Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An emergency liver transplantation was performed in a 22 year-old female for fulminant hepatitis. The donor had had splenectomy with portal vein thrombosis which was diagnosed and removed during portoscopy. Nineteen days later, abdominal pain with shock and hepatic failure occurred. X-rays showed pneumoperitoneum and aeric images in the liver area. Laparotomy disclosed massive liver necrosis with gaz under the Glisson's capsula. The hepatic artery was thrombosed. In spite of emergency retransplantation, the patient died 8 days later, due to systemic aspergillosis. Thrombosis of hepatic artery was particular by the importance of gaz-forming infection, and emphasizes the role of rejection. The discovery of portal thrombosis allows to outline the precautions necessary in case of splenectomized donors. The severeness of aspergillosis is underscored.
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PMID:[Gazeous necrosis of the liver due to hepatic artery thrombosis after liver transplantation]. 176 77

An autopsy case of pulmonary hypertension in a 29-year-old Japanese female with macronodular, posthepatic liver cirrhosis and hepatitis-B antigenemia was presented. No recognizable known cardio-pulmonary disease or portal thrombosis was obtained. Hepatitis-B antigen was demonstrated in the cirrhotic hepatocytes by a specific peroxidase antiperoxidase method. Characteristic pulmonary arterial changes including plexiform lesions with varying developmental stages were widely observed throughout the lungs. Complication of these two distinct disease processes seems to be rarely encountered in the literature. Discussion was focused on the possible interrelationship between the liver cirrhosis with hepatitis-B antigenemia and pulmonary hypertension. Proposed were presumptive underlying humoral, particularly immunological, abnormalities common to these diseases rather than mere incidental complications.
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PMID:Pulmonary hypertension associated with liver cirrhosis and hepatitis-B antigenemia. 634 Feb 45

Splenic Doppler impedance indices are influenced, in portal hypertensive patients, by the resistance of the portal system. The aim of the study was to verify the usefulness of these indices in evaluating the presence of a pathological increase in portal resistance in patients with complications after liver transplantation. Splenic impedance indices have been evaluated in 46 patients before orthotopic liver transplantation (OLT), and 2 days, 1, 4, 8, and 12 to 18 months after transplantation. The results showed that spleen size slowly decreased after liver transplantation. From a baseline longitudinal diameter value of 18.0+/-3.6 cm (M+/-SD), the decrease was by 0%+/-3%, 8%+/-8%, 13%+/-9%, 15%+/-11%, and 14%+/-11% at 2 days and 1, 4, 8, and 12 to 18 months after liver transplantation. Splenic impedance indices-resistance index = (peak systolic - end diastolic) / peak systolic velocity; pulsatility index = (peak systolic - end diastolic) / mean velocity-which were increased before liver transplantation, showed a rapid decrease to normal values: resistance index: from 0.62+/-0.08 to 0.55+/-0.08 after 2 days, and to 0.49+/-0.09, 0.51+/-0.10, 0.54+/-0.10, 0.55+/-0.11 after 1, 4, 8, 12-18 months; pulsatility index: from 0.96+/-0.21 to 0.82+/-0.17 after 2 days, and to 0.69+/-0.19,0.72+/-0.21, 0.81+/-0.26, 0.84+/-0.26 after 1, 4, 8, and 12 to 18 months. Patients who had a good outcome, without any major complications, showed a clear and steady decrease in splenic impedance indices. On the contrary, patients who had complications affecting portal resistance (e.g., acute rejection, relapse of chronic hepatitis C virus-related hepatitis or cirrhosis, stenosis of portal anasthomosis, portal thrombosis), showed a lack of decrease, or, after an initial decrease, a subsequent re-increase in splenic impedance indices to pathological values. Splenic impedance indices measured in patients with complications were higher than those of patients without complications (P < .0004). Specificity and sensitivity of splenic impedance indices in the evaluation of the presence of complications increasing portal resistance were good. In conclusion, after OLT, splenic impedance indices could be useful aspecific parameters for identifying patients with complications that are able to affect or increase portal resistance.
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PMID:Splenic impedance indices: a useful method to monitor patients after liver transplantation? 950 Jun 93

An 82-year-old male patient was admitted for liver dysfunction. Laboratory test showed the following data; aspartate aminotransferase (AST) 79 IU/l, alanine aminotransferase (ALT) 28 IU/l, total bilirubin (T. Bil) 0.9 U, zinc sulfate turbidity test (ZTT) 48.9 U, gamma-globulin 4.9 g/dl, immunoglobulin G (IgG) 5,046 mg/dl, anti-nuclear antibodies x 320, anti-mitochondrial antibodies (-), hepatitis B virus surface antigen (HBsAg) (-), HBcAb (-), anti-hepatitis C virus (anti-HCV) (-), hepatitis C virus (HCV-RNA) (-), anti-hepatitis G virus (anti-HGV) (-), alpha-fetoprotein 306.8 ng/ml, carcinoembryonic antigen (CEA) 2.3 ng/ml, carbohydrate antigen (CA) 19-9 77.2 U/ml. Abdominal ultrasonography and computed tomography showed a large mass occupying most of the right lobe and portal thrombosis in the liver. Liver biopsy revealed cirrhosis with inactive hepatitis in the nontumorous lesion and well-differentiated hepatocellular carcinoma in the tumorous lesion. We report a rare case of an aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma.
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PMID:An aged male patient with autoimmune hepatitis complicated by hepatocellular carcinoma. 1039 80

We describe the radiological features of 201 patients diagnosed as having hepatocellular carcinoma (HCC) in Southern Pakistan. The cases of biopsy-proven HCC were analysed retrospectively for years 1994-1998. Age, sex, underlying cirrhosis, hepatitis markers, and radiological description were recorded. The mean age was 56 years. There were 149 males and 52 females. 82% patients had underlying cirrhosis. The tumour size was measured in at least two dimensions, and the maximum mean tumour size at the time of diagnosis was 8.3 +/- 4.0 cm. Of the tumours 79.5% were more than 5 cm; 56% of primary HCC were multifocal; 51% involved the right lobe only; 15% involved the left lobe; 34% involved both lobes of liver. Portal vein thrombosis was detectable in 17%. There were no significant differences in the radiological patterns amongst patients who had hepatitis B virus related and hepatitis C virus-related HCC except for age.
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PMID:Radiological features of hepatocellular carcinoma in Southern Pakistan. 1167 64

The aim was to study the advantages of the use of a temporary portacaval shunt (PCS) with inferior vena cava (IVC) preservation during the piggyback technique for the anhepatic phase of orthotopic liver transplantation (OLT) performed in cirrhotic patients. Two groups of cirrhotic patients who underwent OLT with piggyback technique were compared; one with a PCS (n = 57) and the other, without PCS (n = 54). Patients with fulminant hepatitis, retransplantation, portal thrombosis, and previous portosystemic shunts were excluded. In both groups graft reperfusion was achieved by simultaneous arterial and venous revascularization. Donor, recipient, and surgical characteristics were similar in both groups. The PCS group had a significantly higher portal venous flow (PVF) than the no-PCS group (773 +/- 402 mL/min vs 555 +/- 379 mL/min, P = .004). Therefore, two subgroups were studied; the high PVF subgroup A (>800 mL/min), mean 1099 +/- 261 mL/min, and the low PVF subgroup B (<800 mL/min), mean 433 +/- 423 mL/min. Subgroup A, who were treated with PCS, required fewer blood transfusions and displayed better postoperative renal function; whereas, no differences were observed among subgroup B patients with versus without PCS. In conclusion, the use of a temporary PCS with piggyback technique during OLT in cirrhotics has advantages in patients who still maintain a high portal venous flow.
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PMID:Portacaval shunt and inferior vena cava preservation in orthotopic liver transplantation. 1638 77

The development of portopulmonary hypertension (PH) in a patient with end-stage liver disease is related to high cardiac output and hyperdynamic circulation. However, PH following liver transplantation is not fully understood. Of 617 pediatric patients receiving transplants between June 1990 and March 2004, 5 (median age 12 yr, median weight 24.5 kg) were revealed to have portopulmonary hypertension (PH) after living-donor liver transplantation (LDLT), as confirmed by echocardiography and/or right heart catheterization. All children underwent LDLT for post-Kasai biliary atresia. In 2 patients with refractory biliary complications, PH developed following portal thrombosis; 2 with stable graft function, who had had intrapulmonary shunting (IPS) before LDLT, were found to have PH in spite of overcoming liver dysfunction due to hepatitis. PH developed shortly after distal splenorenal shunting in 1 patient, who suffered liver cirrhosis due to an intractable outflow blockage. The onset of PH ranged from 2.8 to 11 yr after LDLT, and mean pulmonary artery pressure (mPAP) estimated by echocardiography at the time of presentation ranged from 43 to 120 mmHg. Three of the 5 patients are alive under prostaglandin I2 (PGI2) treatment. Of these, 1 is prepared for retransplantation for an intractable complications of liver allograft, while the other 2 with satisfactory grafts are being considered for lung transplantation. Even after LDLT, PH can develop with portal hypertension. Periodic echocardiography is essential for early detection and treatment of PH especially in the recipients with portal hypertension not only preoperatively but also postoperatively.
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PMID:Development of pulmonary hypertension in 5 patients after pediatric living-donor liver transplantation: de novo or secondary? 1662 93

Portal vein thrombosis (PVT) is a rare event in the general medical setting that commonly complicates cirrhosis with portal hypertension, and can also occur with liver tumors. The diagnosis is often incidental when a thrombus is found in the portal vein on imaging tests. However, PVT may also present with clinical symptoms and can progress to life-threatening complications of ischemic hepatitis, liver failure, and/or small intestinal infarction. This article reviews the pathophysiology of this disorder, with a major focus on PVT in patients with cirrhosis, and presents detailed guidelines on optimal diagnostic and therapeutic strategies.
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PMID:Portal vein thrombosis. 2545 5