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)

The incidence of hepatocellular carcinoma (HCC) in cirrhotic patients is increasing. Despite advances in imaging and laboratory screening which allow earlier diagnosis, the surgeon is all too often confronted with an HCC of advanced stage or arising in the setting of severe cirrhosis. Hepatic resection is still considered the treatment of choice for hepatocellular carcinoma in patients with liver cirrhosis. From 1998 to 2005, 6 patients (5 males, 1 female, age 52-70 years, mean age 64.1 years) with HCC associated severe, but well compensated liver cirrhosis (Child A-- 4 patients, Child B--2 patients) underwent 9 hepatic resection in our department. Mean tumor size was 56 mm (range 23-86 mm). Two of these lesions were in the left liver and four in the right lobe. Doppler ultrasonography was performed in all cases and CT in 3 cases to confirm the extension of the lesions. Laparoscopy was performed in 3 patients under CO2 pneumoperitoneum. The Pringle maneuver was not used. The transection of the liver parenchyma was obtained by the use of Ligasure and harmonic scalpel. Nine hepatic resections were performed: 7 segmentectomy and 2 non-anatomical resections. The resection margin was 1 cm. The mean operative time was 90 minutes (range 60-120). Mean blood loss was 250 ml and 2 patients required blood transfusion. One patient died on the tenth postoperative day from a severe respiratory distress syndrome and hepatic failure. Major morbidities occurred in three patients who developed moderate postoperative ascites, which resolved successfully with conservative treatment in two patients. Limited liver resection in cirrhotic patients with HCC is feasible with a low complication rate when careful selection criteria are followed (tumor size smaller than 8 cm, Child-Pugh A class and the good general conditions of the patients). Other medical and interventional treatments (chemoembolization, chemotherapy) can only slow the progress of HCC.
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PMID:[Liver resection for hepatocellular carcinoma in cirrhotic patients]. 1661 Jan 75

A 78-year-old man had a history of blood transfusion and hepatitis C virus-related liver cirrhosis. He was admitted to the authors' hospital with a hepatocellular carcinoma just below the right hemidiaphragm. Although the lesion was not well visualized with standard sonography, it was clearly defined by performance of sonography with intraarterial injection of carbon dioxide, allowing safe and accurate radiofrequency ablation. To increase the extent of tumor ablation, transcatheter arterial chemoembolization was performed immediately before radiofrequency ablation. By concomitant application of these two techniques, complete tumor necrosis was achieved without the need to perform additional ablation.
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PMID:Carbon dioxide-enhanced sonographically guided radiofrequency ablation plus transcatheter arterial chemoembolization for hepatocellular carcinoma. 1661 57

Cirrhosis is known to be associated with numerous cardiovascular abnormalities. These include increased cardiac output and decreased arterial pressure and total peripheral resistance. Despite this increased baseline cardiac output, patients with cirrhosis show an attenuated systolic and diastolic function in the face of pharmacological, physiological and surgical stresses, as well as cardiac electrical abnormalities such as QT prolongation. These abnormalities have been termed cirrhotic cardiomyopathy. The pathogenic mechanisms that underlie this syndrome include impairment of the beta-adrenergic receptor signalling, cardiomyocyte plasma membrane function, intracellular calcium kinetics, and humoral factors such as endogenous cannabinoids, nitric oxide and carbon monoxide. Cirrhotic cardiomyopathy is believed to contribute to the cardiac dysfunction that can be observed in patients with transjugular intrahepatic portosystemic stent-shunt insertion and liver transplantation. Insufficient cardiac contractile function may also play a role in the pathogenesis of hepatorenal syndrome precipitated by spontaneous bacterial peritonitis. In this review, the clinical features, pathogenic mechanisms, clinical consequences and management options for cirrhotic cardiomyopathy are discussed.
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PMID:Cardiac dysfunction in cirrhosis. 1722 1

Large-conductance calcium-activated potassium channels (BK(Ca)s) are important regulators of arterial tone and represent a mediator of the endogenous vasodilator carbon monoxide (CO). Because an up-regulation of the heme oxygenase (HO)/CO system has been associated with mesenteric vasodilatation of cirrhosis, we analyzed the interactions of BK(Ca) and of HO/CO in the endothelium-dependent dilatation of mesenteric arteries in ascitic cirrhotic rats. In pressurized mesenteric arteries (diameter, 170-350 microm) of ascitic cirrhotic rats, we evaluated the effect of inhibition of BK(Ca), HO, and guanylyl-cyclase on dilatation induced by acetylcholine and by exogenous CO; and HO-1 and BK(Ca) subunit protein expression. Inhibition of HO and of BK(Ca) reduced acetylcholine-induced vasodilatation more in cirrhotic rats than in control rats, whereas inhibition of guanylyl-cyclase had a similar effect in the two groups. CO was more effective in cirrhotic rats than in control rats, and the effect was hindered by BK(Ca) inhibition. The expression of HO-1 and of BK(Ca) alpha-subunit was higher in mesenteric arteries of cirrhotic rats compared with that of control animals, whereas the expression of the BK(Ca) beta1-subunit was lower. In conclusion, an overexpression of BK(Ca) alpha-subunits, possibly due to HO up-regulation with increased CO production, participates in the endothelium-dependent alterations and mesenteric arterial vasodilatation of ascitic cirrhotic rats.
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PMID:Carbon monoxide-mediated activation of large-conductance calcium-activated potassium channels contributes to mesenteric vasodilatation in cirrhotic rats. 1722 79

On the basis of limited experimental and clinical studies, increased activity of the vasodilatory nitric oxide-cyclic guanosine monophosphate pathway is considered to play a key role in the pathogenesis of hepatopulmonary syndrome. We report a 46-year-old woman with Child-Pugh class C cirrhosis and progressive dyspnoea for 12 months. Investigations revealed elevated circulating concentrations of nitric oxide metabolites and exhaled nitric oxide levels, an hyperdynamic circulation with low systemic vascular resistance and mean arterial pressure, a large right to left intrapulmonary shunt fraction on radiolabelled macroaggregated albumin perfusion scanning, positive contrast-enhanced echocardiography, reduced diffusion capacity of carbon monoxide, hypoxaemia and orthodeoxyia, all in keeping with severe hepatopulmonary syndrome. Sequential inhibition of the nitric oxide-cyclic guanosine monophosphate pathway using curcumin (diferuloylmethane), terlipressin and methylene blue was associated with substantial improvements in vascular tone and the hyperdynamic circulation. No improvement, however, in the intrapulmonary shunt was demonstrated. Both hypoxaemia and orthodeoxia were substantially, reproducibly and reversibly worsened with all three treatments. Our findings argue against the contention that intrapulmonary shunting and impairment in arterial oxygenation in hepatopulmonary syndrome are necessarily the consequence of on-going, nitric oxide-cyclic guanosine monophosphate-mediated vasodilatation, at least in the chronic stage, and, given the possibility of substantial worsening of pulmonary oxygen exchange, suggest that inhibition of the nitric oxide-cyclic guanosine monophosphate pathway should be avoided in this setting.
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PMID:Deleterious effect of nitric oxide inhibition in chronic hepatopulmonary syndrome. 1735 1

Nitric oxide (NO) and carbon monoxide (CO) synthesized from L-arginine by NO synthase and from heme by heme oxygenase, respectively, are the well-known neurotransmitters and are also involved in the regulation of vascular tone. Recent studies suggest that hydrogen sulfide (H(2)S) is the third gaseous mediator in mammals. H(2)S is synthesized from L-cysteine by either cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), both using pyridoxal 5'-phosphate (vitamin B(6)) as a cofactor. H(2)S stimulates ATP-sensitive potassium channels (K(ATP)) in the vascular smooth muscle cells, neurons, cardiomyocytes and pancreatic beta-cells. In addition, H(2)S may react with reactive oxygen and/or nitrogen species limiting their toxic effects but also, attenuating their physiological functions, like nitric oxide does. In contrast to NO and CO, H(2)S does not stimulate soluble guanylate cyclase. H(2)S is involved in the regulation of vascular tone, myocardial contractility, neurotransmission, and insulin secretion. H(2)S deficiency was observed in various animal models of arterial and pulmonary hypertension, Alzheimer's disease, gastric mucosal injury and liver cirrhosis. Exogenous H(2)S ameliorates myocardial dysfunction associated with the ischemia/reperfusion injury and reduces the damage of gastric mucosa induced by anti-inflammatory drugs. On the other hand, excessive production of H(2)S may contribute to the pathogenesis of inflammatory diseases, septic shock, cerebral stroke and mental retardation in patients with Down syndrome, and reduction of its production may be of potential therapeutic value in these states.
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PMID:Hydrogen sulfide (H2S) - the third gas of interest for pharmacologists. 1737 2

Hepatopulmonary syndrome (HPS) is found in 4-47% of patients with cirrhosis and is characterized by intrapulmonary vascular dilatations especially in the basal parts of the lung. Liver injury and/or portal hypertension trigger the release of endothelin-l, TNF-alpha, cytokines and mediate vascular shear stress and release of nitric oxide and carbon monoxide, all contributing to intrapulmonary vasodilation. Severe HPS increases mortality (30%) after liver transplantation, especially if Pa O2 is below 50 mmHg. The diagnosis is made by calculating the alveolar-arterial oxygen gradient and by performing a contrast echocardiography. Medical therapy fails and the only long-term treatment available is liver transplantation. More than 85% experience significant improvement or complete resolution in hypoxaemia, but this may take more than 1 year. Portopulmonary hypertension (PPHT) occurs in 2-8% of the patients with cirrhosis. Imbalance between vasodilating (decreased pulmonary expression of eNOS and prostacyclin I2) and vasoconstrictive agents (increased expression of ET-1 and angiotensin 1) may be responsible for misguided angiogenesis and pulmonary hypertension. The diagnosis is made by performing an echocardiography and a right heart catheterisation when systolic pulmonary artery pressure is higher than 30 mmHg on echocardiography. Although prostacyclin analogues are efficacious, adverse effects in terms of safety, tolerability and drug delivery occur. Bosentan is probably the therapy of choice for patients with PPHT because it decreases pulmonary but can also diminish portal hypertension. Sildenafil, a phosphodiesterase-5 inhibitor is used for idiopathic pulmonary hypertension, however, it should be used cautiously in patients with portal hypertension as it may increase portal hypertension by splanchnic vasodilation.
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PMID:Hepatopulmonary syndrome and portopulmonary hypertension: what's new? 1771 35

Pulmonary complications, mainly hepatopulmonary syndrome (HPS), are frequently observed in liver cirrhosis. In this study, the aim was to investigate the frequency of hypoxemia and impairment of pulmonary function tests (PFT) in patients with liver cirrhosis and to examine the relationships of these impairments with liver failure. A total of 39 patients with cirrhosis, 24 males and 15 females, were included in our study. The mean age of the patients was 47.5 +/- 17.2 years. Arterial blood gases, PFT, and carbon monoxide diffusion tests (DLCO) were performed in all patients. Out of 39 cirrhotic patients, 21 (53.8%) had ascites, whereas 18 (46.2%) did not. Seven patients were in the Child-Pugh A group, 21 in the Child-Pugh B group, and 11 patients were in the Child-Pugh C group. Hypoxia was found in 33.3% of the patients. Although the PaO2 and SaO2 values of patients with ascites were lower compared to those without ascites (P < 0.05), no statistically significant difference was determined in the comparison of hypoxia between the groups (P > 0.05). Among the PFT parameters, FEV1/FVC and FEF25-75% values were found to be lower in patients with ascites than those without (P < 0.05). No differences were established between these two groups of patients in terms of DLCO (P > 0.05). While no differences were found in comparison of the DLCO values in between the groups (P > 0.05), there was a statistically significant difference in the ratio of DLCO to the alveolar ventilation (DLCO/VA) in between the groups (P < 0.05). On the other hand, a negative correlation was found between the DLCO/VA and Child points when the relationship between the Child-Pugh score and PFT parameters were investigated (r = -0.371, P < 0.05). Consequently, a relationship was established between the severity of liver failure and diffusion tests showing pulmonary complications invasively. We believe diffusions tests should be performed in addition to the PFT in order to determine pulmonary involvements particularly in patients who are candidates for liver transplantation.
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PMID:The relationship between severity of liver cirrhosis and pulmonary function tests. 1808 Jul 69

Hepatic hydrothorax is defined as the presence of a significant pleural effusion that develops in a patient with cirrhosis of the liver who does not have underlying cardiac or pulmonary disease. There are few published case reports dealing with hepatic hydrothorax treated surgically because patients with hepatic hydrothorax have end-stage liver disease. Recently, we treated two patients with refractory hepatic hydrothorax by directly suturing the diaphragmatic defects during video-assisted thoracoscopic surgery (VATS). During surgery, the diaphragmatic defects were identified using abdominal insufflation of saline with indocyanine green or carbon dioxide. After suture closure using fibrin glue, both right pleural effusions were improved. The patients' postoperative courses were uneventful, and they did not require a drainage tube when they were discharged.
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PMID:Diaphragmatic repair of two cases of hepatic hydrothorax using video-assisted thoracoscopic surgery. 1847 Jun 88

In advanced cirrhosis, decreased lung transfer for carbon monoxide (TLCO) and increased alveolar-arterial oxygen tension difference (PA-aO(2) >or=15 mmHg while breathing ambient air) are frequently detected. Pulmonary membrane diffusion capacity for CO (DmCO) and pulmonary capillary blood volume (Vcap) can be derived from the simultaneous measurement of TLCO and lung transfer for nitric oxide (TLNO). Measurements of single-breath TLNO and TLCO were performed in 49 cirrhotic patients with advanced liver cirrhosis and in 35 healthy controls to derive Vcap, DmCO, and TLNO:TLCO ratio. Twenty-five patients had increased PA-aO(2), of whom 11 had hepatopulmonary syndrome (HPS). Compared with controls, non-HPS patients with normal PA-aO(2) had a significant approximately 10% decrease in TLCO, DmCO, and Vcap but similar TLNO:TLCO ratios. Compared with non-HPS patients with normal PA-aO(2), non-HPS patients with increased PA-aO(2) had lower Vcap and higher TLNO:TLCO ratio but similar DmCO. HPS patients had lower Vcap and higher TLNO:TLCO ratios than both subgroups of non-HPS patients. In cirrhotic patients, TLNO:TLCO ratios correlated positively, and TLCO (percentage of the predicted value) and Vcap (percentage of the predicted value) correlated negatively with PA-aO(2) (r(2) = 0.25, P = 0.0003, r(2) = 0.48, P < 0.0001 and r(2) = 0.57, P < 0.0001, respectively). We concluded that, in cirrhotic patients, lower TLCO and increased PA-aO(2) are associated with lower Vcap. In addition, high TLNO:TLCO ratios in patients with increased PA-aO(2) suggest a decreased thickness of the capillary blood layer in these patients.
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PMID:Nitric oxide and carbon monoxide lung transfer in patients with advanced liver cirrhosis. 1942 34


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