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)

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

Myocardial contractility in cirrhosis is impaired, particularly under stressful situations, in a phenomenon termed cirrhotic cardiomyopathy. Impairment of the cardiac beta-adrenergic receptor and its signaling function appears to be involved in the pathogenesis of this disorder. Additional mechanisms that may have a role include alterations in the physicochemical properties of the cardiomyocyte plasma membrane and abnormalities in circulating humoral factors, such as nitric oxide, carbon monoxide, and catecholamines. The widespread use of orthotopic liver transplantation (OLT) and its associated stresses on the cardiovascular system have highlighted this condition. Cardiac failure has emerged as an important cause of morbidity and mortality in the liver transplant recipient. Unfortunately, pre-OLT recognition of cirrhotic cardiomyopathy is suboptimal because of a lack of sensitive, noninvasive diagnostic tests. Similarly, the management of cirrhotic cardiomyopathy is largely empirical because of a paucity of existing literature. Although evidence suggests that cirrhotic cardiomyopathy may be reversible after OLT, the natural history of this condition warrants further investigation.
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PMID:Cirrhotic cardiomyopathy and liver transplantation. 1091 91

Background/Aim: Hepatic venography with a positive-contrast medium has been reported as a method for evaluating liver disease. However, the contrast medium used in this method provides insufficient portal vein observation and may cause severe liver injuries. Carbon dioxide (CO(2)), a negative-contrast medium, may be able to depict the portal vein system with minimal hepatic toxicity. The aim of this study was to evaluate the usefulness and side-effects of balloon-occluded hepatic venography with CO(2) (CO(2) venography) and to evaluate the correlation between retrograde portogram and liver function in patients with cirrhosis. Subjects and methods: The subjects consisted of 23 biopsy-proven cirrhotic patients (male:female, 16:7; age, 58+/-12 years, range 34-80). The causes of cirrhosis were alcohol intake in ten, HCV infection in ten, HBV infection in one, primary biliary cirrhosis in one and Budd-Chiari syndrome in one. Of these patients, six were complicated with hepatocellular carcinoma (HCC). CO(2) venography was performed with an occlusion balloon catheter, and 25 ml of CO(2) was infused. CO(2) portograms were scored as follows: 0, no visualization of portal veins; 1, visualization of peripheral portal branches; 2, unilateral first portal branch; 3, bilateral first portal branches; 4, main portal vein; 5, left gastric vein, superior mesenteric vein and splenic vein. Hepatic venous pressure gradient (HVPG), cardiac functions, biochemical analysis, blood gas analysis and oxygen (O(2)) saturation monitoring were measured simultaneously. Arterio-portography was also performed. To evaluate the usefulness of CO(2) venography in patients with HCC accompanied by portal vein tumor thrombus (PVTT), three patients were also examined. Results: No significant changes in ALT, AST, O(2) saturation or blood gas data were observed after CO(2) venography. A statistically significant positive correlation was observed between CO(2) portogram scores and Child-Pugh scores (r=0.68, P=0.003). The correlations between CO(2) portogram scores and HVPG, and the forms of gastroesophageal varices in patients without PVTT and major shunts were not significant. The CO(2) portogram score was significantly higher in patients with alcoholic liver cirrhosis than in those with HCV-positive cirrhosis (P=0.04). Cavernous transformation and peripheral portal branches were demonstrated in patients with HCC accompanied by PVTT. These findings could not be observed by arterio-portography. Conclusion: CO(2) venography to obtain retrograde portogram is a safe and useful method for evaluating the portal vein system and liver function in patients with liver cirrhosis.
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PMID:Evaluation of balloon-occluded hepatic venography with carbon dioxide for portography and correlation between retrograde portogram and liver function in patients with liver cirrhosis. 1105 28

A case of disseminated extrahepatic hepatocellular carcinoma (HCC) occurring after ultrasound (US)-guided biopsy and percutaneous ethanol injection therapy is presented. A 72-year-old man with hepatitis-C-virus-related cirrhosis underwent percutanous ethanol injection therapy (PEIT) two times with complete remission: the first for moderately-differentiated HCC in segment six (S6), and the second for well-differentiated HCC in another part of S6. Imaging studies including carbon dioxide (CO(2))-US angiography, incremental computed tomography, and dynamic magnet resonance imaging showed that both HCCs were hypovascular. Twenty-one months after the first PEIT and 7 months after the second, a 5.5x4.5 cm extrahepatic mass interfaced with S6 of the liver was detected by imaging studies. The patient underwent surgery for extrahepatic HCC. Grossly, the main tumor was 5.5x4.5 cm with capsule and septum; the disseminated tumors were detected on the surface of the liver, including the right diaphragm and the falx ligamentosa. Histologically, it was moderately- to poorly-differentiated HCC, which, although not attributed to direct track seeding, was suspected of being induced by the percutaneous US-guided biopsy procedure or by PEIT, irrespective of a hypovascular tumor. Further studies may provide insight into the risk factor engendered by these procedures.
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PMID:A case of disseminated extrahepatic hepatocellular carcinoma after US-guided biopsy and percutaneous ethanol injection therapy. 1134 59

A case of PI in a 57-year-old patient with colonic inertia treated with lactulose for PSE secondary to cirrhosis is described. The colonic inertia led to longer transit time. Retained lactulose and a build-up of carbon dioxide and hydrogen gas occurred in the setting of altered bacterial flora deficient in hydrogen metabolism. The increased gas pressure caused extravasation of air into the intestine, causing PI with pneumoperitoneum. They both resolved with discontinuation of lactulose.
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PMID:Lactulose-induced pneumatosis intestinalis and pneumoperitoneum. 1171 68

Nitric oxide (NO) has diverse physiological and pathophysiological effects. The roles of NO in the renal and cardiac dysfunction found in cirrhosis are reviewed. In the kidneys of experimental animals with cirrhosis, several lines of evidence speak in favour of an enhanced production of NO, through the activation of both endothelial constitutive and inducible isoforms of NO synthase. In contrast with the situation in normal animals, inhibition of NO synthesis in rats with cirrhosis improves sodium and water excretion via blood pressure-dependent and -independent mechanisms, which indicates that the renal sodium and water retention of cirrhosis is related to an excess of NO production. The deleterious effect of excessive NO on the kidney may be mediated by peroxynitrite, a potent oxidant that is readily formed whenever superoxide anions and the *NO radical are produced together. The peroxidation of arachidonic acid by peroxynitrite leads to the formation of F(2a)-isoprostanes, which are powerful renal vasoconstrictors. F(2a)-isoprostane levels are correlated with the severity of liver injury during cirrhosis. However, whether peroxynitrite or F(2a)-isoprostanes are the elusive mediator of the NO-induced renal alterations in cirrhosis remains to be firmly established. NO is also involved in cardiac contractility, probably in the normal heart as well as in disease conditions such as non-cirrhotic and cirrhotic cardiomyopathy. In the latter state, evidence suggests that inducible NO synthase attenuates ventricular contractility, mediated by cGMP. Another gas that transduces its signal through cGMP, carbon monoxide, is also likely to play a role in cirrhotic cardiomyopathy, but the nature of the interaction between NO and carbon monoxide in this syndrome remains unclear.
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PMID:Nitric oxide and renal and cardiac dysfunction in cirrhosis. 1183 41

The derangement of sex hormone serum levels in cirrhotic patients is well-delineated, and increased levels of progesterone and estradiol have been associated to hyperventilation in cirrhotic patients. These hormones have a well-known role in the regulation of vascular tone. The aim of this study was to evaluate whether sex hormone levels contribute to pulmonary vasodilatation (PV) and gas exchange abnormalities in cirrhosis. Contrast transesophageal echocardiography, arterial blood gases, parameters of liver function, pulmonary function test, estradiol and progesterone levels were determined in 45 male cirrhotic patients. Nineteen of 45 patients (42.2%) presented PV. Hyperventilation (pressure arterial of CO2< or =35 mmHg) was correlated to progesterone levels (p<0.05) and pressure arterial of CO2 was high in patients with PV (p<0.005) and Child class B and C (p<0.01). Hypoxemia (pressure arterial of O2<80 mmHg) had inverse correlation with progesterone (p<0.05) and estradiol (p<0.05) levels and pressure arterial of O2 was low in patients with Child class B and C (p<0.05). PV was present in patients with high estradiol levels (p<0.05), high progesterone levels (p<0.005) and Pugh class B and C (p<0.05). Logistic regression analysis identified progesterone as the sole independent factor associated to PV (p<0.0005). Multivariate linear regression showed that PV was the sole independent factor related to both pressure arterial of CO2 (p<0.05) and pressure arterial of O2 (p<0.01) levels. PV was independently associated to gas exchange abnormalities in cirrhosis. Progesterone and estradiol were related with PV in cirrhotic patients.
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PMID:Implications of estradiol and progesterone in pulmonary vasodilatation in cirrhotic patients. 1188 76

During hepatopulmonary syndrome caused by liver cirrhosis, pulmonary endothelial nitric oxide (NO) synthase (NOS) expression and NO production are increased. Increased NO contributes to the blunted hypoxic pressor response (HPR) during cirrhosis and may induce heme oxygenase-1 (HO-1) expression and carbon monoxide (CO) production, exacerbating the blunted HPR. We hypothesized that NO regulates the expression of HO-1 during cirrhosis, contributing to hepatopulmonary syndrome. Cirrhosis was induced in rats by common bile duct ligation (CBDL). Rats were studied 2 and 5 wk after CBDL or sham surgery. Lung HO-1 expression was elevated 5 wk after CBDL. Liver HO-1 was increased at 2 wk and remained elevated at 5 wk. In catheterized rats, the blunted HPR was partially restored by HO inhibition. Rats treated with the NOS inhibitor N(G)-nitro-L-arginine methyl ester for the entire 2- or 5-wk duration had normalized HO-1 expression and HPR. These data provide in vivo evidence for the NO-mediated upregulation of HO-1 expression and support the concept that hepatopulmonary syndrome is multifactorial, involving not only NO, but also HO-1 and CO.
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PMID:Regulation of heme oxygenase-1 by nitric oxide during hepatopulmonary syndrome. 1211 96

Abnormal diffusing capacity is the commonest pulmonary dysfunction in liver transplant candidates, but severe hypoxemia secondary to hepatopulmonary syndrome and significant pulmonary hypertension are pulmonary vascular manifestations of cirrhosis that may affect the perioperative course. We prospectively assessed the extent of pulmonary dysfunction in patients referred for liver transplantation. A total of 57 consecutive patients with chronic liver disease were evaluated. All patients had a chest radiograph, standing arterial blood gas on room air, pulmonary function testing, and Doppler echocardiogram. Those patients with arterial hypoxaemia (PaO(2) < 10 kPa) also underwent (99m)Tc-macroaggregated albumin lung scan, and nine patients had agitated normal saline injection during echocardiography to define further the existence of pulmonary vascular dilatation. Reduced diffusing capacity for carbon monoxide less than 75% of the predicted value was found in 29 of 57 (51%) patients. Although elevated alveolar-arterial oxygen tension difference was detected in 35% (20/57) of the patients, only four (7%) patients had hypoxemia. We were unable to find evidence of intrapulmonary vascular dilatation either on the lung scan or saline-enhanced echocardiography in any of these patients. Reduction in diffusing capacity for carbon monoxide was noted in 75% (18/24) of patients who were transplanted for primary biliary cirrhosis and was accompanied by widened alveolar-arterial oxygen tension in 10 out of 18 (56%) of patients. This study shows that in liver transplant candidates, diffusion impairment and widened alveolar-arterial oxygen tension difference were frequently detected, especially in patients with primary biliary cirrhosis.
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PMID:Pulmonary gas exchange abnormalities in liver transplant candidates. 1220 Jul 82

Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme, catalyzing the oxidative cleavage of heme molecules to biliverdin, carbon monoxide, and iron. The present study was designed to investigate the role of HO-1 in the pathogenesis of renal dysfunction during cirrhosis. Biliary cirrhosis was induced in rats by common bile duct ligation (CBDL). Animals were studied 2 and 5 wk after surgery. In kidney from CBDL rats, HO-1 protein expression increased slightly at 2 wk but was abolished at 5 wk. In addition, we confirmed histologically that HO-1 expression was suppressed in renal tubules and interlobular arterioles in 5-wk-old CBDL rats. Conversely, HO-1 expression in liver was strongly increased. Consistent with the development of cirrhosis and renal dysfunction mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal blood flow (RBF) were decreased in CBDL rats compared with sham-operated controls. In sham rats, treatment with the selective HO inhibitor zinc protoporphyrin markedly decreased GFR and RBF to values similar to those measured in CBDL rats without decreasing MAP. In conclusion, decreased renal HO-1 expression contributes to deteriorated renal function and hemodynamics during cirrhosis. This finding provides a novel mechanism for the pathophysiology of renal dysfunction during cirrhosis.
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PMID:Decreased renal heme oxygenase-1 expression contributes to decreased renal function during cirrhosis. 1237 89


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