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)

Microwave coagulation therapy (MCT) is one of the treatment modalities for patients with hepatocellular carcinoma (HCC). A 67-year-old man with liver cirrhosis underwent MCT during a laparotomy for a deeply located HCC (2.5 cm in diameter) at the border of the anterior and posterior segments of the right hepatic lobe. Two weeks after MCT, he complained of abdominal fullness. Portal vein thrombosis (PVT) was diagnosed because he had massive ascites and an echogenic mass in the portal vein on abdominal ultrasonography. PVT was successfully treated by fibrinolytic therapy with a selective infusion of urokinase via the superior mesenteric artery (SMA). There have been few reports on PVT as a complication of MCT. Attention should be paid to the possible occurrence of PVT as a critical complication after MCT for liver tumors adjacent to the portal vein. Fibrinolytic therapy via the SMA is thus considered to be an effective approach for PVT after MCT.
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PMID:Portal vein thrombosis caused by microwave coagulation therapy for hepatocellular carcinoma: report of a case. 1103 17

Portal vein thrombosis, except in hepatocellular carcinoma and severe cirrhosis, is due to one or several prothrombotic disorders with or without a local precipitating factor. We report a case of a portal and splenic vein thrombosis, without cavernoma and varices which occurred in a 72-year-old man with abdominal pain and weakness. Three prothrombotic states including latent myeloproliferative disorder, antiphospholipid syndrome, and factor II G202101 mutation, were observed. Anticoagulant treatment resulted in complete repermeation of the portal and splenic veins without a hemorrhagic event. This illustrates that several prothrombotic states may occur in a single patient with portal vein thrombosis. Early anticoagulant therapy, in recent portal vein thrombosis, can result in repermeation.
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PMID:[Portal vein thrombosis associated with a myeloproliferative disorder, prothrombin G20210A mutation, antiphospholipid syndrome, with repermeation during anticoagulant therapy]. 1152 Nov 10

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

Between 1995 and 1997 we studied 100 patients with hepatocarcinoma (HCC) and cirrhosis. Of these 74 were males and 26 females with a mean age of 66 years. 13% patients were only HbsAg positive, 75% only anti-HCV positive, 6% HbsAg and anti-HCV and the etiology in 6% of cases was alcoholic. Alpha-foetoprotein was >400 ng/ml in only 18% of cases and portal thrombosis was present in 12%. Mononodular HCC was observed in 63% of cases (small HCC in only 38%) and in 79% was localized to the right lobe. Of the mononodular types, 70% were shown by echography to be hypoechoic, 6% hysoechoic, 6% hyperechoic and 17% mixed patterns. Histologically, 49% were well-differentiated, 45% moderately-differentiated and 6% poorly-differentiated. No correlation was found between histologic pattern and number of nodules. Well-differentiated HCC was found in 51% of mononodular types and in 46% of multinodular types. Moderately-differentiated HCC was detected in 46% and 43% respectively and poorly-differentiated HCC in 3% and 11% respectively. No correlation was found between number of nodules and the degree of Edmonson.
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PMID:Main characteristics of hepatocellular carcinoma and cirrhosis and therapeutic approaches. 1194 47

Thrombosis of the abdominal veins is a rare clinical condition which can be assimilated with the more frequent localization of deep venous thrombosis of the lower limbs. In the last few years great attention has been paid to possible risk factors for thrombosis of the abdominal veins. Two risk factors that have been identified are the presence of internal diseases and congenital and/or acquired abnormalities of haemostasis. The authors describe 3 clinical cases (splenic and portal thrombosis due to congenital thrombophilia, Budd-Chiari syndrome, portal cavernoma consequent to ovarian neoplasia) with different etiopathogenesis to show how this apparently rare condition is today more frequently encountered and easier to recognize. In the presence of thrombosis of major venous structures the search and the identification of intrinsic internal risk factors and of congenital and acquired thrombophilic disorders remains of great importance. Screening for thrombophilia includes blood C and S proteins, AT III, homocysteine, Leiden mutation of the factor V gene, G20210A mutation of the prothrombin gene, antiphospholipid antibodies. The presence of one or more of these risk factors allows the identification of the cases of portal thrombosis (EHPVO) responsible for about 10% of all the cases of portal hypertension, without cirrhosis or other hepatic lesions. The primary diagnostic procedure however remains color-Doppler ultrasonography which represents the most simple and the cheapest diagnostic investigation for the study of the portal and suprahepatic vein system, but it's strictly operator dependent.
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PMID:Dangerous thrombophilic states and internal pathologies: 3 cases of thrombosis of the abdominal veins. 1220 67

Recurrent hepatocellular carcinoma (HCC) deserves multidisciplinary treatment in addition to surgical resection. Radiofrequency ablation (RFA) is an evolving, localized, thermal ablative treatment for unresectable hepatocellular carcinoma (HCC). Though the preliminary results of RFA in clinical studies are encouraging, its serious complications should not be underestimated. Portal vein thrombosis as a result of direct blood vessel injury by RFA is rarely reported and is potentially fatal in patients with limited liver reserve due to underlying liver cirrhosis. We present a case of portal vein thrombosis as a complication of RFA treatment for recurrent HCC and illustrate its underlying possible mechanism.
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PMID:Portal vein thrombosis after radiofrequency ablation for recurrent hepatocellular carcinoma. 1252 97

Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. PVT can be caused by one of three broad mechanisms: (1) spontaneous thrombosis when thrombosis develops in the absence of mechanical obstruction, usually in the presence of inherited or acquired hypercoagulable states; (2) intrinsic mechanical obstruction because of vascular injury and scarring or invasion by an intrahepatic or adjacent tumor; or (3) extrinsic constriction by adjacent tumor, lymphadenopathy or inflammatory process. Usually, several combined factors are necessary to result in PVT. The consequences of portal vein thrombosis are mostly related to the extension of the clot within the vein. Gastrointestinal bleeding from gastroesophageal varices is the most frequent presentation. Noninvasive imaging techniques are currently used for the screening of patients and the initial diagnosis of PVT. The invasive techniques are reserved for cases when noninvasive techniques are inconclusive, before percutaneous interventional treatment, or in preoperative assessment of patients who are candidates for surgery. Recanalization of the portal vein with anticoagulation alone may not be consistent or appropriate in highly symptomatic patients. Catheterization of the superior mesenteric artery (SMA) is helpful for diagnosis as well as for therapy by allowing the intra-arterial infusion of thrombolytic drugs in the same setting. Direct transhepatic portography allows precise determination of the degree of stenosis and extension within the portal vein, as well as pressure measurements. Thrombotic occlusions of the portal, mesenteric, and splenic veins can be managed by mechanical thrombectomy (MT) or pharmacologic thrombolysis. Underlying occlusions because of organized or refractory thrombus or fixed venous stenosis are best corrected by balloon angioplasty and stent placement. Access into the portal venous system can also be established through creating a transjugular intrahepatic portosystemic shunt (TIPS). Creating a TIPS is also important in the setting of PVT associated with cirrhosis to decompress portal hypertension and improve portal venous flow. PVT involving the portal, splenic, and/or mesenteric veins can also complicate a preexisting TIPS in which case the shunt can be readily used as therapy access. Several techniques may be used to recanalize the shunt and portal venous system, including thrombolytic therapy, balloon angioplasty/embolectomy, suction embolectomy, basket extraction of clots, and mechanical thrombectomy with a variety of devices. Advantages of MT include the potential to rapidly remove thrombus without the need for prolonged thrombolytic infusions, and reducing the potential life-threatening complications of thrombolytic therapy. Possible drawbacks include the risk of intimal or vascular trauma to the portal vein, which may promote recurrent thrombosis.
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PMID:Applications of percutaneous mechanical thrombectomy in transjugular intrahepatic portosystemic shunt and portal vein thrombosis. 1277 31

A 78-year-old man was admitted to our clinic because of fatigue. Imaging modalities showed beaded stricture and dilation of the intrahepatic left segmental bile duct. Anomalous pancreatico-biliary ductal union and polycystic kidney disease were absent. Resection of the hepatic left lobe was performed. Grossly, cholesterol stones were impacted in the dilated intrahepatic large bile ducts, and multiple tiny cysts measuring 2-8 mm were noted in the peribiliary areas (peribiliary cysts). Histologically, the cholesterol hepatoliths consisted of cholesterol empty spaces and fibrinous materials, and, in places, foreign body giant cells were seen around the cholesterol crystals. The peribiliary cysts were lined by a layer of cuboidal epithelia. They were intimately intermingled with intrahepatic peribiliary glands, and a close association between the two components was recognized in some places. A mild degree of ascending cholangitis was noted. Bile duct anomalies including von-Meyenburg complexes and simple cysts were not recognized. Peribiliary cysts have been reported in various liver diseases, including portal hypertension, portal thrombosis, cirrhosis, hepatocellular carcinoma, and adult polycystic kidney disease. However, to the best of our knowledge, there have been no reports on peribiliary cysts developing in hepatolithiasis. The present case indicates that peribiliary cysts occur in cholesterol hepatolithiasis, and suggests that they are derived from cystic dilations of intrahepatic peribiliary glands.
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PMID:Cholesterol hepatolithiasis with peribiliary cysts. 1451 24

DIAGNOSTIC CIRCUMSTANCES: Portal vein thrombosis is the second cause of portal hypertension after cirrhosis in Western countries. Diagnosis can be either made at the acute stage in the context of abdominal pain or after appearance of a porto-portal collateral venous circulation leading to the formation of a portal cavernoma, the diagnosis being made in the circumstance of rupture of oesophageal varicose veins or manifestations of hypersplenism. AETIOLOGICAL SURVEY: In the absence of hepatocellular carcinoma, causes that need to be investigated are cirrhosis, local factors (intra-abdominal sepsis, abdominal surgery, splenectomy or pancreatitis), and one or several prothrombotic affections (acquired or inherited prothrombotic states are present in 70% of cases, with myeloproliferative disease ranking first). REGARDING TREATMENT: Anticoagulant therapy generally allows recanalisation of the thombosed veins in recently constituted thrombosis. Some patients at the portal cavernoma stage can also benefit from anticoagulant therapy: patients with a prothrombotic state without large oesophageal-gastric varicose veins. In the case of large oesophageal-gastric varicose veins that have never bled, treatment to prevent haemorrhages due to portal hypertension according to the same modalities as in cirrhosis must be associated with the prescription of an anticoagulant. In the absence of prothrombotic affection or in patients having already suffered from haemorrhages due to portal hypertension, the benefit of anticoagulant therapy is less clearly established.
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PMID:[Portal vein thrombosis]. 1453 80

Portal vein thrombosis (PVT) is the most frequent cause of hypertension portal extrahepatic. It is a rare disorder an the main risk factors are cirrhosis, hepatobiliary malignancies and prothrombotic disorders, which have been identified as major risk. Therapy with anticoagulants must to be considered in acute portal thrombosis or chronic one and proven hypercoagulability. We present the case of a twenty-nine years old patient, with extrahepatic portal hypertension secondary to portal and splenic vein thrombosis, who was diagnosed because of splenomegaly and a coagulation disorder. A protein C deficiency were discovered and anticoagulation and beta-blocker therapy were initiated. One year later the patient had not presented complications concerning to the disease or to the treatment.
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PMID:[Extrahepatic portal hypertension: spleno-portal thrombosis secondary to protein C deficiency]. 1475 3


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