Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

16 coagulant and 7 fibrinolytic parameters were determined in 121 normal subjects and 456 patients with various types of viral hepatitis. The results showed that plasma concentration of F VIII: c, vWF: Ag and vWF: Ag/VIII: c (P less than 0.01) were much higher than those in the controls. Plasma level of other coagulant factors was progressively reduced when the severity of hepatitis was decreased. The changes of fibrinolytic activity suggest that t-PA, PL and FDP were increased, while PAI, PLG, and alpha-PI were decreased. The results of this study may provide an experimental basis for further study of hemorrhage mechanism and prognosis in patients with viral hepatitis.
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PMID:[Changes in plasma coagulant factors and plasma fibrinolytic activity in patients with viral hepatitis]. 166 71

Plasma concentrations of tissue-type plasminogen activator (t-PA), urokinase (u-PA), plasminogen activator inhibitor 1 (PAI-1) and PAI-2 were studied in 53 patients with liver deficiency caused by chronic alcoholism (n = 40), viral hepatitis (n = 10) or malignant disease of the liver (n = 3) and compared to that of a control group (n = 20) of healthy subjects. u-PA and PAI-1 levels were significantly increased in all patients with chronic alcoholism, whereas high t-PA was only observed in combination with disturbed liver function tests or with liver cirrhosis (two and six-fold above control values, respectively). A good correlation was observed between t-PA and gamma glutamyl transferase (r = 0.615; p less than 0.001). In patients with infectious hepatitis or with malignant disease of the liver t-PA was normal whereas u-PA and PAI-1 were increased. PAI-2 levels were close to or below the detection limit (15 ng/ml) in the control group and in most patients. However, in two patients with alcohol induced cirrhosis PAI-2 levels were approximately 45 ng/ml and in one patient with hepatocarcinoma even 66 ng/ml. Thus, in liver disease, marked elevations of t-PA, u-PA and PAI-1 levels may occur, with increased PAI-1 as an early marker of liver defects and t-PA a marker of severe liver defects.
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PMID:Plasminogen activators and plasminogen activator inhibitors in liver deficiencies caused by chronic alcoholism or infectious hepatitis. 251 Mar 45

Chronic liver disease is accompanied by derangement of hepatocyte function including the synthesis of haemostastic factors. It is, however, not known whether the improvement in liver functions as a result of interferon (IFN)-alpha therapy would be reflected in the plasma levels of these factors. To evaluate the effect of IFN-alpha therapy on the plasma levels of natural anticoagulants and on the fibrinolytic parameters, in patients with chronic viral hepatitis. Twenty one patients with chronic viral hepatitis (B and C) were treated with IFN-alpha, and were studied before commencement of therapy (first sample) 3 (second sample) and 6 months (third sample) later. The coagulation screening tests: activated partial thromboplastin time, prothrombin time, thrombin time, reptilase time and plasma fibrinogen and the natural anticoagulants: antithrombin, Protein C and free and total protein S as well as fibrinolytic parameters (tissue type plasminogen activator, plasminogen activator inhibitor type-1 and plasminogen) were measured. An increase in the levels of total protein S at 3 and 6 months after the commencement of IFN therapy was noted but the increase was statistically significant in the latter period. Reptilase time was prolonged in the first (pretreatment) and in the second samples and then began to decrease in the third sample but remained higher than the pretreatment level. Fibrinogen level increased in the second and third samples. No remarkable changes were noted in other haemostatic parameters. Total protein S level is a good marker of response to IFN therapy. IFN therapy does not affect other natural anticoagulants or fibrinolytic parameters. More detailed studies need to be done to confirm these findings.
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PMID:Natural anticoagulants and fibrinolytic activity following interferon therapy in chronic viral hepatitis. 1846 46

Haemophilia patients may develop cardiovascular diseases, suggesting that their clotting defect does not protect them completely from atherosclerosis and its complications. We aimed to evaluate cardiovascular risk factors and, for the first time, the presence of endothelial dysfunction in middle-aged haemophilia patients. We studied 40 patients with haemophilia A and B (24 with moderate-severe disease and 16 with mild disease), and 40 healthy controls. Flow-mediated dilation (FMD), carotid ultrasound (US) intima media thickness (IMT), arterial blood pressure, body mass index (BMI), cholesterol, triglycerides, glucose, insulin, lipoprotein(a) and homocysteine levels were measured, and PAI-1 and t-PA levels before and after venous occlusion (VO), and antibodies to HIV, HBV and HCV were assayed. At least one cardiovascular risk factor was detected in 87.5% of patients, and 2 or more in 47.5% of cases. At US exam, none of the patients had significant carotid stenosis or significant differences in IMT compared to controls. In contrast, all the patients had a significant FMD impairment, associated with a reduced t-PA release after VO in 70% of cases. PAI-1 levels significantly correlated with BMI, triglycerides and insulin values. Fifteen haemophilia patients with chronic viral hepatitis and/or HIV infection showed a significantly lower FMD than patients without active infection. We found an endothelial dysfunction with impaired FMD and t-PA release in our haemophilia patients, usually associated with cardiovascular risk factors. Other pathogenic mechanisms, such as chronic viral infections, are likely to be involved in this endothelial damage, however.
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PMID:Endothelial dysfunction in haemophilia patients. 1862

Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of viral hepatitis, insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that increase risk of hepatocellular carcinoma (HCC). To determine whether and how ER stress contributes to obesity-driven hepatic tumorigenesis we fed wild-type (WT) and MUP-uPA mice, in which hepatocyte ER stress is induced by plasminogen activator expression, with high-fat diet. Although both strains were equally insulin resistant, the MUP-uPA mice exhibited more liver damage, more immune infiltration, and increased lipogenesis and, as a result, displayed classical NASH signs and developed typical steatohepatitic HCC. Both NASH and HCC development were dependent on TNF produced by inflammatory macrophages that accumulate in the MUP-uPA liver in response to hepatocyte ER stress.
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PMID:ER stress cooperates with hypernutrition to trigger TNF-dependent spontaneous HCC development. 2520 16

Membranous nephropathy (MN) associated with malignancies is a well-known entity. However, its association with benign neoplasm is not broadly recognized. A 69-year-old man with recurrent nephrotic syndrome presented with pedal edema and proteinuria of 5 months' duration. Laboratory results showed hypoalbuminemia and hyperlipidemia. Proteinuria was estimated to be protein excretion of 3.5g/d. Studies were negative for viral hepatitis, syphilis, human immunodeficiency virus, autoimmune diseases, and paraproteinemia. Kidney biopsy disclosed MN with negative phospholipase A2 receptor (PLA2R) staining, favoring a secondary form of MN. Computed tomography detected a 7.6-cm duodenal schwannoma. Elective surgical resection was performed. Pathologic study showed that THSD7A (thrombospondin type 1 domain-containing 7A) was positive in both glomeruli and schwannoma. Commonly, secondary MN is related to underlying conditions, including lupus, hepatitis, and neoplasm, and can be medication induced. The risk for developing a concomitant neoplasm among patients with PLA2R-negative MN is up to 12 times higher than in the general population. Most of these neoplasms are malignancies, and the presence of autoantibodies directed at similar tissue targets is hypothesized as the potential mechanism. In our case, THSD7A may be the autoantibody that has linked the schwannoma and the development of MN. Although benign tumors rarely produce renal manifestations, effective treatment may lead to resolution of nephrotic syndrome.
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PMID:Duodenal Schwannoma as a Rare Association With Membranous Nephropathy: A Case Report. 3045 84