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)

Intrahepatic pressure was measured in 148 patients with liver disease (32 outpatients, 116 inpatients) and 13 controls with almost normal liver histology (inpatients), with a 23-gauge needle (inner diameter 0.38 mm). Intrahepatic pressure was significantly elevated in the group order of chronic active hepatitis without bridging necrosis (n = 17, 9.2 +/- 3.0 mm Hg), chronic active hepatitis with bridging necrosis (n = 24, 12.3 +/- 5.7), and posthepatitic liver cirrhosis (n = 65, 18.8 +/- 4.2), compared with controls (n = 13, 6.8 +/- 2.7), whereas it was not elevated in the group of idiopathic portal hypertension (n = 9, 7.8 +/- 2.5 mm Hg), acute hepatitis (n = 10, 8.4 +/- 2.6 mm Hg), and chronic persistent hepatitis (n = 23, 7.9 +/- 2.7 mm Hg), compared with controls. As complications, four patients had abdominal discomfort continuing for more than a day; however, patients were allowed to walk after they had rested on their beds for 30 min. In 37 patients (27 with cirrhosis, seven idiopathic portal hypertension, and three others), portal vein and/or hepatic vein catheterization was performed during the same procedure of intrahepatic pressure measurement. Intrahepatic pressure showed significant correlations with corrected wedged hepatic vein pressure (r = 0.91), portohepatic gradient (r = 0.69), wedged hepatic vein pressure (r = 0.79), and portal vein pressure (r = 0.68). Slopes were 0.97, 0.83, 0.66, and 0.65, respectively. In conclusion, intrahepatic pressure reflects hepatic sinusoidal pressure (corrected wedged hepatic vein pressure), and intrahepatic pressure starts to elevate at the stage of chronic active hepatitis.
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PMID:Measurement of intrahepatic pressure as an index of hepatic sinusoidal pressure. 366 15

Patients with end-stage renal disease combined with tense ascites caused by decompensated liver cirrhosis are sometimes encountered in a hemodialysis center. A big problem for the management of these patients is the tendency of hypotension during ultrafiltration. Subsequent fluid accumulation, especially in the abdominal cavity, causes breathing difficulty and abdominal discomfort. We present a new technique, ascites ultrafiltration, to solve this problem. Using the same equipment as for ordinary hemodialysis, and incurring the same cost, we removed directly approximately 8 L of ascites fluid during each nearly 4-hour session. No hemodynamic instability was noted. We proved this technique to be an effective and safe alternative method for this group of patients.
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PMID:Hemodialysis alternative with ascites ultrafiltration for an end-stage renal failure patient associated with tense ascites secondary to decompensated liver cirrhosis. 895 43

To determine adverse events of ribavirin in the treatment of chronic hepatitis C, 41 patients (18 with cirrhosis), treated with ribavirin at an initial dose of 600-1200mg day(-1), were analysed retrospectively (six patients were treated twice because adverse effects during the first treatment necessitated cessation of ribavirin). Indications for ribavirin included a contraindication (n = 15) an intolerance (n = 11) or a non-response (n = 15) to interferon (IFN). Ribavirin was combined with IFN 3 million units (MU) three times weekly for 15 patients and with azathioprine for six patients (five of whom were transplant patients). No cirrhotics and only one patient treated with ribavirin + IFN received azathioprine. The mean duration of treatment was 5 months (range 1-18 months). Sixteen of 47 treatments (34%) with ribavirin were stopped: four because of vomiting (8.5%), two for psychiatric disorder, one for dry cough, one for an unrelated cause, and eight (at 1-2 months) because of a fall in the level of haemoglobin (Hb) of 4.6 g dl(-1) (range 2.7-5.9 g dl[-1]); however, according to the rules of international protocol, we would have expected only four treatments (two in patients receiving azathioprine) with Hb < 8.5 g dl(-1) to be stopped. The decrease in Hb level occurred more slowly in patients treated with IFN plus ribavirin than in patients treated with ribavirin alone and was of lower clinical significance in patients with cirrhosis than in patients without cirrhosis. After exclusion of patients receiving azathioprine, there was no significant difference in the fall of Hb level between cirrhotic and non-cirrhotic patients and between patients treated with IFN plus ribavirin and patients treated with ribavirin alone. Interestingly, the platelet count of patients treated with IFN plus ribavirin fell less than in patients treated with IFN alone. The most important and expected adverse event associated with ribavirin was haemolysis. Anaemia < 8.5 g dl(-1), requiring cessation of ribavirin therapy, was present in 9% of patients and was worsened by azathioprine. Abdominal discomfort and dry cough were other, potentially important, clinical adverse events found in our study.
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PMID:Effects of cirrhosis, interferon and azathioprine on adverse events in patients with chronic hepatitis C treated with ribavirin. 927 22

Cholestatic liver disease is primarily caused by impaired bile production on the level of hepatocytes and cholangiocytes. Clinically cholestasis can be divided into intrahepatic and extrahepatic forms based on the presence or absence of dilated bile ducts (sonography). Intrahepatic cholestasis is most frequently caused by end stage liver cirrhosis followed by primary cholangiopathies and canalicular transport defects in hepatocytes. The causes of the most important cholangiopathies, such as Primary Biliary Cirrhosis (PBC) and Primary Sclerosing Cholangitis (PSC) are so far not known. Therefore, drug therapy of cholestatic liver disease focuses on the improvement of symptoms such as fatigue, pruritus, abdominal discomfort, jaundice, xanthoma, hypercholesterolemia, portal hypertension, blood count abnormalities, osteoporosis/osteomalacia, and the prevention of complications such as bile-duct strictures in PSC and development of cholangiocarcinoma. The first choice drug in the treatment of cholestatic liver disease of various causes is urosodeoxycholic acid (UDCA), that has been shown to decrease bile acid toxicity in general and prolong the transplant free survival of patients with PBC. If cholestasis persists cirrhosis of the liver is the major complication and liver transplantation may be the definitive treatment in advanced cases of cholestatic liver disease.
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PMID:[Cholestatic liver diseases]. 945 66

Esophageal varices are commonly caused by portal hypertension secondary to cirrhosis. We report the case of a 71-year-old woman who presented with esophageal variceal bleeding due to portal hypertension caused by an arteriovenous fistula. The fistula, which was probably brought about by a liver biopsy performed 18 years previously, was complicated by bleeding. Since this event, the patient has reported right upper quadrant pain. Embolization resulted in elimination of the varices as well as abdominal discomfort.
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PMID:Arterioportal fistula: a rare cause of portal hypertension and abdominal pain. 1168 26

The biochemical, clinical and histological findings are described in nine patients of the Gastroenterology Service of the Guillermo Almenara Irigoyen National Hospital - EsSALUD, with diagnosis of nonalcoholic steatohepatitis (NASH) between January 1996 and April 1998.They did not have significant differences in relation to sex prevalence (5 males and 4 women). Five patients were obese, 2 patients had diabetes mellitus, 5 hyperlipidemic values and a patient was taking prednisone for more than 2 years. Only 2 patients were asymptomatic at the moment of the study; while 4 patients presented with abdominal discomfort, 2 patient had pain in the right upper quadrant (RUQ), 5 patients referred fatigue and hepatomegaly was found on clinical examination. All the patients presented high levels of aminotransferases at the study. All the patients had steatohepatitis in the histology with different combinations of injury to the hepatocyte. Fibrosis and cirrhosis were found in 3 patients. Our results were compared with that described by other authors.
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PMID:[NASH: REPORT OF THE FIRST CASES AT THE GUILLERMO ALMENARA HOSPITAL] 1213 83

Multilobular biliary cirrhosis and portal hypertension are frequent complications of cystic fibrosis liver disease, leading to esophageal varices and splenomegaly. Therapy is focused on variceal bleeding control; however, reduction of spleen volume is also important to restore gastric volume and resolve invalidating abdominal discomfort. We report long-term follow up (median duration, 5.5 years; range, 14 months-21.5 years) of 6 patients with cystic fibrosis (4 men, 2 women; median age, 14 years; range, 8-18 years) who underwent splenectomy with a splenorenal shunt operation. Three patients received elective surgery for massive splenomegaly with important abdominal discomfort, recurrent variceal bleeding, and hypersplenism. Three were urgently treated to control variceal bleeding after several sessions of sclerotherapy. All but 2 received antipneumococcal vaccination before surgery. Four patients had a weight gain of 10% within 3 months of surgery, and 3 developed spontaneous puberty. Lung function remained stable, and there was an overall reduction of respiratory tract infections. The youngest patient, however, died of overwhelming septicemia during treatment with steroids. Although total splenectomy has important risks, in well-selected cases, it can have benefits. Immuno- and chemoprophylaxis, combined with patient awareness of supplementary risk of infections is indispensable to minimize septic complications.
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PMID:Outcome of total splenectomy with portosystemic shunt for massive splenomegaly and variceal bleeding in cystic fibrosis. 1695 92

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease of unknown aetiology characterised by inflammation and fibrosis of the biliary tree. The mean age at diagnosis is 40 years and men are affected twice as often as women. There is a reported annual incidence of PSC of 0.9-1.31/100,000 and point prevalence of 8.5-13.6/100,000. The onset of PSC is usually insidious and many patients are asymptomatic at diagnosis or have mild symptoms only such as fatigue, abdominal discomfort and pruritus In late stages, splenomegaly and jaundice may be a feature. In most, the disease progresses to cirrhosis and liver failure. Cholangiocarcinoma develops in 8-30% of patients. PSC is thought to be immune mediated and is often associated with inflammatory bowel disease, especially ulcerative colitis. The disease is diagnosed on typical cholangiographic and histological findings and after exclusion of secondary sclerosing cholangitis. Median survival has been estimated to be 12 years from diagnosis in symptomatic patients. Patients who are asymptomatic at diagnosis, the majority of whom will develop progressive disease, have a survival rate greater than 70% at 16 years after diagnosis. Liver transplantation remains the only effective therapeutic option for patients with end-stage liver disease from PSC, although high dose ursodeoxycholic acid may have a beneficial effect.
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PMID:Primary sclerosing cholangitis. 1706 36

The Budd-Chiari syndrome (BCS), characterized by hepatic venous outflow occlusion, is rare in children. We describe the cases of 3 patients with BCS who presented at different stages of liver dysfunction that required tailored management. A 10-year-old boy who presented with a weeklong history of abdominal discomfort received an early diagnosis. Treatment with thrombolytic therapy and adjunctive percutaneous interventional radiologic management led to a favorable outcome in this patient. A 2-year-old girl referred with a 6-week illness not amenable to thrombolytic therapy was managed with a pericardial patch atriocavoplasty to restore hepatic venous outflow tract patency. The third patient, a 5-year-old girl, presented with established cirrhosis and massive ascites. After we controlled the ascites with an extracorporeal shunt system and nutritional resuscitation, we conducted an orthotopic liver transplantation on this patient. The stage of disease at diagnosis influences the management strategy, and an early diagnosis offers patients the best possible chance of cure without major surgery. However, a later presentation can still be successfully managed by more radical surgical interventions. The aims of this case report were to emphasize the importance of a high index of suspicion in the diagnosis of pediatric BCS and to highlight the importance of early referral to a specialized pediatric liver unit with the necessary facilities to deal with the medical and surgical aspects of management.
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PMID:The Budd-Chiari syndrome in children: the spectrum of management. 1710 71

The enteric-coated mycophenolate sodium (EC-MPS) is a new formulation of mycophenolic acid with a gastro-resistant enteric coating, which releases the drug in the intestine, reducing the incidence of the gastrointestinal (GI) adverse effects. The present work provided a summary of 20 patients with liver transplantation and more than a 1 year of treatment with mycophenolate mofetil (MMF) who, after presentation of GI complications, were converted to EC-MPS. The patients were followed over a 3-month period after beginning EC-MPS treatment. The mean age of the cohort was 53 +/- 10 years and included 75% men. The reasons for transplantation were ethanol cirrhosis (70%), hepatitis C cirrhosis (30%), hepatocarcinoma (5%), and Wilson's disease (5%). At baseline, all patients were being treated with cyclosporine (CsA). CsA doses and levels were reduced during follow-up: baseline dose 179 mg/day versus 143 mg/day at 3 months; levels: 90.4 ng/mL versus 85.8 ng/mL, respectively (P = .017). The administered dose of EC-MPS was 720 mg/day in all cases. The GI complications at baseline were: diarrhea 60% (92% moderate-severe), abdominal discomfort 60% (58% moderate), abdominal pain 45% (44% moderate-severe), gas 40% (38% moderate-severe), nausea 20% (25% moderate), and dyspepsia 20% (mild). After 3 months of EC-MPS treatment, only two patients (10%) displayed moderate diarrhea. The renal evolution was favorable, serum creatinine was reduced, and 24-hour creatinine clearance significantly increased (creatinine: 1.78 +/- 1.6 mg/dL at baseline versus 1.30 +/- 0.3 mg/dL at 3 months, P = .002; creatinine clearance: 72.8 +/- 18 mL/min versus 79.6 +/- 13 mL/min, P = .001). Conversion of MMF to EC-MPS in liver transplant recipients solved the GI tolerability problems and improved renal function during the first 3 months, probably due to the concomitant reduction of anticalcineurinic dose.
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PMID:Clinical evolution in the first 3 months of patients after liver transplantation in maintenance phase converted from mycophenolate mofetil to mycophenolate sodium due to gastrointestinal complications. 1788 75


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