react to a rise in occupational workload and acute exposure to stressful life events by increased gastric secretion which, in turn, leads to ulceration and symptoms. Cigarette smoking, intake of aspirin and related drugs, dietary salt, and alcohol abuse represent additional environmental risk factors, which form the etiologic link of the association of peptic ulcer with chronic lung disease, rheumatoid arthritis, hypertensive disease, and liver cirrhosis, respectively.
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PMID:Factors which influence the incidence and course of peptic ulcer. 307 62

To clarify the role of endotoxaemia and congestion of the stomach in the development of acute haemorrhagic gastritis in cirrhotic patients and to investigate the mechanisms of gastric mucosal haemorrhage, the present study was undertaken using rats. Congestion of the stomach was produced by the ligation of gastric veins. Congestion of the stomach or endotoxaemia could not produce gastric mucosal haemorrhage by itself. However, petechial haemorrhage was induced when endotoxin was given to the rats with congestion of the stomach, and the gastric mucosal haemorrhage was largely prevented by administration of gabexate mesilate, an anti-kallikrein drug. Administration of bromelain, which releases prekallikrein and high molecular weight kininogen, instead of endotoxin, also induced gastric mucosal haemorrhage. These findings suggest that the cause of acute haemorrhagic gastritis may be the coexistence of endotoxaemia and congestion of the stomach due to liver cirrhosis and portal hypertension. The mechanisms of the haemorrhage may be as follows: Endotoxin-induced bradykinin acts on the dilated capillaries and small veins in the mucosa and markedly increases their permeability.
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PMID:An experimental study into the cause of acute haemorrhagic gastritis in cirrhosis. 309 56

Our patient, with cirrhosis, portal hypertension, varices, and chronic gastrointestinal bleeding from hemorrhagic gastritis, illustrates an important therapeutic principle. Since the gastritis is related to vascular changes and congestion of the stomach wall secondary to increased portal pressure, and not inflammation, measures aimed at local healing or surgical removal of the bleeding area fail. One must attempt to lower portal pressure with drugs such as propranolol and/or undertake portal decompressive surgery.
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PMID:Persistent hemorrhagic gastritis in a patient with portal hypertension and esophagogastric varices: the role of portal decompressive surgery. 326 69

A retrospective study of the causes and the risk factors for upper digestive hemorrhage (UDH) was carried out by post-mortem investigations in 39 consecutive cases of liver cirrhosis (LC), in comparison with a control group of 40 patients with LC, free of UDH. The patients' age and the disease duration in the cases with ruptured esophageal varices or with hemorrhagic erosive gastritis (the main causes of UDH in the group studied) were longer than in the controls. The causes of UDH were: rupture of esophageal varices (in 43.7% of the cases), hemorrhagic erosive gastritis (41%), both (10.2%), and active duodenal ulcer (5.1%). The frequency of small esophageal varices among the ruptured ones (23%) was higher than that detected by endoscopic studies (13-15%), owing to the peculiarities of the group investigated and to the methods of evaluation. Ascites can be considered a risk factor for UDH, as an expression of portal hypertensions. Liver carcinoma, jaundice, prothrombinemia, albuminemia, bilirubinemia and Child index are not risk factors for UDH, some of them reflecting only a longer evolution of the disease.
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PMID:Study of the risk factors for upper digestive hemorrhage, determined by post-mortem investigations in 39 cases of liver cirrhosis. 326 Oct 33

It is controversial whether the occurrence of ascites and gastrointestinal bleeding in cirrhosis is related to the severity of portal hypertension. Portal pressure was examined in 124 unselected patients with portal hypertension due to chronic liver disease to evaluate this issue. Portal pressure was less in patients without complications of chronic liver disease (11.7 +/- 3.0 mmHg, n = 16) as compared to patients who had bled from varices or erosive gastritis (16.6 +/- 3.4 mmHg, p less than 0.001, n = 49), who had ascites (16.2 +/- 3.0 mmHg, p less than 0.001, n = 78) or both (16.5 +/- 3.0 mmHg, p less than 0.001, n = 19). Portal pressure was similar in patients bleeding from varices and erosive gastritis (16.7 +/- 3.4 mmHg, n = 43; vs 16.2 +/- 4.0 mmHg, n = 6, respectively) and in patients with refractory and nonrefractory ascites (16.2 +/- 3.5, n = 21; vs 16.2 +/- 3.5 mmHg, n = 57). The lowest portal pressure recorded in a patient with variceal bleeding was 9.0 mmHg. The lowest portal pressure recorded in a patient with ascites was 8.0 mmHg. Esophageal varices (graded 0-4 at endoscopy) were larger in patients with a history of bleeding from esophageal varices as compared to patients without such a history (3.2 +/- 0.7 vs 2.0 +/- 0.9, p less than 0.001). Serum albumin concentration was greater in patients without ascites as compared to patients with ascites (33 +/- 5 vs 26 +/- 5 g/l p less than 0.001) but was similar in patients with refractory and nonrefractory ascites (25 +/- 7 vs 26 +/- 5 g/l, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Portal hypertension: a permissive factor only in the development of ascites and variceal bleeding. 349 Jun 15

Intestinal permeability was investigated with a chromium-51-EDTA (edetic acid) absorption test in 36 non-intoxicated alcoholic patients without liver cirrhosis or overt clinical evidence of malabsorption or malnutrition. Patients abstaining from alcohol for less than 4 days almost invariably had higher intestinal permeability than controls, and in many the abnormality persisted for up to 2 weeks after cessation of drinking. The presence of gastritis did not correlate with the presence of increased permeability. The site of altered intestinal permeability was shown by an in-vitro permeability test to be the small bowel. The increased intestinal permeability to toxic "non-absorbable" compounds of less than 5000 molecular weight may account for some of the extraintestinal tissue damage common in alcoholic patients.
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PMID:The leaky gut of alcoholism: possible route of entry for toxic compounds. 614 32

Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.
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PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

One hundred consecutive patients (predominantly men, aged 60 years and older), who were admitted to the Hsinhua Hospital, Shanghai, with acute bleeding from the gastrointestinal tract during a three-year period, were reviewed. The most common causes of bleeding were peptic ulcers, chronic gastritis, prolapse of gastric mucosa, and other benign conditions. In 22 patients, bleeding was either due to oesophageal varices, or was a complication of cor pulmonale. The incidence of malignant disease was 23% (higher than that reported from the United States or the United Kingdom). The mortality rate in patients with benign causes of gastrointestinal bleeding (after exclusion of patients with malignant disease, cor pulmonale, and hepatic cirrhosis) was 4.4%--much lower than the British rate, but slightly higher than that reported in an Australian study. It is hoped that, with the increasing interest in geriatrics, and closer attention to acute bleeding from the gastrointestinal tract in the aged, the mortality rate from this condition will decline.
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PMID:Acute upper gastrointestinal bleeding in the aged. A retrospective analysis of 100 cases. 660 Dec 27

The current medical literature states that upper gastrointestinal bleeding in patients with cirrhosis and portal hypertension originates from a variety of sources. Although variceal bleeding has been recognized as the principal source, acute erosive gastritis and peptic ulcer are said to be the bleeding site in a large percentage of cases. In 140 consecutive patients with endoscopically documented esophageal varices who came to our service with upper gastrointestinal hemorrhage, varices were the source of bleeding in approximately 90%, regardless of whether the underlying liver disease was due to alcoholism or not. We conclude that: 1) patients with varices almost always bleed from varices, and 2) the incidence of erosive gastritis and peptic ulcer as a cause of bleeding in this group has been overemphasized.
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PMID:Upper gastrointestinal bleeding in patients with portal hypertension: a reappraisal. 660 62

The natural history of gastrointestinal bleeding in cirrhosis has been studied using prospectively collected data of 532 patients included in a randomized clinical trial with a regular follow-up of up to 12 yr. Of the total 199 patients who experienced gastrointestinal bleeding, 95 (48%) bled from esophageal or gastric varices, 67 (34%) bled from peptic ulcer or gastritis, and 37 (18%) had either insufficient evidence of the source (33) or mixed sources (4). In the total group of patients the cumulative percentage of patients in whom varices had been demonstrated of patients in whom varices had been demonstrated by radiography increased from 12 to 90 in 10 yr, while that of bleeding from varices increased from 7 to 40. In 104 patients who bled for the first time during the trial period (trial bleeding patients) the median number of bleeding episodes was one (range 1-8). In these patients the fatality from bleeding from varices was 82%. The risk of rebleeding from varices was 81%, and 4 yr after the first bleeding the cumulative survival had decreased to less than 10%. Rebleeding was significantly less frequent and survival significantly higher in patients bleeding from sources other than varices. Prednisone reduced the occurrence rate of varices, bleeding from varices, and death from bleeding varices in nonalcoholic females without ascites, 40% of whom fulfilled the histologic criteria of chronic active hepatitis. Prednisone significantly increased the occurrence rate of varices inpatient with ascites and of bleeding from varices in alcoholic patients. Prednisone significantly increased the occurrence rate of peptic ulcer in males and in patients without chronic active hepatitis.
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PMID:Aspects of the natural history of gastrointestinal bleeding in cirrhosis and the effect of prednisone. 702 43


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