Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The operative procedure of terminal esophagoproximal gastrectomy (TEPG) with extensive esophagogastric devascularization and splenectomy is described in detail and its rationale is discussed. Late results of this operation performed therapeutically on 64 patients with posthepatitic cirrhosis revealed that (1) operative mortality rate (death within a month) was 11%, mostly being contributed by poor-risk patients; (2) over-all survival was 65% at 5 years and 59% at 10 years; (3) gastrointestinal bleeding recurred in nine patients, five of whom had major and four minor hemorrhages; (4) portasystemic encephalopathy was seen frequently after shunts had never occurred, and the hepatic encephalopathy was only a sequel of major gastrointestinal bleeding or a manifestation of terminal-stage liver insufficiency; and (5) ascites was not a major clinical problem after this operation; mild esophagitis was an occasional complication.
 ...
PMID:The late results of terminal esophagoproximal gastrectomy (TEPG) with intensive devascularization and splenectomy for bleeding esophageal varices in cirrhosis. 108 26

Portal hypertension is characterised by alterations in the splanchnic and systemic circulation resulting in the development of portosystemic collateral channels, the most important of which are found in the lower oesophagus and stomach. The major clinical complication of gastro-oesophageal varices is bleeding and over the last decade there has been considerable interest in the pharmacological management of this complication. The factors currently implicated in the development of gastro-oesophageal varices in patients with cirrhosis include a) increased portal vascular resistance, b) splanchnic and systemic vasodilatation and c) changes in the lower oesophageal venous anatomy [palisade and perforating venous zones]. In a patient with gastrointestinal bleeding, endoscopic examination of the upper gastrointestinal tract will confirm the diagnosis of portal hypertension by confirming the presence of gastro-oesophageal varices. Cirrhosis is the most common aetiological factor for gastro-oesophageal varices, but imaging techniques, including Doppler ultrasound, computerised tomography and venous phase angiography, may be required to exclude extrahepatic portal venous obstruction from the differential diagnosis. Although the pathogenesis of variceal rupture remains unclear, several risk factors for variceal haemorrhage have been identified, including a) increased size, b) high intravariceal-portal pressure, c) increased varix wall tension characterised by the presence of red spots observed at endoscopy (particularly in large varices since wall tension is related to variceal size), and d) poor liver function. Although oesophagitis may be observed at endoscopy, an erosive mechanism is no longer considered to be of pathogenic significance. A high portal pressure in the immediate postbleeding period is now recognised as predictive of rebleeding. Periodic elevations in intravariceal pressure, associated with the release of enhanced endogenous vasoactive compounds, or beta-adrenergic-mediated stress-related increases in portal pressure, may contribute to the rupture mechanism. Consequently, portal hypertension is now being more widely considered as a multiorgan disorder associated with changes in blood flow within both systemic and splanchnic vascular beds. This article reviews the factors currently implicated in the development of portal hypertension and the approach to diagnosis. The pathogenesis of variceal bleeding will also be considered.
 ...
PMID:Mechanisms and consequences of portal hypertension. 138 66

We present a case of disseminated tuberculosis with peritoneal and intestinal involvement in a homosexual patient who presented micronodular fibrosis and was infected by HIV, with an AIDS diagnosis since he had previously presented an esophagitis caused by candida. Diagnosis was made from a sample obtained from an ulcerated lesion from rectum-sigmoid region by colonoscopy, and when stained with Ziehl-Nielsen revealed acid-alcohol resistant bacilli (AARB) identified as M. tuberculosis. The torpid evolution of the process, which was complicated by the uncompensation of the cirrhosis determined the patient's death inspite of treatment. The characteristics of intestinal tuberculosis in HIV infected patients is reviewed.
 ...
PMID:[Intestinal tuberculosis in acquired immunodeficiency syndrome]. 178 2

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis and a major cause of death in such patients. The main sites of bleeding are esophageal varices, gastritis, and peptic ulcers. In order to determine the prevalence of either potential bleeding lesions or of other endoscopic findings in hemodynamically stable individuals with various etiologies of cirrhosis, 510 consecutive cirrhotic patients, evaluated for possible orthotopic liver transplantation (OLTx) underwent an upper gastrointestinal endoscopy for combined diagnostic and therapeutic purposes. The patients were divided into two main groups: 319 patients with parenchymal liver disease and 191 patients with cholestatic liver disease. Gastritis was found significantly more often in patients with parenchymal liver disease than in those with cholestatic liver disease (49.8% vs 30.9%; P less than 0.001). In contrast, the prevalence of esophagitis, esophageal and gastric varices, gastric ulcer, duodenal ulcer, and duodenitis was similar in both groups. Normal endoscopic findings were present in 5.0% of the parenchymal group and 11.5% of the cholestatic group (P less than 0.02). Ascites and encephalopathy were found significantly more often in subjects with parenchymal liver disease as compared to those with cholestatic liver disease. Portal hypertension and its degree, as assessed by the presence and size of esophageal varices, was similar in both groups, and in both groups there was a statistically significant qualitative trend of increasing prevalence of esophageal varices with increasing severity of disease as estimated using Pugh-Child's criteria.
 ...
PMID:Prevalence of endoscopic findings in 510 consecutive individuals with cirrhosis evaluated prospectively. 234 4

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.
 ...
PMID:[Candidiasis of the esophagus. Prospective study of incidence, type of complaints and predisposing factors]. 373 73

The results of the examinations do not depend on the peptic theory of the haemorrhage of the oesophageal varices in patients with liver cirrhosis, since the relative frequency of reflux troubles and of gastrooesophageal reflux in patients with liver cirrhosis and haemorrhage of the oesophageal varices was not found greater than in patients with liver cirrhosis and oesophageal varices without haemorrhage as well as the combination of reflux oesophagitis and oesophageal varices was rarely to be observed in the endoscopic material.
 ...
PMID:[Gastroesophageal reflux--cause of hemorrhaging esophageal varices?]. 387 38

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.
 ...
PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

The study included 11 patients with AIDS who underwent gastric emptying studies for solid food, endoscopy (esophagogastroduodenoscopy), and gastric biopsy whenever gastritis was diagnosed on endoscopy. All studies were performed within 1 week. The studies were retrospectively reviewed to analyze the changes in gastric emptying secondary to Kaposi's sarcoma (KS) with or without opportunistic infections. Two patients with KS only had rapid gastric emptying (T1/2 6.7 and 45 minutes). Two other patients with KS and opportunistic infections had normal gastric emptying (T1/2 56.7 and 70 minutes), and one patient with KS and opportunistic infections had rapid gastric emptying (T1/2 25.9 minutes). Four patients with gastritis secondary to opportunistic infections and no KS had delayed gastric emptying (T1/2 622, 92, 266.5, and 179.4 minutes). The remaining two patients had endoscopy showing gastritis not proven by biopsy, and both had rapid gastric emptying. One patient had gastric ulcer (T1/2 39 minutes), and the other had chronic active hepatitis and early cirrhosis (T1/2 15 minutes). Esophagitis was present in 6 out of 7 patients who had gastritis. Esophageal candidiasis was confirmed in three patients, and cytomegalovirus was confirmed in one patient. The findings suggest that gastroduodenal KS is associated with fast gastric emptying in patients with AIDS. However, normal gastric emptying study does not reflect normal gastric physiology in patients with AIDS.
 ...
PMID:Gastric emptying patterns in Kaposi's sarcoma and gastroenteritis secondary to human immunodeficiency virus infection. 798 15

Twenty-five adult patients with liver cirrhosis, and another 30 patients with no liver disease but referred with symptoms suggestive of gastroesophageal reflux disease were selected at random. Twenty-four hour ambulatory intra-esophageal pH measurement and upper gastrointestinal endoscopy were carried out on all patients recruited. Applying the former test, 16 (64%) of the patients with liver cirrhosis have gastroesophageal reflux disease. This figure is comparable with the 70% (21/30) rate recorded in the group of dyspeptic patients clinically thought to have the disorder. A positive endoscopic diagnosis was much lower at 12% and 23%, respectively. No significant differences were observed among liver disease patients when they were subdivided in accordance with the etiology of liver cirrhosis and the grade of esophageal varices. We conclude that gastroesophageal reflux disease occurs at a high frequency (64%) in patients with liver cirrhosis and portal hypertension, irrespective of the etiology of cirrhosis and the grade of esophageal varices. It is therefore considered to be the main cause of esophagitis in these patients, and that it might play a role in initiating a variceal bleeding episode. The latter hypothesis needs further evaluation.
 ...
PMID:Frequency of gastroesophageal reflux in patients with liver cirrhosis. 827 Feb 39

The portal vein (PV) velocity was measured by duplex Doppler ultrasound to predict the severity of portal hypertension. A total of 143 patients with liver cirrhosis were studied from January 1991 to June 1992. There were 104 males and 39 females with a mean age of 52 years old (range 23-76). The maximal PV velocity was significantly lower in patients with moderate and severe varices, cardiac varices, red-color signs on varix, esophagitis and congestive gastropathy. The patients with bleeding esophageal varices or upper gastrointestinal tract were found to have a significantly maximal PV velocity. Comparing patients without ascites or victims with controllable ascites. The maximal PV velocity in Child's C or mortality cases was also significantly lower than that in Child's A, Child's B and surviving cases. If we set the cut off value of PV velocity at 15 cm/sec, we could get the accuracy of 67.8%, 62.2%, 67.8% and 73.5% in the prediction of massive ascites, varices severity, Child C class and mortality respectively. In conclusion, PV velocity may reflect the severity of clinical portal hypertension in cirrhotic patients; it could be a prognostic factor in cirrhotic patients.
 ...
PMID:Portal vein velocity by duplex Doppler ultrasound as an indication of the clinical severity of portal hypertension. 852 31


1 2 3 Next >>