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)

Standard therapy for variceal bleeding includes endoscopic sclerotherapy and esophageal balloon tamponade. In addition, pharmacologic therapies, including arginine vasopressin (AVP), are frequently used in hemodynamically unstable patients or where sclerotherapy has been unsuccessful. A case is described herein of a 30-year-old woman with a history of ethanol abuse, hematemeisis, and biopsy-proven hepatic cirrhosis in which the addition of AVP to an antivariceal regimen of octreotide was associated with a paradoxical episode of hypotension, bradycardia, and hypoxia. Indeed, within 15 minutes after initiation of an AVP infusion, the patient exhibited hypotension with a systolic blood pressure of 80 mmHg, a relative bradycardia to 76 beats per minute, and a desaturation of blood oxygen to 84%. The AVP infusion was discontinued 2 hours later and blood pressure, heart rate, and oxygen saturation rapidly returned to baseline. This temporal correlation between the onset and termination of the physiologic effects and the initiation and discontinuation of the AVP infusion suggests a causal relationship. The paradoxical physiologic effects might reflect cardiac ischemia secondary to vasospasm and/or central suppression of the autonomic nervous system induced by AVP.
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PMID:Paradoxical hypotension and bradycardia after intravenous arginine vasopressin. 954 67

Mesenteric vein thrombosis (MVT) is a rare cause of intestinal ischemia. Because of its nonspecific symptoms, diagnosis is often delayed. We describe a patient with liver cirrhosis who developed acute MVT while waiting for liver transplantation. Surgical intervention carried a high risk because of her underlying cirrhosis. Mesenteric venous thrombectomy and thrombolysis were performed with an AngioJet (Possis Medical, Minneapolis, MN) thrombectomy device and streptokinase infusion through transjugular route. The patient subsequently received an orthotopic liver transplant. We also present a review of the literature about the occurrence and treatment options for MVT.
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PMID:Percutaneous mesenteric venous thrombectomy and thrombolysis: successful treatment followed by liver transplantation. 956 61

We studied the influence of intermittent ischemic injury on thioacetamide-induced liver cirrhosis in rats. Wistar rats were divided into group A, intermittent ischemic injury to liver cirrhosis, and group B, continuous ischemic injury to liver cirrhosis. Total ischemic time was 60 min in both groups. In group A, ischemic injury consisted of a repetition 4 times of 15 min ischemia and 5 min reperfusion. The ATP level of the liver was measured before ischemia, before reperfusion, and 60 min after reperfusion. Bile was collected to determine bile flow rate. The ATP level in the liver tissue 60 min after reperfusion was significantly (p < 0.05) higher in group A than in group B. The ATP level immediately before reperfusion was also significantly (p < 0.05) higher in group A than in group B. The survival rate 1 week after ischemic injury and bile flow rate 60 min after reperfusion were significantly (p < 0.01) higher in group A compared with those in group B. The energy level was much higher in intermittent ischemic injury than in continuous ischemic injury immediately before reperfusion and after reperfusion. Survival rate and bile flow rate were higher in intermittent ischemic injury than in continuous ischemic injury. Therefore it suggests that the viability of the liver was maintained better in intermittent ischemic injury than in continuous ischemic injury.
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PMID:Influence of intermittent ischemia on thioacetamide-induced rat liver cirrhosis. 962 15

The paper describes the technique of anatomical liver segmentectomies based on the extraparenchymal clamping, at the hepatic hilum, of the afferent vascular pedicles. The resection is started on the liver surface along the demarcation line caused by the ischemia. During parenchymal transection the technique of hemihepatic vascular occlusion has been undertaken. The results obtained with 125 segmentary hepatic resections performed for hepatocellular carcinoma arised on cirrhosis are also reported. The overall operative mortality has been 6.4%. The actuarial 1 and 3 year survivals were 93.3% and 70.4% respectively. Hepatic segmentary resections are recommended for limited hepatic lesions, mainly in well compensated cirrhotic patients.
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PMID:Hepatic resective surgery in cirrhotic patients. Techniques and results of anatomical segmentectomies. 964 39

Propranolol, a beta-adrenergic blocking agent commonly used in the treatment of hypertension, decreases mesenteric blood flow during exercise, at rest, and in cirrhosis. Widespread idiopathic myointimal hyperplasia of mesenteric veins produces intestinal ischemia in otherwise healthy individuals. This report describes a 42-year-old woman who died suddenly and unexpectedly while attending a ball game. She had hypertension treated with propranolol and no other clinically apparent disorders. Autopsy revealed mild mesenteric venous myointimal hyperplasia and segmental jejunal infarction. Recent clinical and experimental studies are used to propose possible mechanisms for this death which combine the effects of propranolol and mesenteric venous myointimal hyperplasia.
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PMID:Unexpected sudden death during propranolol therapy in a patient with mild mesenteric venous myointimal hyperplasia. 967 May 18

The inducible nitric oxide synthase (iNOS) gene is expressed by hepatocytes in a number of physiologic and pathophysiologic conditions affecting the liver including septic and hemorrhagic shock. The molecular regulation of iNOS expression is complex and occurs at multiple levels in the gene expression pathway. The cytokines TNF-alpha, IL-1beta, and INF-gamma synergistically activate iNOS expression in the liver, and the human iNOS gene was first cloned from cytokine-stimulated hepatocytes. iNOS expression requires the transcription factor NF-kappaB and is down-regulated by steroids, TGF-beta, the heat shock response, p53, and nitric oxide (NO) itself. In vivo, hepatic iNOS induction is differentially regulated from the typical acute-phase reactants and is not expressed as a mandatory component of the acute phase response. Thus, numerous mechanisms have evolved to regulate iNOS expression during hepatocellular injury. Studies of the effects of NO in the liver demonstrate that induced NO synthesis plays an important role in hepatocyte function and protects the liver during sepsis and ischemia reperfusion. Its cytoprotective role is best exemplified in a rodent model of endotoxemia. Here the addition of the nonspecific NOS inhibitors significantly increased hepatic damage. NO exerts a protective effect through its ability to prevent intravascular thrombosis by inhibiting platelet adhesion and neutralizing toxic oxygen radicals. NO also exerts a protective effects both in vivo and in vitro by blocking TNF-alpha-induced apoptosis and hepatotoxicity, in part by a thiol-dependent inhibition of caspase-3-like protease activity. These studies demonstrate the cytoprotective effects of NO in the liver and suggest hepatic iNOS expression functions as an adaptive response to minimize inflammatory injury. In addition, NO has anti-tumor effects as well as known mutagenic effects, is involved in the systemic vasodilatation of cirrhosis, and has potent antimicrobial properties.
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PMID:Inducible nitric oxide synthase in the liver: regulation and function. 972 29

The usefulness in cirrhotic patients of hemodynamic measurements by Doppler ultrasonography (US) is still not defined. We investigated the relationships between Doppler measurements and the severity of ascites. Portal blood flow velocity and volume, and hepatic and renal arterial resistance indexes (RI) were measured in 57 cirrhotic patients (19 without ascites, 28 with responsive ascites, and 10 with refractory ascites) and 15 healthy controls. The renal arterial RI were obtained for the main renal artery, interlobar vessels, and cortical vessels. Cirrhotic patients had decreased portal blood flow and an increased congestion index (CI). Only the CI was correlated to the severity of ascites, showing that it is also a reliable measure of the severity of portal hypertension in patients with ascites. The hepatic and renal artery RI were increased in cirrhotic patients, and the two values were correlated (r = .68; P = .00001). The RI of renal interlobar and cortical vessels were higher in patients with refractory ascites than in patients without ascites (P < .02 and P < .009), and correlated with sodium excretion rate (r = -.45; P < .003), the renin-aldosterone system, and creatinine clearance (r = -.62; P < .0002). The RI decreased from the hilum of the kidney to the outer parenchyma in healthy subjects and patients with responsive ascites, but this difference disappeared in patients with refractory ascites. This indicates that the degree of renal vasoconstriction varies in different areas according to the severity of the ascites. Cortical vessels are involved mainly in patients with refractory ascites, suggesting that the intrarenal blood flow distribution in cirrhosis tends to preserve the cortical area and that severe cortical ischemia is a feature of refractory ascites.
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PMID:Reduction of renal cortical blood flow assessed by Doppler in cirrhotic patients with refractory ascites. 979 6

Repeat open-heart operations are becoming more frequent with a patient population at higher risk. Sternal re-entry poses the risk of possible damage to vital structures. These include laceration of the myocardium, especially the right ventricle, tearing of patent grafts and internal mammary grafts in particular, or dislodgement of emboli from patent vein grafts. To minimize the risk associated with sternal re-entry, we adopted the method of establishing femoral artery-femoral vein cardiopulmonary bypass (CPB) in order to achieve cardiac decompression prior to sternotomy. Between June 1994 and October 1997, 94 patients underwent repeat open-heart operations at our institution. Of these, seven were a second time reoperation. Mean age was 62 years (range 31-80 years), and 65 were male. Fifty-nine patients had coronary bypass, 27 had aortic valve replacement, 45 had mitral valve replacement, and nine had other procedures (these numbers include patients having combined procedures). In patients with no known vascular disease, the femoral vessels were exposed, and if found suitable, were cannulated, and the patients connected to CPB. The sternum was opened with an oscillating saw, and on penetration through the posterior table, the heart was drained to allow for decompression. If the femoral vein cannula did not allow full bypass, ventilation was maintained until the right atrium was exposed and cannulated and full bypass was achieved. Femoro-femoral bypass was established in 75 patients. In 19 patients it was not done for the following reasons: eight patients had a diseased femoral artery, in one patient the femoral vein could not be cannulated, nonuse of CPB altogether occurred in three patients, and it was because of surgeon's preference in seven patients. In one patient a high pressure developed in the arterial line, requiring conversion to aortic cannulation during the course of CPB, without any negative consequences. There were no problems associated with sternal re-entry, no patient had limb ischemia or venous thrombosis. Two patients (2.6%) had complications related with femoral cannulation, with one having trauma to an atherosclerotic femoral artery requiring repair with vein interposition, and the other a tear of iliac vein requiring laparotomy. Groin wound infection occurred in five patients (6.6%), and groin hematoma in four patients (5.3%). All complications were treated successfully with no permanent damage. Operative mortality was 9% (seven patients). Causes of death included myocardial infarction (2), infection (3), respiratory (1), and cirrhosis (1). We conclude that femoro-femoral bypass prior to sternotomy is a safe and easy method to reduce the risk of sternal re-entry by allowing early decompression of the heart, and in unstable patients it offers better myocardial protection by earlier connection to CPB. Proper selection of patients is important in order to minimize related comorbidity. We recommend this method in redo patients in whom femoral cannulation is feasible.
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PMID:Femoro-femoral bypass for repeat open-heart surgery. 988 93

The causes and pathologic changes leading to fibrosis and cirrhosis after orthotopic liver transplantation (OLT) are not fully defined. The computerized pathology files were searched for cases of fibrosis/cirrhosis after OLT. Of 493 grafts from 435 patients, 35 grafts from 32 patients of posttransplantation liver fibrosis/cirrhosis were identified and retrieved (7%). Detailed histopathologic examinations of all post-OLT liver biopsy specimens were performed in conjunction with clinical, virologic, serologic, and molecular diagnostics information. Two cases with subcapsular septa and fibrous tissue close to hilum were excluded as false positives. Fibrosis/cirrhosis was confirmed in the remaining 33 grafts. In 20, the underlying cause was recurrent viral hepatitis, including eight with hepatitis C, 10 with hepatitis B, and two with combined hepatitis C and B. Another two with pretransplantation chronic hepatitis B developed cirrhosis without detectable virologic markers after OLT; these were biliary type secondary to obstruction in one, and chronic changes due to severe graft ischemia in one. Three patients acquired hepatitis C after OLT, with molecular confirmation available in two. In five patients, the underlying causes were Budd-Chiari syndrome and autoimmune hepatitis, recurrent autoimmune hepatitis, recurrent primary biliary cirrhosis, alcohol-induced liver disease, and recurrent bile duct carcinoma. Three cases had centrilobular fibrosis but without bridging septa or cirrhosis as a result of chronic rejection. It was concluded that (1) Cirrhosis after OLT is uncommon (7%). (2) Chronic rejection does not lead to cirrhosis, but it may result in centrilobular fibrosis. (3) In most (70%) cases, cirrhosis after OLT is attributed to recurrent or acquired viral hepatitis.
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PMID:Fibrosis/cirrhosis after orthotopic liver transplantation. 992 25

Acutely increased intraabdominal pressure can lead to multisystem organ dysfunction. Organ dysfunction consists of acute pulmonary failure secondary to compressive atelectasis and associated with high peak inspiratory pressures and impaired gas exchange, acute renal failure with marked oliguria without hypernaturia, intestinal and hepatic ischemia possibly leading to bacterial translocation or necrosis with peritonitis, increased intracranial pressures which may cause brain dysfunction or aggravate head injury edema, venous thrombosis and thromboembolism, and abdominal wall ischemia or necrosis. The diagnosis is made clinically in a patient with high peak inspiratory pressures, oliguria and an apparently tight abdomen, although urinary bladder pressure > or = 20 cm H2O pressure is suggestive. However, chronically increased intraabdominal pressure as is seen in the morbidly obese, pregnancy and cirrhosis may be misleading. As to treatment, once the diagnosis is made, the patient's abdomen should be opened and the tension relieved. The intestinal contents need to be protected and evaporative water loss minimized by either closing the skin and not the fascia or, if this is not possible, using an impermeable protective dressing. If the abdomen is difficult to close at the primary operation, it is best to prevent the development of an acute abdominal compartment syndrome by closing only the skin or leaving it open and using an impermeable dressing. In conclusion, the acute abdominal compartment syndrome has become increasingly recognized as a cause for multisystem organ failure. Recognition of the problem or prevention is mandatory for optimal patient survival.
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PMID:Multisystem organ failure secondary to increased intraabdominal pressure. 1144 Mar 93


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