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Biomedical subjects

S A Vasil'ev

Publications and source records attributed to S A Vasil'ev.

At least 19 recordsLinked to original sources
PubMed2006

[Chronic myeloproliferative diseases and pregnancy].

AIM: To analyse the course of pregnancy in chronic myeloproliferative diseases (CMPD) with hyperthrombocytosis, primarily, essential thrombocytemia. MATERIAL AND METHODS: The analysis of thrombogenic risk factors covered literature data and 8 cases observed by the authors. RESULTS: Six pregnant women received long-term treatment with preparations of interferon-alpha in a dose 9-20 million IU a week (both before and during pregnancy). Rapid reduction of hyperthrombocytosis (1100-4000 x 10(9) l) and the absence of a negative effect on development of the fetus were seen in all the cases. Normal delivery on week 37-39 was in 4 patients, spontaneous abortion on week 24 was provoked by a car accident. Three gravidas (gestational week 28, 33 and 34) are still under observation. Lupus anticoagulant or elevation of anticardiolipin antibodies level was detected in 4 of 8 patients, 2 patients had heterozygous mutation of methylentetrahydrofolatereductase genes and factor V (Leiden). These patients were given lannacher, faxiparine, folic acid and discrete plasmapheresis (in 2 cases). CONCLUSION: Gravidas with hyperthrombocytosis, if not contraindicated, must be treated with aspirin and interferon-alpha preparations at any gestational term. Moreover, it is necessary to exclude additional most prevalent causes of thrombophilia for adequate prevention of thromboses.

Adult↗
PubMed2005

[Thromboembolism of the pulmonary artery in Willebrand's disease].

AIM: To ascertain risk factors of thromboembolism of the pulmonary artery (TPA) in Willebrand's disease (WD). MATERIAL AND METHODS: We made a retrospective analysis of hospitalizations of WD patients for 10 years. We analysed causes of the patients' admission, interventions, registered maximal levels of factor VIII (FVIII) and Willebrand's factor (FW) in which the interventions were made, cases of TPA. RESULTS: Thirty four patients with WD were hospitalized 45 times. Three patients were treated conservatively because of gastrointestinal bleeding, the rest patients received surgical therapy. All the patients were given FVIII concentrates, cryoprecipitate, fresh-frozen plasma. In the course of the treatment, FW and FVIII levels were determined in 38% cases, FW--in 23%, FVIII--in 27%, coagulation was studied in 12% without test for FVIII and FW levels. Maximal concentration of FW was 72.1 +/- 11.8%, FVIII--125 +/- 15.8%. TPA developed in 2 (4.4%) of 45 patients. In both cases we observed a marked rise of plasmic concentration of FVIII due to therapy (250 and 240%). CONCLUSION: In patients with WD thromboembolic complications risk factors are age, obesity, surgical interventions, immobilization, etc. Simultaneous administration of several drugs containing FW and FVIII was also among the risk factors. Overdosage of FVIII is one of the causes of thrombotic complications in WD. FW and FVIII correlations in FVIII preparations must be considered. Prophylactic heparin therapy is recommended in patients with a high risk of thrombotic complications upon achievement of normal hemostasis.

Adult↗
PubMed2004

[Possibility of diagnosis and treatment of thrombotic complications in primary mediastinal B-cell lymphosarcoma].

AIM: Efficacy of the treatment of primary mediastinal B-cell lymphosarcoma depends to a great extent on early diagnosis and treatment policy. In this study we evaluated possibilities of diagnosis and treatment of thrombotic complications of primary mediastinal B-cell lymphosarcoma (PMBL). MATERIAL AND METHODS: 61 patients were examined using roentgenography, computed tomography, chest ultrasound investigation,coagulogram, allelle specific polymerase chain reaction, ultrasound investigation of the jugular, subclavian, brachial veins, vena cava superior to detect mutation of genes II, V factors and methylentetrahydrofolatereductase. RESULTS: In 7 cases prechemotherapy examination detected thrombosis of the internal jugular and subclavian veins. In 4 of 7 cases there was a combined thrombosis of the left internal jugular and subclavian veins, in 3 cases one the vessels was affected with thrombosis. In 2 cases, in the course of polychemotherapy, there was recurrent thrombosis and development of pulmonary artery thromboembolism (PATE). In progression of the disease there was thrombosis of the left subclavian vein (1 case) and PATE (a case). Coagulologically, hypercoagulation syndrome signs were registered. 5 patients with PMBL complicated by thromboses showed gene mutations. CONCLUSION: In PMBL there is a tendency to formation of venous thrombosis and development of PATE. This is explained by tumor process and hereditary factors of thrombogenicity. Therefore, specific antitumor treatment should include anticoagulation therapy.

Adolescent↗
PubMed2002

[Plasmapheresis in combine therapy of hypercoagulation syndrome in hematogenic thrombophilia].

AIM: To specify indications to plasmapheresis (PA) and to assess its efficiency in patients with hypercoagulatory syndrome in hematogenic thrombophilia (HT). MATERIAL AND METHODS: 18 patients (11 males, 7 females, age 26-50 years) with various forms of HT received standard antiaggregation, anticoagulatory therapy plus therapeutic PA. By PA technique the patients were divided into two groups. RESULTS: A positive trend in clinical, instrumental and laboratory indices was observed in all the patients. CONCLUSION: Therapeutic PA in hypercoagulation syndrome in HT patients leads to fast normalization of the clinical picture and reestablishment of patency of thrombus-affected vessels.

Adult↗
PubMed2002

[Disorders of protein C anticoagulant system in various clinical conditions].

A study was carried out on activity of protein C4 in 73 surgical patients (coagulation test, reagents of company PEHAM). The reduction in activity of protein C was observed in patients with focal liver lesion related to disturbance of protein formation function. This percent of disturbances in protein C system is more often found in patients with vascular pathology. This is explained by the mechanism of its action and implication of vascular endothelium into the process. Disturbances in patients with injury infection are stipulated with activity of C and S proteins and availability of mutant factor V--factor Leiden in patients with diabetes. In the first days after surgical intervention the activity of C protein was much reduced. The obtained results emphasize the importance of research in the system of protein C in surgical patients.

Blood Coagulation Disorders↗
PubMed2001

[Screening test on protein C].

A method for obtaining protein C (PrC) activator from Agkistrodon contortrix contortrix venom, based on ion exchange chromatography, has been developed specificity and sensitivity of a reagent based on ellagic acid and soybean phosphatides to disorders in PrC system has been studied. A simple and convenient screening test for analysis of PrC system has been developed.

Humans↗
PubMed2000

[Effect of composition of reagents for activated partial thromboplastin time on their sensitivity during analysis of blood coagulation factors].

Brain cephaline-based reagents for evaluating activated partial thromboplastin time (APTT) and soybean phosphatides with ellagic acid complex activator with intermediate metal ions have been studied. The sensitivity of these reagents to internal clotting factors (VIII and IX) and heparin is determined by phospholipid nature and type of metal. The results help obtain highly active and sensitive APTT reagents.

Factor IX↗
PubMed1999

Production of soluble P-selectin by platelets and endothelial cells.

The distribution of a soluble form of a cell adhesion molecule, P-selectin, in human platelets and cultivated endothelial cells has been studied by enzyme-linked immunosorbent assay (ELISA). The concentration of soluble P-selectin in the blood plasma of healthy donors and patients with abnormal platelet count has also been determined. P-selectin was measured in the Triton X-100 lysate of platelets and endothelial cells (total P-selectin), in the 100,000g supernatant obtained after sedimentation of the membrane fraction from the homogenate of sonicated platelets and endothelial cells (intracellular soluble P-selectin), in the supernatant of activated and nonactivated platelets, and in the culture medium of endothelial cells. A soluble form of P-selectin which did not coprecipitate with the membrane fraction was detected in platelets and accounted for approximately 10% of the total P-selectin. Platelet activation by thrombin, ADP, or a thromboxane A2 analog resulted in the secretion of 30-50% of the intracellular soluble P-selectin. Measurements of P-selectin in endothelial cell culture revealed that endothelium from aorta contained about twofold more P-selectin than endothelium from umbilical vein. Intracellular soluble P-selectin was identified in both types of endothelial cells. In endothelial cells from the umbilical vein this form made up approximately 10% of the total P-selectin. Soluble P-selectin was also detected in the medium of cultivated endothelial cells, where its content correlated with the total cellular P-selectin. Concentration of P-selectin in blood plasma strongly correlated with the platelet count in the blood of healthy donors and patients with thrombocytosis and thrombocytopenia. These data indicate that platelets serve as one of the main source of plasma P-selectin. However, the presence of P-selectin in the plasma of patients with severe thrombocytopenia suggests that endothelium can also be involved in plasma P-selectin production. Thus, in vitro experiments as well as measurements of plasma P-selectin have shown that both platelets and endothelial cells can produce a soluble form of the protein. Platelet-derived soluble P-selectin and plasma P-selectin were shown to react with antibodies against the cytoplasmic domain of P-selectin. These data prove that at least part of soluble P-selectin is produced by synthesis employing special mRNA which lacks the sequence encoding the transmembrane domain, but not by the proteolytic shedding of the extracellular portion of membrane P-selectin.

Antibodies↗
PubMed1998

[Coagulation system in patients with blood malignancies treated with estrogens in the course of cytostatic therapy].

AIM: To evaluate the effect of estrogen gestagenic drugs (EGD) on blood coagulation in patients with blood malignancies treated by polychemotherapy. MATERIALS AND METHODS: 32 females of reproductive age treated with ovarioprotector marvelon during cytostatic therapy. The following indices were determined: activated partial thrombin time, prothrombin index of the ethanol test, fibrinogen and antithrombin III levels, factor XIIa dependent time of fibrinolysis, thrombin time. Dopplerography of the lower limb vessels was carried out. RESULTS: No significant alterations in coagulograms of the patients treated with cytostatics in combination with EGD were recorded. CONCLUSION: It is safe to use EGD as ovarioprotectors in females with hematological malignancies in hypercoagulation.

Adolescent↗
PubMed1995

[Evolutionary programming for finding "structure-activity" relationships in a series of 3-phenoxychromone and 3-phenoxy-4-hydroxycoumarin derivatives].

Based on a set of compounds possessing hypolipidemic activity, it was demonstrated that evolutionary algorithms can be successfully used to compile an informative set of molecular parameters. The parameter sets selected using the method of potential functions allowed correct prediction of the activity of test molecules.

4-Hydroxycoumarins↗
PubMed1994

[Circulating complexes of plasma fibronectin (fibronectin-fibrin) in human diseases].

The study of circulating complexes fibronectin-fibrin in 21 patients with immunocomplex affections revealed their high levels which occurred in inverse relationships with fibronectin concentrations in the blood, but in direct correlation with indicators of inflammation (fibrinogen, cialic acid). It is suggested that the complexes are involved in the development of fibrosis at the sites of chronic inflammation in immune disorders.

Adult↗