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)

A remarkable progress was made in the palliative treatment of unresectable hepatocellular carcinoma using transcatheter arterial chemoembolization (TAC). The combination of doxorubicin as cytotoxic drug and of Lipiodol as carrier, which is selectively accumulated within the tumors is an effective treatment. Prolonged survival has been demonstrated in several clinical studies. In a prospective trial the effect of regional TAC with temporary ischemia of the liver was evaluated concerning liver function, systemic reactions and tumor response. Temporary ischemia of the liver was well tolerated even in patients with liver cirrhosis. Revascularization of the liver after TAC was observed in all cases. Systemic side effects of the cytotoxic drug were mild. In patients with Child C cirrhosis or tumor volume of more than 60% of the liver no impact of the treatment on the survival time was observed. In the entire patient group a survival rate of 70% after 15 months was achieved.
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PMID:[Chemoembolization in primary liver cell carcinoma. Results of a prospective study]. 753 59

The pathogenesis of congestive cirrhosis is generally thought to be a reaction of the hepatic stroma to hypoxia, pressure, or necrosis. This does not explain the poor correlation between symptoms and severity of fibrosis and the irregular distribution of fibrosis within the liver. We have observed healed hepatic vein (HV) thrombosis in patients with congestive heart failure (CHF). The purposes of this study were to document hepatic vascular lesions in autopsy livers of patients with chronic CHF, to determine the role of these lesions in the pathogenesis of congestive cirrhosis, and to refine the definition of congestive cirrhosis. Twenty-five livers were studied, 13 with multiple large blocks 4 x 5 cm. Sections were graded for parenchymal fibrous septa, sinusoidal fibrosis, and intimal fibrosis of portal veins (PVs) and HVs. Fibrous septa were found in livers of 7 of 13 patients with CHF and in none of 12 controls without CHF (P = .007). Parenchymal fibrosis was highly variable in distribution, often with severe septation in some areas and nearly normal morphology in others. Intimal fibrosis and obstruction of small- and medium-HVs were found only in livers of patients with CHF. The vascular lesions were confined to regions with fibrous septation and had morphology suggestive of organized thrombosis. Acute thrombi in sinusoids were noted in livers of 4 patients with CHF and in livers of 2 patients without CHF. These findings support the hypothesis that congestive cirrhosis is a response to intrahepatic thrombosis. The pattern of disease suggests that thrombus begins in sinusoids, occasionally propagates to HVs, and causes secondary local PV thrombosis, ischemia, parenchymal extinction, and fibrosis.
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PMID:Role of thrombosis in the pathogenesis of congestive hepatic fibrosis (cardiac cirrhosis). 773 28

We studied 30 patients with cirrhosis to determine the effect of nitroglycerin on portal and gastric mucosal hemodynamics. Systemic hemodynamics, portal venous pressure (PVP), the hemoglobin index (IHB), and the oxygen saturation index (ISO2) of the gastric mucosa were measured before and after a continuous infusion of nitroglycerin. The patients were divided into two groups according to the presence or absence of major portal-systemic collateral routes on portograms. Nitroglycerin caused a reduction in PVP in all patients. Although there was no significant difference in systemic hemodynamic changes between the two groups, the reduction in PVP in patients with major portal-systemic collaterals was significantly higher than in those without major collaterals. A nitroglycerin infusion, at a dose of 1.0 micrograms/kg per min for 10 min, produced a reduction in both IHB (-16%, P < 0.001) and ISO2 (-13%, P < 0.001) in the gastric mucosa, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. These findings suggest that the continuous infusion of nitroglycerin reduces PVP in cirrhotic patients, particularly in those with major portal-systemic collaterals, and reduces the congestion of the gastric mucosa in patients with portal hypertension.
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PMID:Influence of nitroglycerin on portal pressure and gastric mucosal hemodynamics in patients with cirrhosis. 801 7

The radiographic appearance of intestinal edema, including colonic edema, has been well described in the literature. Severe wall circumferential thickening can occur within the colon in a number of conditions. This includes edema secondary to colitis, allergy, ischemia, and infiltrative neoplastic processes. Edema may be secondary to low protein levels, as from protein losing enteropathy, nephrotic syndrome, and hepatic cirrhosis. The following case, in which there was severe ascending colonic wall thickening due to edema, is unusual in two respects: it had well-developed demonstrated "protective" right colonic varices and a normal protein level.
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PMID:CT demonstration of ascending colon varices. 818 Aug 60

113 consecutive elective liver resections were performed in 107 patients over a period of 8 and half years. The indication was a malignant tumor in 75.2% of cases and a benign lesion in 24.8%. The remnant liver was pathologic in 22.1% of cases (16 steatosis, 8 cirrhosis and 1 fibrosis). The extent of liver resection was major (> or = 3 segments according to Couinaud classification) in 60 cases and minor in 45 cases. No intraoperative mortality occurred. Hospital mortality was 4.4%. Major complications, including death, occurred in 36.3% of cases (41/113). Statistical analysis of various risk factors was performed, regarding age, type of liver disease, cholestasis, surgical approach, extent of resection, type of hepatic vascular clamping, liver ischemia, quality of the remnant liver, intraoperative hemorrhage and length of the procedure. Multivariate analysis demonstrated three major statistically significant risk factors: pre operative cholestasis (r = 0.373; p = 0.0012), extent of liver resection (r = 0.377; p = 0.0011), and intra operative blood transfusion (r = 0.364; p < 0.008) with a global correlation coefficient of 0.582 (p < 0.0001). These results should lead to better surgical selection for liver resection and reduced morbidity and mortality.
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PMID:[Risk factors of hepatectomies: results of a multivariate study. Apropos of 113 cases]. 825 43

Hepatic regeneration of cirrhotic liver following partial hepatectomy was evaluated in the rats following portal triad cross clamp (Pringle's maneuver). Cirrhotic rats were induced by repeated intraperitoneal injection of thioacetamide. Sixty eight percent of partial hepatectomy was performed under general anesthesia with or without total hepatic normothermic ischemia. Pringle's maneuver consisted of 4 times repetition of the combination of 15-minute ischemia and 15-minute reperfusion. Rats were sacrificed on 1, 7, and 28 postoperative days. The increasing rate of regenerated liver, the labeling index (LI) by histochemical measurement of BrdU positive hepatocyte, biochemical tests of the blood were evaluated in non cirrhotic and cirrhotic rats. Cirrhotic rats tolerated Pringle's maneuver well, without portal congestion as observed in non cirrhotic rats, suggesting the formation of porto-systemic shunt in cirrhotic rats. The inhibition in DNA synthesis and hepatic regeneration rate was observed in liver cirrhosis. However, no statistical significant difference in hepatic regeneration was observed in cirrhotic rats with or without Pringle's maneuver. In conclusion, the rat with cirrhotic liver tolerated Pringle's maneuver well and the maneuver itself was not harmful for hepatic regeneration following the partial resection.
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PMID:[Effect of ischemia and reperfusion on hepatic regeneration following partial hepatectomy in cirrhotic rat liver]. 831 1

We report two cases of ischemic hepatitis in patients with alcoholic cirrhosis. In both, hepatic ischemia was induced by hemorrhagic shock and severe sepsis. Despite control of the bleeding and restoration of normal hemodynamics, liver failure deteriorated to hepatic coma and death in both cases. Ischemic hepatitis occurred in 1.5% of 130 consecutive cases of cirrhosis admitted for hemorrhage on our medical intensive care unit. Although cirrhotic patients run an increased risk of ischemic hepatitis, our experience and our review of the literature indicate that this condition is rare in these patients.
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PMID:Ischemic hepatitis in cirrhosis. Rare but lethal. 840 9

Seventeen patients with chronic liver disease underwent prolonged warm ischemia of hemi-lobe during liver resection. Those included 15 cirrhotic patients and two with chronic hepatitis. The hemi-hepatic ischemia was carried out with a liver clamp. The normothermic liver ischemia time of 40 to 70 minutes (53.8 +/- 10.4 minutes, mean +/- SD) were tolerated well with an acceptable postoperative course and no mortality. The liver with cirrhosis or chronic hepatitis can tolerate a hemi-hepatic ischemia of up to 70 minutes for patients with no high-risk factors.
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PMID:Tolerance of chronically-diseased liver to prolonged hemihepatic ischemia during hepatectomy. 853 Feb 22

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67

We investigated the viability of rat cirrhotic livers preserved cold using an isolated rat liver perfusion model. Cirrhosis was induced by intravenous thioacetamide injection. Normal and cirrhotic livers were reperfused immediately or following 6 h of preservation through the portal vein with Krebs-Henseleit buffer and hyaluronic acid added. Cirrhotic livers with short cold ischemia showed higher portal venous resistance than their normal counterparts (p < 0.05), while cirrhotic livers preserved for 6 h exhibited marked elevation of the portal venous resistance as compared with their fresh counterparts or normal liver preserved cold for 6 h (p < 0.05). Similarly, the oxygen consumption of cirrhotic livers with short cold preservation was lower than that of normal livers (p < 0.05), which was further reduced by 6 h of cold preservation (p < 0.05). The bile output was not different between normal and cirrhotic livers. The sinusoidal endothelial cell function of cirrhotic livers as assessed by the clearance of hyaluronic acid was impaired even after a short period of cold ischemia. Histologically, cirrhotic livers showed severe sinusoidal endothelial cell damage, hepatocellular swelling, and marked septal edema which became more prominent by cold preservation. We conclude that the viability of the cirrhotic liver is impaired even by a short cold exposure, and that the prolongation of cold ischemia of the cirrhotic liver leads to further deterioration of the viability.
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PMID:Tolerance of the cirrhotic liver to cold ischemia: ex vivo analysis in rats. 883 68


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