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)

A 35-year-old man with acute promyelocytic leukemia received an allogeneic bone marrow transplant (BMT) in second complete remission. The donor was his 18-year-old brother, a chronic hepatitis B virus (HBV) carrier with detectable serum hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg) and hepatitis B virus DNA (HBV DNA). Before BMT, the recipient was immune to HBV, with serum antibody to HBsAg (anti-HBs), antibody to HBeAg (anti-HBe) and normal liver function. Examination of the recipient serum drawn 2 months after BMT revealed reverse seroconversion from anti-HBs/anti-HBe to HBsAg/HBeAg, which remained positive thereafter. Upon reducing cyclosporin 6 months after BMT, acute hepatitis occurred with HBV DNA in serum as evidence of active HBV replication; the patient then developed chronic hepatitis which progressed to cirrhosis and hepatic decompensation within 8 months. Transfusion of HBV DNA/HBeAg-positive bone marrow is thus harmful even when the recipient has anti-HBs prior to BMT.
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PMID:Reverse seroconversion of hepatitis B virus infectious status after allogeneic bone marrow transplantation from a carrier donor. 152 9

Much progress has recently been made in understanding the biochemistry and physiology of endogenous fibrinolysis. As a result, a better understanding of the mechanisms and clinical consequences of disordered fibrinolysis has emerged. Increased fibrinolytic activity is an uncommon but important cause of hemorrhagic disease. Congenital disorders of fibrinolysis which cause bleeding include increased plasma plasminogen activator activity and deficiency of alpha-2 antiplasmin. Acquired disorders associated with increased fibrinolytic activity and bleeding include liver cirrhosis, amyloidosis, acute promyelocytic leukemia, some solid tumors, and certain snake envenomation syndromes. Increased fibrinolysis is important to recognize because epsilon-aminocaproic acid (EACA) may be required to prevent or control bleeding. Diminished fibrinolytic activity has been associated with a variety of thrombotic disorders, but a direct cause-and-effect relationship has yet to be established. Congenital abnormalities of fibrinolysis associated with thrombosis include plasminogen deficiency, decreased endothelial generation of plasminogen activator activity, and certain abnormal fibrinogens. Thrombosis in these disorders is effectively managed with warfarin. Diminished fibrinolysis has also been reported in "idiopathic" venous thrombosis, oral contraceptive-induced and post-operative venous thrombosis, coronary artery disease, cerebrovascular disease, systemic lupus erythematosus, and thrombotic thrombocytopenic purpura, but the significance of abnormal fibrinolysis in these disorders is uncertain. Large, prospective studies of fibrinolytic variables as risk factors for vascular and thrombotic disease are needed to determine whether pharmacologic augmentation of impaired fibrinolysis could be useful in the prevention or treatment of these disorders.
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PMID:Clinical disorders of fibrinolysis: a critical review. 252 71

Hemostatic plugs consist of platelet aggregates and fibrin mesh containing blood cells and plasma components. Hemostatic efficiency depends on the rate of formation of hemostatic plugs as well as the structural integrity and stability of the formed hemostatic plugs. Fibrin elements are major constituents contributing to the structural integrity and stability, but they are subject to fibrinolytic activity occurring spontaneously after fibrin formation. Fibrinolysis is usually suppressed by endogenous inhibitors. Increase of a profibrinolytic component or deficiency of an inhibitor would result in an accelerated fibrinolysis, causing a premature lysis of hemostatic plugs before restoration of injured vessels, leading to a hemorrhagic tendency. Such a state can be seen typically in patients with congenital deficiency of alpha 2-plasmin inhibitor or a hereditary increase of plasminogen activator, and it is also seen in acquired situations such as amyloidosis, liver cirrhosis, disseminated intravascular coagulation (particularly in patients with acute promyelocytic leukemia) and thrombolytic therapy. The hemorrhagic tendency can be well controlled by an administration of an antifibrinolytic agent: epsilon-aminocaproic acid or tranexamic acid. In contrast to an accelerated fibrinolysis causing a hemorrhagic tendency, retarded fibrinolysis may predispose an individual to a thrombotic tendency. Retarded fibrinolysis may be due to either an increase in plasminogen activator inhibitors or decrease of plasminogen activators. Quantitative or qualitative deficiency of plasminogen may also lead to a thrombotic tendency.
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PMID:Hemostasis associated with abnormalities of fibrinolysis. 265 Jul 72

We describe a case of phlegmonous colitis occurring in a 70-year-old man with liver cirrhosis, hepatocellular carcinoma and acute promyelocytic leukemia. He developed an acute abdominal emergency and died during the first day of admission. Autopsy revealed a colon lesion characterized by suppurative inflammation associated with marked edema and hemorrhage in the submucosa. These findings were identical both macroscopically and microscopically to those of phlegmonous colitis.
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PMID:Phlegmonous colitis in a patient with liver cirrhosis, hepatocellular carcinoma and acute promyelocytic leukemia. 754 39

We report a 47-yr-old woman with a 30-yr history of cryptogenic cirrhosis who sustained a cerebral infarction shortly before undergoing liver transplantation. Anticardiolipin antibody titers were positive prior to transplantation (IgG = 24 GPL; IgM > 80 MPL; IgA < 10 APL). After liver transplantation, however, the titers dropped to normal (< 10 PL units). This report suggests that cirrhotic patients with high anticardiolipin antibody titers may be at risk for thrombotic events, and that this tendency may be reversed by liver transplantation or post-transplant immunosuppressive agents.
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PMID:Anticardiolipin antibody-associated cerebral infarction in cirrhosis: clearance of anticardiolipin antibody after liver transplantation. 817 57

Promyelocytic leukemia protein (PML) is a major component of PML nuclear bodies (PML NBs). Fusion of promyelocytic leukemia alpha gene (PML) with retinoic acid receptor gene with the t (15;17) translocation causes disassembly of PML NBs, leading to development of acute promyelocytic leukemia. In contrast, PML overexpression as well as different morphological changes of PML NBs were described in a few solid tumors. In this study, the expression of PML through the multistep hepatocarcinogenesis was analyzed in 95 cases of human hepatocellular carcinomas (HCCs) for comparison along with dysplastic nodules (DNs) and background liver cirrhosis (LC) or chronic hepatitis by immunohistochemistry and immunoblot. In addition, cases of HCCs were further evaluated according to their histologic grade and etiology. The amount of PML as well as the number and size of PML NBs increased gradually through the progression from LC, DNs to HCCs. The overexpression of PML in HCCs was much more closely associated with HBV infection than HCV infection or alcoholic liver disease. The PML expression, however, was not correlated with histologic grade of HCCs. These results suggest that PML is involved in the early stage of multistep hepatocarcinogenesis, and HBV infection may be associated with the overexpression of PML and the morphological alteration of PML NBs.
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PMID:Overexpression of promyelocytic leukemia protein and alteration of PML nuclear bodies in early stage of hepatocarcinogenesis. 1151 88

Elevated levels of serum cobalamin may be a sign of a serious, even life-threatening, disease. Hematologic disorders like chronic myelogeneous leukemia, promyelocytic leukemia, polycythemia vera and also the hypereosinophilic syndrome can result in elevated levels of cobalamin. Not surprisingly, a rise of the cobalamin concentration in serum is one of the diagnostic criteria for the latter two diseases. The increase in circulating cobalamin levels is predominantly caused by enhanced production of haptocorrin. Several liver diseases like acute hepatitis, cirrhosis, hepatocellular carcinoma and metastatic liver disease can also be accompanied by an increase in circulating cobalamin. This phenomenon is predominantly caused by cobalamin release during hepatic cytolysis and/or decreased cobalamin clearance by the affected liver. Altogether it can be concluded that an observed elevation of cobalamin in blood merits the a full diagnostic work up to assess the presence of disease.
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PMID:Significance of elevated cobalamin (vitamin B12) levels in blood. 1463 71

Although all-trans retinoic acid (ATRA) is widely used in acute promyelocytic leukemia (APL), there is little data as to whether or not ATRA is useful for patients with liver and renal failure. A 63-year-old APL patient, complicated by Child-Pugh class A liver cirrhosis and chronic renal failure (creatinine 3.2 mg/dL), was successfully treated with 45 mg/m(2)/day of ATRA. With three courses of chemotherapy, complete remission has been maintained for four years in this patient. Serum trough and maximum ATRA concentration, and the area under the curve (AUC) were not elevated. These observations suggest that full-dose ATRA therapy might be safely applicable to such a complicated case with APL.
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PMID:Successful treatment by all-trans retinoic acid in a patient with acute promyelocytic leukemia complicated by liver cirrhosis and polycystic kidney. 1975 76

Successful escape from immune response characterises chronic hepatitis C virus (HCV) infection, which results in persistence of infection in about 80% of the patients. The deleterious consequences are cirrhosis and hepatocellular carcinoma. HCV accounts the most frequent cause for hepatocellular carcinoma (HCC) and liver transplantation (LT) in the western world. The underlying molecular mechanisms how HCV promotes tumor development are largely unknown. There is some in vitro and in vivo evidence that HCV interferes with the tumor suppressor PML and may thereby importantly contribute to the HCV-associated pathogenesis with respect to the development of HCC. The tumor suppressor protein "promyelocytic leukemia" (PML) has been implicated in the regulation of important cellular processes like differentiation and apoptosis. In cancer biology, PML and its associated nuclear bodies (NBs) have initially attracted intense interest due to its role in the pathogenesis of acute promyelocytic leukemia (APL). More recently, loss of PML has been implicated in human cancers of various histologic origins. Moreover, number and intensity of PML-NBs increase in response to interferons (IFNs) and there is evidence that PML-NBs may represent preferential targets in viral infections. Thus, PML could not only play a role in the mechanisms of the antiviral action of IFNs but may also be involved in a direct oncogenic effect of the HCV on hepatocytes. This review aims to summarise current knowledge about HCV-related liver carcinogenesis and to discuss a potential role of the nuclear body protein PML for this this hard-to-treat cancer.
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PMID:Hepatitis C-associated liver carcinogenesis: role of PML nuclear bodies. 2525 37

Although all-trans retinoic acids (ATRA) are most commonly used as agents in acute promyelocytic leukemia (APL), there are few reports on the administration of ATRAs to patients with liver insufficiency. We report two cases of APL; a 57-year-old man with APL complicated by liver cirrhosis (Child-Pugh class B) and hepatocellular carcinoma who is receiving transcatheter arterial chemoembolization (TACE) and a 50-year-old man with APL complicated by liver cirrhosis (Child-Pugh class B) who is being prepared for receiving a living-donor liver transplantation. Both patients were successfully treated with a normal dosage of ATRA alone during remission-induction therapy. Because the total bilirubin and hepatic transaminases in the two cases were almost at normal levels; the patients received three courses of ATRAs plus a 42%-70% dose of anthracyclines as a consolidation therapy. At 1 year after receiving intermittent ATRA therapy, the patients are maintaining molecular remission. These cases suggest that the administration of ATRA and modifications of doses of chemotherapeutic agents are applicable to APL patients with liver dysfunction.
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PMID:[Successful treatment of acute promyelocytic leukemia complicated by liver cirrhosis with all-trans retinoic acid and reduced-dose anthracycline chemotherapy]. 3062 89


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