Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The variations of the main plasma inhibitors of coagulation were prospectively studied in 33 cirrhotic patients, of which 9 presented with hepatocellular carcinoma, 5 of those associated with portal vein thrombosis. The mean prothrombin index was 49 +/- 16 percent. All plasma values of inhibitors were diminished, but to varied degrees: the mean values were: protein C (PC): 33 +/- 15 percent, antithrombin III (AT III): 50 +/- 23 percent, total protein S (PST): 67 +/- 20 percent. The more severe the cirrhosis, the more decreased were the values of antithrombin II and protein C. According to Child classes A, B, and C, antithrombin III plasma values were 64 +/- 20, 50 +/- 21 and 26 +/- 11 percent and protein C values were 43 +/- 16, 32 +/- 8 and 19 +/- 9 percent, respectively. We were able to define expected plasma values of the plasma inhibitors as a function of coagulation factors during cirrhosis; AT III (percent) = 1.16 x factor II (percent) - 7.85; PC (percent) = 0.49 x AT III (percent) + 8.96; PC (percent) = 0.55 x factor II (percent) + 5.55; PST (percent) = 0.76 x factor II (percent) + 28.74. However those equations cannot be extrapolated to patients presenting with cirrhosis complicated with portal thrombosis.
...
PMID:[Changes in levels of blood coagulation inhibitors in cirrhosis. Prospective study in 33 patients]. 131 44

A simple and fast method for the quantitative determination of protein C activity in plasma is here described. The first step consists in the conversion of protein C in the test sample into activated protein C by means of an activator isolated from Southern Copperhead venom. Subsequently, the degradation of factor Va, in presence of protein C-deficient plasma, is measured by the prolongation of the prothrombin time which is proportional to the amount of protein C in the sample. The dose-response curve showed a linear relationship from 6 to 150% protein C activity and the inter- and intra-assay reproducibility was 3.5% and 5.6% respectively. In normal subjects, a mean of protein C level of 98 +/- 15% of normal pooled plasma was found. Comparison with the anticoagulant assay in samples of patients with oral anticoagulant, liver cirrhosis, disseminated intravascular coagulation and severe preeclampsia revealed an excellent correlation (r = 0.94, p less than 0.001). Also, a similar correlation (r = 0.93, p less than 0.001) existed between amidolytic assay and the method here proposed for all the samples studied without including the oral anticoagulant group. These results allowed us to infer that this method evaluates the ability of protein C to interact with protein S, phospholipids, calcium ions and factor Va.
...
PMID:A novel functional assay of protein C in human plasma and its comparison with amidolytic and anticoagulant assays. 161 82

A functional assay for the selective measurement of the active form of protein S in plasma, based on the prolongation of an APTT, was previously developed. This assay is sensitive, reproducible and specific, not affected by other clotting factors including FVIII. This method was applied to the measurement of protein S activity in congenital and acquired disorders. Results of protein S activity were compared to those of total and free antigen measured by ELISA. In 30 controls, there was an excellent correlation between protein S activity and free antigen. In patients with inflammatory disease, protein S activity and free antigen were normal, despite high levels of both C4b-binding protein and total protein S antigen. In dicoumarol-treated patients, protein S activity was lower than free antigen due to the presence of acarboxylated forms. Surprisingly, in liver cirrhosis, free antigen was only slightly decreased whereas protein S activity was significantly reduced. In 23 patients with congenital deficiency, protein S activity was consistently decreased, from less than 5% to 60% and showed good correlation with the free antigen. This functional assay allows the rapid diagnosis of congenital or acquired deficiency of protein S.
...
PMID:Functional assay of protein S in 70 patients with congenital and acquired disorders. 183 22

Sixteen patients with mesenteric venous thrombosis were reviewed retrospectively during a period from 1983 to 1987. Twelve patients had progressive abdominal pain, three had gastrointestinal bleeding, and one had general malaise. Seven of these 16 patients had previous deep-vein thrombosis. After negative routine gastrointestinal and hepatobiliary evaluation, 11 patients underwent an infusion computerized tomographic scan. Of these, 10 had superior mesenteric vein thrombosis; three of these 10 patients had portal vein thrombosis. Selective arteriography was done in two patients because of gastrointestinal bleeding, and a diagnosis of mesenteric vein thrombosis was made on the venous phase of the examination. The remaining four patients developed acute abdominal symptoms requiring surgical exploration, at which time mesenteric venous thrombosis was discovered. An identifiable coagulopathy was detected in nine patients (protein C deficiency in six, protein S deficiency in two, and factor IX deficiency treated with factor IX concentrate in one). No case of congenital antithrombin-III deficiency was identified. Six of these nine patients had a past history of deep venous thrombosis. Of five patients who underwent surgical exploration, all required bowel resection. In follow-up, two patients died of intestinal necrosis and a third died of associated pancreatic cancer. Thirteen patients were discharged from the hospital. Treatment of coagulopathy was by heparin in three patients and sodium warfarin (Coumadin) in four patients. Long-term anticoagulation was not instituted because of gastrointestinal bleeding in three and cirrhosis in three patients. Mesenteric venous thrombosis can occur without gangrenous bowel. Diagnosis should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes and a coagulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Mesenteric venous thrombosis. 172 86

Beta 2-microglobulin determinations in ascitic fluid (A) and serum (S) collected on the same day, were performed in 24 patients suffering from alcoholic liver cirrhosis. Ascitic beta 2-m concentration varied from 0.4 to 4.6 mg/l for patients with a normal renal function. Much higher values were found in patients with chronic renal failure. No correlation could be established between ascitic beta 2-m level and the clinical evolution of the cirrhosis. Comparative measurements of beta 2-m S/A ratio and albumin, transferrin, total protein S/A ratios suggests a local synthesis of beta 2-m in ascitic fluid. This is confirmed by an immuno-cytochemical technique which reveals the localisation of beta 2-m in the cytoplasm of peritoneal cells. The presence of beta 2-m in ascitic fluid seems to be related to an ultrafiltration across the peritoneal membrane as well as a local polyclonal activation of the immune system.
...
PMID:Beta 2-microglobulin in liver cirrhosis: study of a local synthesis in ascitic fluid. 330 Aug 9

A new one-step ELISA using two monoclonal antibodies specific for distinct epitopes of the free form of protein S (ELISA-m) has been developed for the direct measurement of free protein S in untreated plasma. This assay has been compared with the classic method using polyclonal antibodies to protein S (ELISA-p). The latter method has the drawback of requiring PEG precipitation of plasma which is time-consuming, difficult to perform with accuracy and therefore poorly reproducible in most laboratories. Results of both ELISAs were compared with those of a functional assay. In 30 normal subjects, there was an excellent correlation between ELISA-m and ELISA-p (r = 0.95) as well as between ELISA-m and the functional assay (r = 0.96). In twelve patients with a congenital deficiency, the levels of free protein S antigen were similarly decreased with ELISA-m and ELISA-p and in good agreement with those of protein S activity. In 20 patients with miscellaneous inflammatory diseases, the levels of free proteins S were normal with good correlation between both ELISAs and PS activity, despite high levels of C4bBP-protein S complexes. As expected, in 15 dicoumarol-treated patients, there was a significant and parallel decrease of free protein S antigen with both ELISAs, with even lower levels of protein S activity. In 14 patients with liver cirrhosis, the mean values for free protein S antigen were normal using both assays, but with wide extreme values, whereas protein S activity was significantly lower.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Clinical applications of a direct assay of free protein S antigen using monoclonal antibodies. A study of 59 cases. 751 89

Membranous obstruction of the inferior vena cava is a rare disease. The etiology of the membrane is believed to be thrombotic or congenital. In three of 11 siblings from a single family, symptoms of membranous obstruction of the inferior vena cava developed during early adult life. All had signs of more long-standing disease, as judged by the presence of collaterals, cirrhosis and, in one case, hepatocellular carcinoma. On family screening no further cases of membranous obstruction of the inferior vena cava were found. There was also no evidence of inherited defects in the natural coagulation inhibitors (protein C, protein S and antithrombin III) and plasminogen deficiency. This familial occurrence of membranous obstruction of the inferior vena cava supports a congenital etiology, although a thrombotic etiology cannot be totally excluded.
...
PMID:Familial occurrence of membranous obstruction of the inferior vena cava: arguments in favor of a congenital etiology. 766 59

In patients with liver cirrhosis a decrease of the coagulant potential is well-documented and has been linked to the high bleeding tendency among these patients. Whether the decrease of the coagulant potential is only due to a reduced hepatic synthesis of coagulation factors or also to its consumption by disseminated intravascular coagulation is debatable. We investigated hemostasis activation markers thrombin-antithrombin III complexes (TAT), fibrin degradation products (D-Dimer) and plasmin-alpha 2-antiplasmin complexes (PAP) in 41 outpatients with liver cirrhosis (Child-Pugh index 1 n = 18, 2 n = 15, 3 n = 8). Compared to controls similar in terms of age and sex, TAT, D-Dimer and PAP was elevated in the whole group of patients. A progressive increase of D-Dimer and PAP from Child 1 to 3 indicates a relationship between the severity of cirrhosis and the amount of hemostasis activation. Investigation of the natural anticoagulant potential showed significant decreases of antithrombin III (AT III), protein C, and protein S, most pronounced in Child 3 patients. Statistical analysis revealed significant negative correlations between levels of D-Dimer and both AT III and protein C, indicating that hemostasis activation is linked to the loss of anticoagulant potential.
...
PMID:Hemostasis activation in patients with liver cirrhosis. 774 May 19

Eighteen patients with an acute thrombosis of the splanchnic veins were reviewed. Most of apparently idiopathic cases of splanchnic vein thrombosis are related to an increased coagulation related to a congenital or acquired defect of haemostasis. The aim of this study was to assess the effects of a new and effective treatment. Nine male and 9 female patients (range of age: 19 to 81 years) experienced a mesenteric venous thrombosis. There were 14 mesenteric vein thromboses with infarction, two transient mesenteric venous ischaemias without bowel infarction and two acute thromboses of the splanchnic veins without bowel ischaemia. A coagulopathy was detected in seven patients: oral contraception, protein C (PC) or antithrombin III (AT III) congenital deficiencies, acquired deficiency of AT III, PC and protein S (PS), polycythaemia in the post-partum period and primary myeloproliferative disorder. No coagulopathy was associated with thrombosis in eight cases: mesenteric haematoma, splenomegaly, cirrhosis, appendicectomy, cholescytectomy, chronic heart failure, treatment with beta-adrenergic receptor antagonist and digitalis, stenosis of the portal anastomosis after liver transplantation. Twelve patients required surgery: eight intestinal bowel resections with immediate anastomosis, four resections without immediate anastomosis. Only one patient underwent a second look for a repeat bowel resection. No death occurred in the early postoperative period and 17 out of 18 patients were alive after 12 years. An oral anticoagulant therapy was undertaken from two months to seven years. However, three patients suffered a recurrent thrombosis. Two of them required a long-term anticoagulation. Six patients experienced a portal hypertension and oral anticoagulants were discontinued in three of them because of bleeding oesophageal varices. Six patients were treated only by unfractionated heparin (UFH) or low molecular weight heparin (LMWH) followed by oral anticoagulants. After laparotomy, two were only treated with UFH without any bowel resection, as mesenteric venous ischaemia was too extensive. These observations suggest that the choice between an appropriate medical or surgical treatment is important and must be discussed. Since 1989, the therapeutic choice has been modified by ultrasonography and contrast enhanced computed tomographic scan which confirms diagnosis, allows to follow up and check the effects of anticoagulation and to choose the time for surgery. When the diagnosis is established and the patient's risk is low, the IU . kg(-1) . d(-1) to obtain an antifactor Xa activity between 0.3 and 0.6 antiXa IU mL(-1). When the diagnosis is uncertain and the patient's risk if high a laparotomy is required.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:[Mesentric venous thrombosis. Risk factors, treatment and outcome. An analysis of 18 cases]. 781 2

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.
...
PMID:Plasma protein S-antigen (PS:Ag) in selected disease states. 808 8


1 2 3 4 Next >>

---