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

From history-taking and from analysis of plasma salicylate levels it is shown that a link exists between aspirin and gastrointestinal bleeding in 68% of cases. Salicylate levels alone indicate that aspirin has been taken in 22% of cases. Plasma salicylate measurement and endoscopy allow a better understanding of haemorrhagic lesions due to aspirin. Aspirin is responsible especially for haemorrhage from ulcers and acute gastritis or duodenitis. Aspirin is seen to be dangerous in a moderate number of susceptible individuals: those with peptic ulcer constitution or cirrhosis.
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PMID:Aspirin and gastrointestional bleeding. Interest of plasma salicylate determination. 31 93

The renal effects of aspirin and acetaminophen are minor. With a major overdose of acetaminophen, uncommonly renal failure may occur that cannot be ascribed to hepatic failure; its mechanism is unknown. Aspirin may cause a transient shedding of renal tubular cells, alterations in urate excretion, inhibition of spironolactone action, and, in certain clinical settings, a reversible decline in renal function manifested as a fall in glomerular filtration that may be accompanied by mild water, sodium, and potassium retention. Active systemic lupus erythematosus, advanced cirrhosis, and chronic renal insufficiency seem to predispose patients to the effects on renal function, and there is direct or indirect evidence in those conditions that prostaglandin synthesis is an important part of the body's attempt to preserve renal blood flow. Study of these effects has provided new insight into the way in which the kidneys may use prostaglandins to preserve renal function when it is threatened.
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PMID:Acute effects of aspirin and acetaminophen on renal function. 700 35

Cephalic duodenopancreatectomy is certainly the operation of choice in cases of adenocarcinoma of the pancreatic head. We evaluated the results of this operation in order to justify its indication and to pinpoint the factors that have an influence on the patients' prognosis after the operation. From 1982 to 1992, 386 patients were hospitalized in our department with the diagnosis of pancreatic cancer, all histological types included. Of these, 21 men and 18 women, mean age 65 years, underwent cephalic duodenopancreatectomy for adenocarcinoma. Associated with these operations were 3 liver metastasis excisions, 2 vascular resections, 1 colectomy and 1 splenectomy. All the tumors were operated on whenever technically possible, except those associated with distant metastasis. Postoperatively, only one patient died (on the 29th day, of viral meningitis). Postoperative morbidity was 51% with 23% local complications. There was one leakage of the anastomosis. Age, weight loss, history of pancreatitis or cirrhosis, anesthetic risk (ASA) and tumor staging were not found to be factors increasing the risk of postoperative complications. Survival after 1 year was 34% and after 5 years 6%. The degree of histological differentiation was the only factor that had any significant influence on the postoperative survival rate in our study. We conclude that cephalic duodenopancreatectomy is the treatment of choice which is capable of improving the quality, and to a lesser extent the length, of survival of patients suffering from pancreatic cancer, with acceptable postoperative mortality and morbidity rates.
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PMID:[Cephalic duodenopancreatectomy for pancreatic adenocarcinoma]. 774 Feb 89

Liver fibrogenesis is a delicately balanced process, in which mainly the non-parenchymal liver cells are implicated. Either increased synthesis or decreased catabolism of matrix proteins results in the enhancement of ECM. As further consequence the formation of continuous diffusion and filtration barriers along the Disse space will hinder the bidirectional exchange of macromolecules. Normal structure of ECM is necessary to the normal function of hepatocytes. The quantitative and qualitative changes of ECM observed in liver fibrosis are able to inhibit the liver specific functions of hepatocytes. The mechanisms involved in this effect are not yet clearly understood. In animal experiments liver cirrhosis is reversible and theoretically the chance is open for humans, as well if we will be able to influence the specific steps of fibrogenesis.
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PMID:[Fibrogenesis in the liver--fibrosis, cirrhosis]. 841 83

Effects of inhibitors of arachidonic acid (AA) metabolism on the development of fatty liver, cirrhosis, glutathione-S-transferase placental form (GST-P)-positive nodules and the generation of 8-hydroxydeoxyguanosine (8-OHdG) and thiobarbituric acid-reactive substances (TBARS), caused by a choline-deficient, L-amino acid-defined (CDAA) diet, were examined in male Fischer 344 rats by feeding CDAA diets supplemented with the inhibitors for 12 and 30 weeks. Acetylsalicylic acid (ASA) (at doses of 0.1 and 0.2%) and p-bromophenacylbromide (BPB) (0.1 and 0.2%) were used as inhibitors of, respectively, cyclo-oxygenase and phospholipase A2, and quercetin (QU) (0.75 and 1.5%) and nordihydroguaiaretic acid (NDGA) (0.1 and 0.2%) as inhibitors of lipoxygenase. None of the inhibitors affected the development of fatty liver caused by the CDAA diet. ASA at a doe of 0.2% almost completely prevented the appearance of cirrhosis, GST-P-positive nodules, 8-OHdG and TBARS in seven out of 11 (63.7%) rats. BPB at a dose of 0.2% also exerted inhibitory effects on all of these lesions but to a lesser extent than ASA. QU and NDGA exerted inhibitory effects limited to the GST-P-positive nodule case. The results indicate that a perturbed AA metabolism, particularly of the cyclo-oxygenase pathway, derived secondarily from depletion of labile methyl groups or phosphatidylcholine, might play key roles in the cirrhosis, hepatocarcinogenesis and oxidative stress caused by a CDAA diet. The results also indicated a possible involvement of the lipoxygenase pathway in hepatocarcinogenic processes.
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PMID:Inhibition by acetylsalicylic acid, a cyclo-oxygenase inhibitor, and p-bromophenacylbromide, a phospholipase A2 inhibitor, of both cirrhosis and enzyme-altered nodules caused by a choline-deficient, L-amino acid-defined diet in rats. 863 Nov 32

Hepatic necrosis is a common reaction to liver injury of various etiologies. The response is regeneration. As reviewed earlier, reconstitution of liver mass may proceed via two mechanisms: (1) re-entry of surviving, functionally intact differentiated liver cells into the cell cycle, where they may remain for several rounds of replication, and (2) recruitment of hepatic progenitor cells, whereby the liver mass is replaced by extensive proliferation and differentiation of more primitive cell types. Although both mechanisms appear to share a number of regulatory factors, distinct differences exist that are reflected in the complex and intricate networks of interacting cells, cytokines, and ECM molecules constituting the regenerative process. The development of liver fibrosis or cirrhosis is probably an unwanted but frequent byproduct of the regenerative process, similar to scar formation in any other tissue following extensive damage. Although intensive research in recent years has yielded a wealth of information about regenerative processes, a better understanding of the elements regulating the regenerative process is crucial for effective intervention to prevent or minimize fibrosis while providing optimal conditions for regeneration. Because our only experimental tool is observation in human studies, we must continue the use of experimental animal models including those of transgenic mice to further elucidate the complex interactions of cytokines, ECM, and target cells in the development of liver fibrogenesis, cirrhosis, and cancer.
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PMID:Hepatic regeneration. The role of regeneration in pathogenesis of chronic liver diseases. 879 75

Meta-analysis is increasingly used in hepatogastroenterology. Meta-analysis is of value to provide a systematic review of related trials and to display their results in an objective, easily understandable manner. When the trials are sufficiently homogeneous, meta-analysis can document the superiority, (a), or the lack of superiority (b) of a treatment with respect to another (e.g., (a) Interferon plus ribavirin vs Interferon for chronic hepatitis; (b) 5-ASA vs sulfasalazine for maintaining remission in ulcerative colitis). However the interpretation of meta-analysis requires caution. Meta-analysis can be unreliable or unstable if based on a few, small trials (e.g., Tamoxifen vs non-active treatment for hepatocellular carcinoma), or if distorted by confounding variables and publication bias (e.g., glucocorticoids vs standard treatment in alcoholic hepatitis). Eventually, qualitative heterogeneity makes the pooled results of meta-analysis meaningless or questionable (e.g., endoscopic sclerotherapy for prevention of first variceal bleeding in cirrhosis) and should prompt the search for its sources to plan future studies. Finally, meta-analysis of trials measuring the treatment effect of a drug vs a placebo when an active drug is available for comparison provides the limited informative content for the physician of the individual trials (e.g. 5-ASA vs placebo for maintaining remission in ulcerative colitis).
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PMID:Meta-analysis as a source of evidence in gastroenterology: a critical approach. 1073 May 66

Disadvantages related to CO2 pneumoperitoneum in high risk patients (anesthesiologic classification in III and IV ASA), have led to the development of the abdominal wall retractor, a device designed to facilitate laparoscopic surgery without conventional pneumoperitoneum. A case of a patient with acute cholecystitis, well-compensated liver cirrhosis, and high respiratory and cardiologic risk (ASA III class), submitted to laparoscopic cholecystectomy with gasless technique is reported.
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PMID:[Gasless laparoscopic cholecystectomy. Selective intervention in a high surgical risk patient]. 1083 83

The liver undergoes pathogenic changes such as hepatitis, fibrosis and cirrhosis under continuous stimulation by hepatitis virus or alcohol intake, leading to the development of hepatocellular carcinoma. The metastatic potential of HCC can be positively or negatively regulated by pathogenic alterations of liver. We investigated whether the metastatic abilities of HCC after orthotopic implantation can be influenced in the fibrotic liver by continuous injection of carbon-tetrachloride (CCl4) for seven weeks. The incidence of lung metastasis after orthotopic implantation of murine HCC (CBO140C12) fragments into CCl4-treated livers was higher than into normal livers. The amount of mRNA for MMP-2 increased in the CCl4-treated livers as compared with normal livers, and CBO140C12 cells constitutively expressed mRNA for MT1-MMP in early amplification cycles by RT-PCR. In addition, we found that the culture of CBO140C12 cells on the substrates pre-coated with ECM components increased the expression of MMP-2 mRNA. Thus, enhanced incidence of lung metastasis in the fibrotic liver might be partly due to: i) over-expression of MMP-2 in the fibrotic liver in cooperation with MT1-MMP on the CBO140C12 cell surface, ii) over-expression of MMP-2 in CBO140C12 cells, possibly mediated by the interaction of tumor cells (surface integrins) with accumulated ECM in the fibrotic liver. This is the first report showing that increase of MMP-2 in the fibrotic liver can influence the metastatic potential of HCC cells.
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PMID:Accumulation of extracellular matrix in the liver induces high metastatic potential of hepatocellular carcinoma to the lung. 1140 24

Proteoglycans are macromolecules formed by a protein core to which sugar chains are covalently attached. They are present on the cell surface and in the ECM of living things. In normal liver syndecan-1 is the dominant transmembrane proteoglycan, trace amounts of ECM proteoglycans are in the stromal components. The amounts of proteoglycans we studied increase in liver cirrhosis. In liver cancer abnormal localization of syndecan-1 and stroma rich in agrin was characteristic. The core proteins as well as the sugar chains of proteoglycans interact with and modulate the effect of regulatory factors. This implies that structural alterations of proteoglycans contribute to the development of malignant phenotype. Heparan sulfate chains of liver cancer are undersulfated with decreased or altered biological activity. Their binding capacity for transcription factor decreases, and they do not inhibit topoisomerase I enzyme. Truncated form of syndecan-1 lacking the extracellular domain of the molecule induces differentiation of hepatoma cell line and inhibits the shedding of syndecan-1. This phenomenon calls attention to the importance of syndecan-1 shedding in the regulation of cell behavior.
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PMID:[Proteoglycans in the liver]. 1552 Aug 70


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