Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From January 1st, 1975, up to January 1st, 1986, a meso-caval interposition shunt was performed in 86 patients (electively with one exception), using a 16 or 18 mm lumen Dacron prosthesis. The criteria for selection for operation were a liver volume of 1000-2500 ml, a residual portal perfusion of 15 to 30%, exclusion of an activity of the liver process and stenosis of the hepatic artery or coeliac trunk. The cause of portal hypertension was liver cirrhosis in 77 patients (89.5%), prehepatic block in five (4.5%), liver fibrosis in three patients (3.5%), and myeloproliferative disease in one patient (1%). The study represents a prospective assessment and included 52 men and 32 women with a mean age of 43 years. Intraoperative flow measurement demonstrated a residual portal perfusion in all 17 patients measured after the shunt. In-hospital mortality was 8%, late mortality 39%; the fate of four patients is unknown. The main causes of death were liver failure and hepatocellular carcinoma. The rate of encephalopathies over the whole period was 10.5%. The actual survival rate was over 70% for five and over 50% for ten years. Postoperative angiographic studies confirmed by sequential scintigraphy demonstrated a residual portal perfusion in 75% of the patients postoperatively, 60% after six months and in 38% after two years. Thus it could be demonstrated that the meso-caval interposition shunt is converted to a total shunt in the long term. The total shunt patency rate was 90%. The meso-caval interposition shunt is certainly no ideal procedure but is useful in the selective or semiurgent management of patients with liver cirrhosis and portal hypertension.
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PMID:Prognosis after meso-caval interposition shunt. Experience of eighty-six consecutive cases over a period of ten years. 296 34

We have presented a working hypothesis showing the possible interrelations between proliferative, aproliferative and autoimmune disorders that may follow infection with lymphotropic herpesviruses. Aproliferative disorders in this context may also indicate immune or hematopoietic deficiency. Although this hypothesis can currently be best documented with the lymphotropic viruses (herpesviruses as well as similarly HTLV and HIV), the model may apply as well--with certain variations--to other viral infections such as with hepatitis virus B or C with acute or chronic infectious diseases, post-infectious arthritis, aplastic anemia, and other autoimmune liver diseases, as well as neoplastic diseases (hepatocellular carcinoma, chronic lymphocytic leukemia). The working hypothesis as depicted in Figure 2 permits a preview of which combinations of symptoms may occur in an individual disease independent of its initial classification and what clinical testing should be done respectively, and it also permits certain prognostic considerations. The above-mentioned transitions or combinations of various disease patterns have been repeatedly described in the medical literature (to refer to only a few examples: APL and MPD, HD and MDS, SLE and aplastic anemia, SLE and Kikuchi's disease; 23, 80-83). Finally the hypothesis can ideally serve as the basis for future planning of clinical research.
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PMID:A unifying concept of viral immunopathogenesis of proliferative and aproliferative diseases (working hypothesis). 789 76

The presence of serum antiphospholipid antibodies is associated with arterial and venous thrombosis. We report two cases of portal vein thrombosis associated with serum antiphospholipid antibodies. In our two patients, systemic lupus erythematosus, chronic liver disease, hepatocellular carcinoma, myeloproliferative disorders and coagulation inhibitor deficiency were excluded after extensive tests were performed to diagnose portal vein thrombosis and after a follow-up period of 6 and 7 years, respectively. The test for serum antiphospholipid antibodies was positive on two occasions in both patients. Both patients were treated with endoscopic sclerotherapy for bleeding esophageal varices and with long term anticoagulant therapy for the prevention of recurrent thrombosis. These two cases suggest that serum antiphospholipid antibodies should be investigated in patients with portal vein thrombosis of unexplained etiology.
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PMID:[Portal thrombosis disclosing antiphospholipid syndrome. 2 cases]. 899 Nov 50

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

The Budd-Chiari syndrome was primarily described as hepatic vein thrombosis within the liver, but it now includes inferior vena cava (IVC) thrombosis and other conditions that cause hepatic vein outflow obstruction. This author and several others maintain that primary hepatic vein thrombosis and primary IVC thrombosis represent two different clinical disorders. Primary thrombosis of the IVC most commonly occurs in its hepatic portion, which seems to be predisposed to thrombosis and has been called membranous obstruction of IVC, because the thrombus organizes into a fibrous and frequently membranous occlusion of the IVC. The hepatic vein orifices are affected to varying degrees, resulting in congestive liver damage. The cause of IVC thrombosis may be a hypercoagulable state such as coagulation factor deficiency and myeloproliferative disorders, but is more often idiopathic. In Nepal, it is endemic with a suspected association with infections. To consider IVC thrombosis and the congestive liver damage as a disease entity, this author proposes the term obliterative hepatocavopathy, separate from hepatic vein thrombosis. Clinically obliterative hepatocavopathy is less severe in its acute phase compared with hepatic vein thrombosis, but it aggravates occlusion of hepatic vein orifices with recurrent thrombosis. Primary hepatic vein thrombosis and obliterative hepatocavopathy display different hemodynamics of the hepatic veins, IVC, and portal vein; dilatation of the subcutaneous veins in the body trunk is more pronounced in obliterative hepatocavopathy because the ascending lumbar vein becomes the major collateral route. Congestive liver cirrhosis develops after a long clinical course that may be complicated by hepatocellular carcinoma.
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PMID:Inferior vena cava thrombosis at its hepatic portion (obliterative hepatocavopathy). 1192 76

Large regenerative nodules are benign liver lesions that are frequently seen in Budd-Chiari syndrome and less commonly in other vascular disorders of the liver or systemic conditions such as autoimmune disease, myeloproliferative disorders, and lymphoproliferative disorders. They are usually multiple, with a typical diameter of 0.5-4 cm. At pathologic analysis, large regenerative nodules are well-circumscribed, round lesions that may distort the contour of the liver. Only a minority of these nodules are detected at cross-sectional imaging. At multiphasic helical computed tomography, large regenerative nodules are markedly and homogeneously hyperattenuating on arterial dominant phase images and remain slightly hyperattenuating on portal venous phase images. Large regenerative nodules are bright on T1-weighted magnetic resonance images and show the same enhancement characteristics after intravenous bolus administration of gadolinium contrast material. They are predominantly isointense or hypointense relative to the liver on T2-weighted images. There is no evidence that large regenerative nodules degenerate into malignancy. If these nodules are misdiagnosed as multifocal hepatocellular carcinoma, patients might be denied transplantation or offered inappropriately aggressive therapy such as transcatheter arterial chemoembolization. Understanding the clinical setting and imaging appearance of large regenerative nodules can help avoid misdiagnosis as other hypervascular masses.
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PMID:Benign regenerative nodules in Budd-Chiari syndrome and other vascular disorders of the liver: radiologic-pathologic and clinical correlation. 1211 Jul 14

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

Myeloproliferative disorder, liver cirrhosis with portal hypertension, deficiency of natural anticoagulant proteins, gene mutation and hepatocellular carcinoma are the most frequent causes of portal vein thrombosis (PVT). Higher accuracy of the diagnostic methods is the reason why today the cause of PVT can be found more frequently. With imaging methods, PVT with or without cavernous transformation can be diagnosed. Fresh thrombus can be undetected in sonography due to the low echogenity but can be recognized in color Doppler sonography, especially with contrast-enhancing agent. Contrast-enhanced 3D MR angiography allows a comparable accuracy in the detection of PVT as digital subtraction angiography. Therapeutical options of PVT consist of mechanical recanalization of the portal vein, local fibrinolysis with or without placement of transjugular intrahepatic portosystemic stent shunt (TIPS), combination of mechanical recanalization and local fibrinolysis, systemic thrombolytic therapy, anticoagulation alone and surgical thrombectomy. Once PVT is found in sonography, Doppler sonography may be performed in order to distinguish benign from malignant thrombus. If further information is needed, MR angiography or contrast enhanced CT is the next step. If these tests are unsatisfactory, digital subtraction angiography should be performed. Until the early nineties, shunt surgery was recommended in patients with PVT who bled despite endoscopic treatment. Today, in symptomatic noncavernomatous PVT, recanalization with local methods is recommended. Additional implantation of TIPS should be performed when the patient is cirrhotic. In recent PVT in non-cirrhotic patients anticoagulation alone is recommended. It is expected that in old PVT anticoagulation can prevent further extension of the thrombus.
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PMID:Portal vein thrombosis: etiology, diagnostic strategy, therapy and management. 1596 89

Portal vein thrombus has been detected in patients with liver cirrhosis, pancreatitis, ulcerative colitis, septicemia, myeloproliferative disorder, and neoplasm. The formation of portal tumor thrombus by hepatocellular carcinoma is well recognized, because of its high incidence, and subsequent development of portal hypertension such as rupture of varices, ascites and liver failure indicates the poor prognosis. In gastric cancer, portal hypertension as an initial presentation is extremely rare. Herein we report a case presenting as portal hypertension caused by tumor thrombus without invasion of liver parenchyma. It is presumed to be intraluminal tumor thrombus originating from primary foci of gastric adenocarcinoma. Tumor thrombus in the portal vein is demonstrated on the PET-CT.
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PMID:[A case of gastric adenocarcinoma presenting as portal hypertension]. 2283 99

Prothrombotic haematological disorders, in particular myeloproliferative disorders, are identified in a significant proportion of patients with Budd-Chiari syndrome and portal vein thrombosis (PVT). Multiple prothrombotic disorders may coexist. PVT is diagnosed in one fourth of patients with cirrhosis and is more common with advanced liver disease and hepatocellular carcinoma. PVT in cirrhosis can precipitate decompensation. Intrahepatic microthrombosis may play a role in the pathogenesis of hepatic fibrosis. Sinusoidal obstruction syndrome is usually a complication of myeloablative treatment before haematopoietic stem cell transplantation. Post-transplant lymphoproliferative disorders can complicate liver transplantation and are related to Epstein-Barr virus infection. Hepatitis B reactivation in patients receiving chemotherapy for haematological malignancies is very common without pre-emptive treatment, and can lead to liver failure. Liver involvement is common in primary haematological diseases, such as haemolytic anaemias, lymphomas and leukaemia.
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PMID:Liver in haematological disorders. 2409 Sep 39


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