Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over a 30-month period, 60 patients (30 in each group) suffering from end-stage liver disease or primary hepatic malignancy and scheduled for liver transplantation were enrolled in a prospective, randomized study to compare two methods of liver preservation: histidine-tryptophan-ketoglutarate (HTK) solution versus University of Wisconsin (UW) solution. Entry criteria for both groups were: age (18-65 years), elective surgery (transplantable or urgent category of the recipients), first transplantations and harvesting procedure performed by the same team. The parameters under investigation were the clinical and laboratory data pre- and post-transplantation, as well as follow-up data such as complications and survival. There were no significant differences in the two groups as far as the evaluation criteria were concerned, even when cold ischemia time was more than 15 h (n = 7). A slight, yet not significant, increase in late complications of the biliary anastomoses could be seen in the UW group. Hepatocellular injury (SGOT, SGPT, GLDH, lactate) appeared to be more marked in the HTK group. These results suggest that both HTK and UW solutions are appropriate for clinical use in liver transplantation, even if cold ischemia time is more than 15 h.
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PMID:Comparison of histidine-tryptophan-ketoglutarate (HTK) solution versus University of Wisconsin (UW) solution for organ preservation in human liver transplantation. A prospective, randomized study. 806 Apr 66

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

Hepatocyte growth factor (HGF) is the most potent mitogen of mature hepatocytes in primary culture, and is a molecule composed of 69 kD alpha-chain and 34 kD beta-chain. HGF predominantly acts on various epithelial cells as a mitogen, motogen and a morphogen. HGF mRNA and HGF protein increases rapidly in the liver and plasma of rats with liver injury such as hepatitis, ischemia, physical crush and partial hepatectomy. Production of HGF in the liver occurs in Kupffer cells, sinusoidal endothelial cells, and Ito cells, but not in hepatocytes. HGF mRNA is also rapidly increased in the intact organs such as lung, kidney and spleen. Thus, HGF may act as a hepatotrophic factor for liver regeneration through two mechanisms: a paracrine mechanism and an endocrine mechanism. Moreover, intravenously injected HGF enhances liver regeneration and protects hepatitis in vivo. Consequently, HGF may prove to be useful for the clinical treatment of patients with liver disease. Recently, we found a factor which specially appears in the blood of rats with organ injury and increases the synthesis of HGF, and it was named "injurin". IL-1 alpha and IL-1 beta are also positive regulators for the expression of the HGF gene, while TGF-beta and Dexamethazone down-regulate HGF expression.
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PMID:[Molecular biology of hepatocyte growth factor (HGF)]. 838 41

During the last decade intensive work on the relationships between the liver and the arachidonic acid cascade has greatly expanded our knowledge of this area of research. The liver has emerged as the major organ participating in the degradation and elimination of arachidonate products of systemic origin. The synthesis in the liver of arachidonate products derived from the cyclooxygenase, lipoxygenase and cytochrome P450 system pathways has been demonstrated. The participation of leukotriene B4 and cysteinyl-leukotrienes as mediators of liver damage and the possible therapeutic usefulness of prostaglandins (PGs) in acute liver injury has attracted the interest of clinicians. This article reviews the essential features regarding the role of arachidonate metabolites in liver disease and specially focuses on the cytoprotective effects on the liver displayed by PGE2, PGE1, PGI2 and synthetic PG analogs in experimental models of liver damage induced by ischemia-reperfusion injury, carbon tetrachloride, bacterial lipopolysaccharide and viral hepatitis and on the possible mechanisms underlying liver cytoprotection in these experimental models. The therapeutic usefulness of PGs in clinical practice is critically analyzed on the basis of available evidence in patients with fulminant hepatic failure and primary graft nonfunction following liver transplantation.
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PMID:Liver cytoprotection by prostaglandins. 841 74

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

Orthotopic liver transplantation is an established therapy for end-stage liver disease. This study evaluated the range of cardiovascular abnormalities in patients undergoing evaluation for orthotopic liver transplantation and determined the prognostic implications of abnormal echocardiographic features, including ischemia during dobutamine stress echocardiography, in predicting postoperative cardiac events. Two-dimensional echocardiography was performed in 190 patients for assessment of left ventricular function, valvular pathology, and pulmonary hypertension. Dobutamine stress echocardiography was performed in 165 patients for evaluation of inducible ischemia. Contrast echocardiography for detection of intrapulmonary shunting was performed in 125 patients at rest and in 99 during dobutamine stress. Left ventricular dysfunction, significant valvular regurgitation, and inducible ischemia were identified in <1O% of patients. Pulmonary hypertension, left ventricular hypertrophy and > or = moderate intrapulmonary shunting were present in 12%, 16%, and 26% of patients, respectively. Severe intrapulmonary shunting predicted death prior to transplantation (P=0.01). Of the 71 transplanted patients, major perioperative events included global left ventricular dysfunction in four patients and myocardial infarction in one patient with normal coronary arteries. No preoperative echocardiographic parameters, including ischemia on dobutamine echocardiography, predicted these perioperative events. No cardiac events related to obstructive coronary artery disease occurred in the 154 patients without ischemia on dobutamine stress echocardiography. The majority of patients with end-stage liver disease, including those with alcoholic cirrhosis, have normal cardiac function on two-dimensional echocardiography. Severe intrapulmonary shunting portends a poor prognosis in patients awaiting transplantation. A negative dobutamine stress echocardiogram appears useful in excluding patients at risk for perioperative cardiac events related to obstructive coronary artery disease.
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PMID:Two-dimensional and dobutamine stress echocardiography in the preoperative assessment of patients with end-stage liver disease prior to orthotopic liver transplantation. 861 Apr 15

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

The peribiliary vascular plexus plays an important role in physiology of bile flow. Disturbance of the microcirculation may contribute to ductal injury, but little is known about alterations in the vascular supply of small bile ducts in liver disease. Immunoperoxidase stains for vascular endothelium (Ulex europaeus, factor VIII-related antigen, CD34) were used to study the peribiliary vascular plexus in 20 cases of primary sclerosing cholangitis (PSC) and 27 cases of primary biliary cirrhosis (PBC), two diseases characterized by bile duct destruction. Normal liver from 10 autopsy cases of sudden cardiac death was used as a control. Interlobular bile ducts (20- to 80-microm diameter) were identified on AE1/AE3 immunostain; vessels adjacent to the basement membrane of these ducts were counted. Normal interlobular bile ducts had an average of 2.15 vessels per duct (range, 1.68 to 2.71). Few PBC or PSC cases had a normal number of peribiliary vessels. There was a trend toward vasopenia at higher stage, although vascular loss was noted in early stages as well. The pattern of vascular loss was different for the two diseases; in PSC, the periductal capillaries were often preserved but were pushed away from the basement membrane by concentric deposits of collagen. Small residual vessels could be identified within fibrous scars of obliterated bile ducts in PSC. In 4 stage 3 or 4 PSC cases with little bile duct injury, vessel/duct ratio approached normal levels. In PBC, vessels were obliterated in areas of granulomatous inflammation and heavy lymphocytic infiltrate around bile ducts. In conclusion, loss of peribiliary vessels is common in PSC and PBC. Vessel loss is seen in early stages and may contribute an element of ischemia to continued small bile duct loss but is probably secondary to the inflammatory process.
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PMID:Peribiliary vascular plexus in primary sclerosing cholangitis and primary biliary cirrhosis. 922 46

Liver transplantation is an accepted therapy for end-stage liver disease. After allografting, a variety of clinical problems may require laboratory involvement for accurate and timely diagnosis and intervention. Critical factors in the choice of a laboratory test menu to support a transplant program include turnaround times that support clinical decisionmaking, real diagnostic value, and real value for money. Particular clinical problems, whose early presentation must be anticipated, include graft ischemia, primary nonfunction, and hepatic artery thrombosis. Acute rejection is common at 5-10 days posttransplantation, the principal target being the biliary tree. Longer-term problems are associated with the therapeutic drug measurement of cyclosporin A and, increasingly, tacrolimus (FK506); the side effects of immunosuppressant therapy also require monitoring. A successful liver transplant program can be adequately supported with a simple battery of automated tests that are cheap, fast, and available at all times.
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PMID:Clinical chemistry and post-liver-transplant monitoring. 926 7

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


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