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)

We tested an in vitro system simulating bleeding time reported by Kratzer et al. Primary hemostasis was studied perfusing an artificial vessel with citrated blood under a constant pressure of 40 mmHg, measuring the blood volume perfused (bleeding volume) and the time until blood flow stopped (bleeding time). The artificial vessel consists of a glass capillary simulating arteriole and a filter covered with collagen type I to provide a surface for the adhesion of platelets. The bleeding volume (mean +/- SD microliters) was 317.7 +/- 93.8 in controls (n = 19), 487.3 +/- 242.1 in idiopathic thrombocytopenic purpura (n = 9), 666.8 +/- 224.1 in aplastic anemia and paroxysmal nocturnal hemoglobinuria (n = 4), greater than 820 in von Willebrand's disease (n = 3), 231.0 +/- 74.5 in hemophilia A (n = 3), 499.0 +/- 269.4 in liver cirrhosis (n = 6), and 457.7 +/- 229.0 in myeloproliferative disorders (n = 11). When citrated blood was applied to this system after incubation with monoclonal antibodies (MoAb) to von Willebrand factor or platelet membrane glycoprotein Ib (GPIb), bleeding volume was significantly increased while no effects were observed after incubation with MoAb to GPIIb/IIIa, factor VIII: CAg and factor XIIIa. These data suggest that in vitro model of primary hemostasis could be used for not only diagnosing bleeding disorders although 'time' is not reliable, but also investigating the mechanisms of hemostasis.
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PMID:[Bleeding time and volume in vitro by THROMBOSTAT]. 231 3

The authors characterized antiplatelet membrane antibodies in the sera of patients with idiopathic thrombocytopenic purpura (ITP) and cirrhosis of the liver. Antibodies were detected in five of the 22 patients with chronic ITP and in none of the eight patients with cirrhosis of the liver. The authors report a patient with chronic ITP in complete remission. Antibody to platelet glycoproteins (GP), with molecular weights of 55 and 49 kDa, was detected in the serum. The patient's immunoglobulin G (IgG) alone could cause the aggregation of platelet-rich plasma. Anti-GPIIb/IIIa antibody (LJ-CP8) inhibited the aggregation of platelet-rich plasma induced by the patient's IgG in a dose-dependent manner. The F(ab')2 of the patient's IgG had a synergetic effect on the aggregation of PRP induced by adenosine 5-diphosphate. This demonstrates that in ITP, the binding of IgG via its fragment of antigen binding site portion may activate platelets.
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PMID:Autoimmune antibody in a patient with idiopathic thrombocytopenic purpura reacted to the platelet low molecular weight glycoproteins and activated platelets. 813 99

One of frequently occurring hematological disorders accompanying advanced liver diseases is thrombocytopenia (TP). Immunological disorders in patients with liver cirrhosis, loss of tolerance to own antigens, and the change of platelet antigenicity enable antiplatelet antibody formation under the influence of continuous activation. The aim of the study was to determine the rate of autoimmunological thrombocytopenia occurrence in patients with liver cirrhosis and TP. Antiplatelet autoantibody occurrence were determined in blood serum with the use of ELISA method in 15 patients with liver cirrhosis and TP (mean plt number 67.9 +/- 24.9 x 10(3)/microliter). Three patients (20%) presented anti-GPIIb/IIIa antibodies and 2 patients--anti-GPIa/IIa. These patients had liver failure (stage C according to Child-Pugh classification) and splenomegaly. Plt morphological parameters were also evaluated. The significant decrease of plt crit as well as the decrease of mean platelet volume (MPV) was observed in liver cirrhosis with thrombocytopenia. The increase of megathrombocyte population (MPV > 20fl) up to 5.5% of all plt was also observed. Megathrombocytes in healthy individuals were 2.25% of platelet population. Examinations confirmed that autoimmunological factors play an important role in the development of thrombocytopenia in liver cirrhosis.
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PMID:Platelet autoantibodies in liver cirrhosis and thrombocytopenia. 1171 41

Thrombocytopenia (TP) often accompanies chronic liver diseases. The causes are numerous and include impaired production of blood platelets, spleen sequestration, and the immune factors, e.g. antiplatelet autoantibodies. ELISA (GTI-PAKPLUS) examinations were conducted in order to estimate the rate of autoimmune thrombocytopenia occurrence in patients with thrombocytopenia in the course of chronic hepatitis (10 patients) and liver cirrhosis (20 patients). Blood platelet activity was also evaluated as well as the expression of platelet glycoproteins (GPIIb, GPIIIa, and GPIX) in platelets of the patients and the controls. It was observed that autoimmune TP occurred in 30% of patients with liver cirrhosis and in 10% of patients with chronic hepatitis, in which anti-GPIIb/IIIa, GPIa/IIa, and HLA class I antibodies were detected. In all patients there occurred significant/marked platelet activation with CD61P expression. Thrombocytopenia in patients showed a similar activity after thrombin stimulation to that in healthy individuals. Expression on GPIIb platelet receptors was markedly increased and GPIX decreased in patients in comparison to the controls. There was no correlation between the occurrence of certain types of anti-platelet autoantibodies and the expression of GP on thrombocytes in these patients.
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PMID:[Autoimmune thrombocytopenia in chronic liver disease]. 1189 44

Thrombocytopenia is a common manifestation in patients with liver cirrhosis (LC), but its underlying mechanism remains controversial. This study examined the role of anti-platelet autoimmunity in cirrhotic thrombocytopenia by determining the autoantibody response to GPIIb-IIIa, a major platelet surface autoantigen recognized by anti-platelet antibodies in patients with idiopathic thrombocytopenic purpura (ITP). Circulating B cells producing anti-GPIIb-IIIa antibodies as well as platelet-associated and plasma anti-GPIIb-IIIa antibodies were examined in 72 patients with LC, 62 patients with ITP, and 52 healthy controls. In vitro anti-GPIIb-IIIa antibody production was induced in cultures of peripheral blood mononuclear cells (PBMCs) by stimulation with GPIIb-IIIa. The frequency of anti-GPIIb-IIIa antibody-producing B cells in patients with LC was significantly greater than in healthy controls (10.9 +/- 6.2 vs. 0.4 +/- 0.3/10(5) PBMCs; P <.0001) and was even higher than the frequency in patients with ITP (8.2 +/- 5.2; P =.007). Anti-GPIIb-IIIa antibodies in the patients with LC and ITP were mainly present on the surfaces of circulating platelets rather than in the plasma in an unbound form. Furthermore, PBMCs from patients with LC and ITP produced anti-GPIIb-IIIa antibodies on antigenic stimulation with GPIIb-IIIa in vitro, and the specific antibodies produced had the capacity to bind normal platelet surfaces. In conclusion, the similar profile of the anti-GPIIb-IIIa autoantibody response in patients with LC and ITP suggests that autoantibody-mediated platelet destruction may contribute at least in part to cirrhotic thrombocytopenia.
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PMID:A role of autoantibody-mediated platelet destruction in thrombocytopenia in patients with cirrhosis. 1277 4

The aim of this study was to explore application value of detecting platelet associated antibody and platelet membrane glycoprotein in the diagnosis and prognosis for immune thrombocytopenia. The platelet associated immunoglobulin (PAIg) and platelet membrane glycoprotein (CD41, CD61, GPIIb/IIIa) in 76 cases of immune thrombocytopenia and 30 healthy subjects were determined by FCM. The results showed that PAIg level in ITP patients included PAIgG (31.25 +/- 18.06)%, PAIgM (32.41 +/- 15.51)%, PAIgA (23.39 +/- 16.67)% which were remarkedly higher than in health control (10.48 +/- 5.05)%, (9.40 +/- 4.42)% and (7.23 +/- 3.61)% (P < 0.001). In patients with secondary immune thrombocytopenia (chronic aplastic anemia, SLE, Evans syndrome, liver cirrhosis hypersplenism, etc), PAIg level was higher than that in control group, while the platelet membrane glycoprotein in the blood of these patients was lower than that in control group. The level of PAIg decreased (P < 0.05) after treatment, but platelet membrane glycoprotein increased (P < 0.01). The result suggested that measurements for platelet membrane glycoprotein and platelet associated antibody by FCM were practical with high sensitivity, rapidity and simplicity used as a routine method in diagnosis and evaluation of the therapeutic effects in immune thrombocytopenia patients.
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PMID:[Significance of detecting platelet associated antibody and platelet membrane glycoprotein for diagnosis of immune thrombocytopenia]. 1515 39

Forty-five individuals with hepatosplenic schistosomiasis mansoni were studied with the aim of measuring levels of von Willebrand factor antigen (vWF:Ag), detecting abnormalities in platelet morphology and aggregation, and identifying changes to surface antigens. Haemograms, platelet aggregation tests, flow cytometry investigations of CD41/CD42b antibody and vWF:Ag assays were performed. Mean platelet counts were low (77,522/mm3) and 82.2% of patients presented thrombocytopenia. An inverse relationship between spleen size and platelet count was seen. Macroplatelets were found in 57.1% of patients, indicating good bone-marrow response, but were insufficient to compensate for the decrease in platelets due to splenomegaly. Decreased or absent platelet aggregation was seen in 50% of patients, probably due to low platelet counts. Markers for GPIIb/IIIa were normal in more than 90% of patients, not supporting the increased capture and destruction of platelets in the spleen that is hypothesized to occur with cirrhosis. Similar to cirrhosis, vWF:Ag levels were high or very high in 70.5% of patients. High levels of vWF:Ag were associated with platelet counts <100,000/mm3, larger spleen diameter and oesophageal varices. In conclusion, hepatosplenic schistosomiasis leads to a lower platelet count due to pooling in the spleen and, consequently, impaired aggregation, but not to increased capture and destruction of platelets in the spleen. High vWF:Ag levels probably promote stabilization of platelet microaggregates and prevent minor manifestations of thrombocytopenia such as petechiae, ecchymosis and gingival bleeding.
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PMID:Platelet function and the von Willebrand factor antigen in the hepatosplenic form of schistosomiasis mansoni. 1911 53