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)

Vascular complications after liver transplantation are relatively rare. Thrombosis of the host-transplant arterial anastomosis is the most frequently encountered vascular complication whereas only a few observations of infected anastomotic aneurysms, often leading to death by massive bleeding or loss of the transplant, have been reported. We report herein the case of a patient with an infected false anastomotic aneurysm of the hepatic artery associated with dissection of the celiac artery following orthotopic liver transplantation in a 35-year-old man who had received a liver transplantation for end-stage liver disease secondary to posthepatitis cirrhosis in March 1989. Starting at day 30, he had signs of infection associated with hemocultures positive for Staphylococcus aureus. A subhepatic collection was found on sonography and CT scan and also cultured positive for the same germ. Arteriograms demonstrated a celiac artery dissection associated with a false anastomotic aneurysm of the hepatic artery. Surgical treatment consisted of arterial reconstruction using a saphenous vein graft between the right renal artery and the hepatic artery of the transplant, followed by resection of the hepatic artery aneurysm and the celiac artery. Hepatic ischemia was 12 min. The immediate postoperative course was uneventful and postoperative angiograms showed that the reconstruction was patent at 5 years.
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PMID:Infected false hepatic artery aneurysm after orthotopic liver transplantation treated by resection and reno-hepatic vein graft. 914 Jun 7

We report on the successful regrafting of a transplanted liver. The donor liver was first grafted into a patient suffering from cryptogenic cirrhosis; the patient died 1 day after the elective transplantation of cerebral bleeding. The well-functioning graft was harvested again and transferred to our institution. After another 12 h of cold ischemia, the liver was reperfused in an urgently registered patient with recurrence of hepatitis B in his first graft. The transplantation was successfully performed and the patient is now doing well, more than 5 months after regrafting with the reused liver.
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PMID:Successful regrafting of a transplanted liver. 916 69

From January 1991 to May 1994, we have operated on 15 cases of Type B aortic dissection. In 10 of these patients, thoracoabdominal repair was performed. According to Crawford's classification, 2 patients fell into Type I, 6 patients into Type II, and 2 patients into Type III. The aneurysms were exposed through a left thoracotomy extending into the retroperitoneum with the hemidiaphragm divided circumferentially. The operations were performed under femoro-femoral partial cardiopulmonary bypass. In 6 of these cases selective perfusion of the visceral branches was used. The celiac axis was reconstructed in 10 patients, superior mesenteric artery in 9, right renal artery in 7, left renal artery in 6. Abdominal vessels were reconstructed by the "inclusion" technique described by Crawford in 2 patients, by "beveling" the distal prosthetic end in 6 and by the "interposition" technique in 4 patients. Vessels arising from the false lumen were reconstructed by the "interposition" technique. To prevent paraplegia, the evoked spinal cord potentials by direct stimulation of the cord (ESPs-dsc) were monitored perioperatively and the aneurysms were repaired sequentially in segments. In all patients except 2 with Crawford type III aneurysms, spinal cord ischemia was detected by ESPs-dsc. In 7 of these patients, 2 to 8 pairs of intercostal/lumbar arteries (I/L aa.) that arose from the "responsible" aortic segment were reconstructed. Reconstruction techniques included the "inclusion" technique in 2 patients, the "beveling" technique in 1, the "interposition" technique in 1 and the "on lay grafting" technique in 3 patients. One hospital death occurred in a patient who had chronic renal insufficiency and liver cirrhosis preoperatively. Spinal cord injury occurred in 5 patients, including 4 paraparesis and 1 delayed-onset paraplegia. In 2 of these patients, responsible I/L aa., were not reconstructed correctly despite ESPs changes, and injury might have been prevented if reconstruction of the "responsible" arteries had been performed. Thoracoabdominal repair for chronic Type B aortic dissection could be performed safely with an acceptable mortality rate. Spinal cord injury remains an unsolved problem.
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PMID:Operative results of thoracoabdominal repair for chronic type B aortic dissection. 920 Nov 25

Ischemia is known to be a cause of hepatocellular apoptosis and atrophy in experimental animals, but the effect of vascular obstruction on such lesions in the normal or cirrhotic human liver has not been studied. The purpose of this study was to investigate the role of ischemia in the development of apoptosis, atrophy, and nodular hyperplasia in cirrhotic and noncirrhotic human livers. Apoptosis, focal atrophy, and nodular hyperplasia were semiquantitated in 203 liver specimens obtained at transplantation, segmental resection, or autopsy. These parameters were correlated with etiology, stage, activity, and acute and healed portal vein thrombosis (PVT). Large numbers of apoptotic cells were found in livers with acute PVT (17.2/medium-power field [MPF]) and in infarcts of Zahn caused by obstruction of portal veins (PVs) by tumor (16.4/MPF). Smaller numbers of apoptotic cells were found in cirrhosis of various etiologies (3.8-10.0/MPF) and rarely in normal livers (0.16/MPF). Evidence of healed PVT was found in 47% of cirrhotic livers and was associated with nodular hyperplasia (58% vs. 32%, P < .01) and focal atrophy (79% vs. 49%, P < .002). Apoptotic cells were found equally in those with and without healed PVT (40% vs. 38%, not significant). These observations suggest that apoptosis is a transient response to acute ischemia and that atrophy and nodular hyperplasia are chronic responses to ischemia. Vascular obstruction may be an important cause of the apoptosis and atrophy, which are found in nodular regenerative hyperplasia (NRH), infarct of Zahn, chronic hepatitis, and cirrhosis.
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PMID:Role of ischemia in causing apoptosis, atrophy, and nodular hyperplasia in human liver. 925 44

Sarcoidosis often involves the liver with mild elevation of serum enzymes and granulomas histologically. Rarely, chronic cholestasis, portal hypertension, cirrhosis, or nodular hyperplasia may be found. The pathogenesis of the portal hypertension and of the cirrhosis are not understood, in part because large samples of tissue have seldom been described. We describe the clinical and anatomic findings of four patients with sarcoid liver disease in whom the whole livers were available for examination. One patient had cirrhosis, one had diffuse nodular hyperplasia, and two had small regions of parenchymal fibrosis. The first two of these had a history of variceal bleeding and healed portal vein thrombosis. One had chronic cholestasis without cirrhosis. We suggest that the cirrhosis and focal fibrosis were caused by ischemia secondary to primary granulomatous phlebitis of portal and hepatic veins. The portal hypertension in two patients was likely secondary to portal vein thrombosis, because cirrhosis was absent at the onset of variceal bleeding.
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PMID:The role of granulomatous phlebitis and thrombosis in the pathogenesis of cirrhosis and portal hypertension in sarcoidosis. 930 82

Adhesion molecules are cell surface glycoproteins that are critical for the localization of leukocytes at sites of inflammation. This review discusses the current knowledges of adhesion molecule expression in normal liver and its upregulation on individual liver cell types during liver inflammation. Cytokines, chemokines, complement factors, and lipid-derived mediators are critical for increased gene transcription and activation of constitutively expressed adhesion molecules. The specific role of selectins, integrins, and members of the immunoglobulin gene superfamily in sinusoidal and venular leukocyte sequestration, transendothelial migration, and adherence to target cells in the liver is described. Increased understanding of these basic mechanisms of communication between resident liver cells and infiltrating leukocytes (neutrophils, lymphocytes, macrophages) not only advances our insight into the pathophysiology of hepatic inflammation but also identifies promising new targets for therapeutic interventions and expands the spectrum of diagnosis and treatment of liver diseases, including alcoholic hepatitis and cirrhosis, viral hepatitis, ischemia-reperfusion injury (transplantation, tumor resection, shock), sepsis- or endotoxin-induced liver injury, acute and chronic rejection, primary biliary cirrhosis, and primary sclerosing cholangitis.
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PMID:Cellular adhesion molecules: regulation and functional significance in the pathogenesis of liver diseases. 934 Oct 49

The arterial ketone body ratio (AKBR) has been proposed as an accurate indicator of liver mitochondrial redox potential. However, the efficacy of the AKBR as a biochemical marker has been recently called into question. To resolve this issue, we studied the effect of temporary vascular occlusion on the AKBR during hepatectomy. Twenty patients undergoing hepatectomy were divided into two groups: those with hepatocellular carcinoma with a history of hepatic cirrhosis (n = 10; cirrhotic group) and those with liver disease without cirrhosis (n = 10; non-cirrhotic group). To minimize blood loss during hepatectomy, temporary vascular occlusion was applied using the Pringle maneuver. Acetoacetate and beta-hydroxybutyrate concentrations in the arterial blood and the AKBR were determined before and after vascular occlusion. In 25% of the two groups combined, the AKBR increased following normothermic ischemia, as compared with the levels prior to clamping; in 20% of cases in the cirrhotic group, it increased immediately following reperfusion, as compared with the levels prior to clamping. Changes in the AKBR during hepatectomy did not correlate with preoperative hepatocellular function. An AKBR of less than 0.7 prior to clamping which persisted during surgery was not a consistent risk factor for postoperative complications. The AKBR was not a useful predictor of liver viability in partial liver resection with temporary vascular occlusion.
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PMID:Arterial ketone body ratio during hepatectomy. 935 69

The aim of this study was to evaluate the tolerance of normothermic liver ischemia with different degrees of hepatic function in cirrhotic rats. Liver cirrhosis was induced by administering carbon tetrachloride (CCl4) in water solution to male Wistar rats. Hepatic function was graded using the plasma levels of antithrombin III, albumin, and bilirubin and the presence of ascites. Rats were distributed in four groups: noncirrhotic (control group), compensated cirrhosis (group A), decompensated cirrhosis (group B), and decompensated cirrhosis with ascites (group C). Groups A, B, and C were significantly different in all four parameters studied (P < .003). Subtotal liver ischemia was performed for periods of 0, 30, 45, 60, and 75 minutes. At the end of the procedure, the nonischemic lobes were resected. Postoperative evolution of alanine aminotransferase, aspartate aminotransferase, and bilirubin levels was also recorded. Survival rates after the same periods of ischemia were statistically different (P < .05): control group, 7 of 7 after 45 minutes (100%), 7 of 7 after 60 minutes (100%), and 4 of 9 after 75 minutes (44%); group A, 7 of 7 after 45 minutes (100%) and 1 of 7 after 60 minutes (14%); group B, 7 of 7 after 0 minutes (100%), 5 of 7 after 30 minutes (71%), and 1 of 7 after 45 minutes (14%); and group C, 0 of 5 after 0 minutes (0%) and 1 of 7 after 30 minutes (14%). No differences were found in the postoperative course of transaminases. However, bilirubin levels found 24 hours and 7 days after ischemia were significantly greater in cirrhotic rats, and this was directly related to the degree of hepatic insufficiency (P < .001). Histological examination of the livers exposed to CCl4 showed features of liver cirrhosis with ductal proliferation. The ischemia time tolerated by cirrhotic rat livers is shorter than the time tolerated by normal rats. Tolerance to hilar vascular occlusion depends on the degree of hepatic insufficiency. Rats with decompensated cirrhosis and ascites do not tolerate any surgical procedure.
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PMID:Vascular occlusion in hepatic resections in cirrhotic rat livers: an experimental study in rats. 940 63

We investigated the long-term efficacy and the contraindications of single-session percutaneous ethanol injection (PEI) under general anesthesia in hepatocellular carcinoma (HCC). One hundred patients were treated from October, 1991, to April, 1996: 24 patients had a single capsulated HCC, 4.5 to 10 cm phi (group A); 62 had a single infiltrating tumor or multiple lesions (3 to 6), with 10 cm maximum phi (group B); 14 patients were in an advanced stage because of Child class C or of infiltrating tumors with portal thrombosis, with 14 cm lesion maximum phi (group C). Group A patients were treated because they were not operable or refused surgery. Three to 22 injections were performed (mean: 13) depending on tumor size and ethanol spread. The maximum injected volume of ethanol was 190 ml (mean: 57 ml). The procedure took 20 to 50 minutes (mean: 30 minutes). The mean hospital stay was 3.5 days. Tumor necrosis was complete in 58% of encapsulated tumors and > 70% in infiltrating lesions. The greatest lesion with complete post-PEI necrosis was 8.2 cm phi. A transient and variable increase in transaminase, bilirubin, white cell and D-dimer levels and a decrease in red cell, platelet, hemoglobin, fibrinogen and haptoglobin levels were observed. These changes were due to hepatic cell necrosis, hemolysis and focal thrombosis. One death (bleeding esophageal varices in the Child C patient)(1%) and four major complications (one peritoneal bleeding, one liver decompensation, two chemical segmentectomies with pain)(4%) were observed. 1, 2, 3 year survival rates for groups A, B and C were: 80, 63, 63%; 70, 50, 30% and 58, 14 and 0% respectively. In our experience, PEI was an efficacious procedure. The risk conditions are: superficial lesion site with severe coagulation defects, severe portal and/or pulmonary hypertension, esophageal varices at risk of bleeding, cardiac ischemia, advanced cirrhosis.
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PMID:[Single-session alcohol administration for hepatocarcinoma]. 942 44

Mesenteric vein thrombosis is a rare disorder which can develop rapidly with intestinal infarction or subacutely with abdominal pain due to intestinal ischemia. Despite the availability of modern diagnostic tools, which allow an early diagnosis in most cases, the mortality from this disease has not significantly diminished over the years. The problem is that the syndrome is rare and unusual and the clinical presentation is usually vague or confusing. Particularly in cirrhotic patients, this diagnosis requires the exclusion of several other complications of liver disease, like spontaneous bacterial peritonitis, tense ascites or portal thrombosis. Here, we report the occurrence of acute mesenteric vein thrombosis in two patients with liver cirrhosis. Severe subcontinuous abdominal pain out of proportion to the physical findings and abdominal distension were the major symptoms in both patients. Magnetic resonance imaging in one case and ultrasound scan with color Doppler followed by computed tomography in the other patient confirmed the diagnosis and enabled an appropriate early therapy to be undertaken.
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PMID:Mesenteric vein thrombosis: a rare cause of abdominal pain in cirrhotic patients--two case reports. 949 85


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