fibrin and Pericardial-Effusion

Occlusion of chest drainage tubes by thrombus is not uncommon after open heart operations. It has been suggested that by coating the tube with phosphatidylcholine (PC), the most prominent phospholipid in the erythrocytes outer membrane, it may be possible to overcome the blood-material interaction responsible for thrombus formation. To test this hypothesis 102 patients (75 males; mean age, 57 +/- 10 years) were randomly allocated to receive either PC-coated or noncoated 32F chest drainage tubes. Preoperative status, type and length of operation, and duration of drainage were similar in the two groups as was postoperative blood loss. Patients receiving PC-coated tubes, however, had less residual blood clot in the tube after removal (0.7 +/- 0.1 versus 3.1 +/- 0.3 g; p < 0.001), a reduced incidence of pericardial effusions (17.6% versus 41.2%; p < 0.01), fewer postoperative supraventricular arrhythmias (2 of 51 versus 10 of 51; p < 0.002), and a shorter hospital stay (8.4 +/- 0.3 versus 9.7 +/- 0.5 days; p < 0.05). Late cardiac tamponade developed in 2 patients in the noncoated group 6 and 10 days postoperatively, which required reexploration. The data show that PC-coated chest drainage tubes are less susceptible to occlusion by thrombus and their use is associated with a significant reduction in postoperative morbidity.

Topics: Aged; Arrhythmias, Cardiac; Biocompatible Materials; Blood Platelets; Chest Tubes; Drainage; Erythrocytes; Female; Fibrin; Heart Diseases; Humans; Incidence; Length of Stay; Male; Microscopy, Electron, Scanning; Middle Aged; Pericardial Effusion; Phosphatidylcholines; Postoperative Care; Postoperative Complications; Prospective Studies; Surface Properties

Topics: Echocardiography, Three-Dimensional; Fibrin; Humans; Male; Middle Aged; Pericardial Effusion

Different macromolecules were administered intraperitoneally to stimulate formation of protein-rich ascitic fluid in rodents. Stimulatory effect of plant lectins depended on the attachment to cell surface carbohydrates, Canavalia ensiformis (ConA) lectin was used in the majority of experiments. The time course of ConA-induced ascites was divided into an early (up to 4 h) and a late (from 6 h on) phase, with a transitional period between the two. Water and protein accumulation showed parallel time courses: volume of the ascitic fluid peaked at around 3 h, and fibrin threads appeared after 6 h. Viscosity of the ascitic fluid and its supernatant increased with time, reaching maximal fibrinogen concentration at around 16 h. Peritoneal permeability, followed by pleural and pericardial effusions, was elicited only by lectins that form soluble complexes with serum glycoproteins, whereas the effect of serum-precipitating lectins was restricted to the peritoneum. Macromolecules with serial positive charges (e.g., polylysine or polyethyleneimine) enhanced peritoneal permeability by ionic interactions with cell surface molecules. Viscosity of the polycation-induced ascitic fluid did not tend to increase with time and corresponded to the early phase of the ConA-induced ascites. Polyglutamate, a polyanionic macromolecule, inhibited the effect of polycations, but not that of ConA. The most efficient stimulatory macromolecules appear to induce ascites by noncovalent cross-linking of cell surface glycoproteins or glycosaminoglycans or both. A similar mechanism may operate in the maintenance of basal secretion to prevent eventual desiccation. Noncovalent cross-linking appears to be a common denominator of both basal and enhanced permeability.

Topics: Animals; Ascites; Ascitic Fluid; Female; Fibrin; Injections, Intraperitoneal; Mice; Pericardial Effusion; Peritonitis; Permeability; Plant Lectins; Pleural Effusion; Polymers; Rats; Rats, Wistar; Serum Albumin; Time Factors; Viscosity

We have shown that the thrombin G-protein coupled receptors (GPCR) designated as protease-activated receptors (PAR-1) are expressed in primary cancer cells isolated from peritoneal and pleural malignant effusions. Here, our main goal was to evaluate several coagulation and thrombin activation effectors and markers in a series of 136 malignant effusions from cancer patients with gastrointestinal, lung and mammary carcinomas. All these patients present a highly activated coagulation system in blood and their malignant effusions, as indicated by high levels of prothrombin F1.2 fragments and D-dimers. Notably, we detected in the effusions all the coagulation factors of the tissue factor pathway inducing thrombin activation, namely factors VII, V, X and II, as well as high VEGF levels and IGF-II in mature and precursor forms. Fibrin clot formation also correlated with higher levels of free ionized calcium (iCa), suggesting that iCa and its binding protein albumin are regulatory factors for fibrinogenesis in effusions. Consequently, thrombin, VEGF and IGFII appear to converge in the promotion of survival and invasivity of the metastatic cancer cells from blood to the malignant effusions. Thus, we add new insights on the interconnections between blood coagulation disorders in cancer patients and thrombin activation in malignant effusions, including their functional interaction with PAR in metastatic cancer cells. Based on these data we propose to counteract the metastatic cascades by targeted invalidation of key effectors of the coagulation system. Therefore, potential therapeutic approaches include the application of thrombin protease inhibitors, VEGF-blocking antibodies, and drugs targeting the VEGF and thrombin signaling pathways, such as tyrosine kinase or GPCR inhibitors.

Topics: Aged; Antineoplastic Agents; Antithrombins; Ascitic Fluid; Blood Coagulation; Blood Coagulation Factors; Breast Neoplasms; Calcium; Case-Control Studies; Factor V; Factor VII; Factor X; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Gastrointestinal Neoplasms; Humans; Insulin-Like Growth Factor II; Lung Neoplasms; Male; Middle Aged; Neoplasm Invasiveness; Neoplasm Metastasis; Neoplasms; Peptide Fragments; Pericardial Effusion; Pleural Effusion, Malignant; Proteins; Prothrombin; Serum Albumin; Thrombin; Thromboplastin; Vascular Endothelial Growth Factor A

Scleroderma renal crisis (SRC) can lead to end-stage renal disease (ESRD) and subsequent need for dialysis and/or renal transplantation. We review all reported cases of renal transplantations in scleroderma patients from PubMed search, present UNOS data on transplant outcomes, and identify predictors for allograft SRC. Of the five cases with recurrent SRC, all developed ESRD within a year of onset of native kidney SRC, whereas none of those who developed ESRD more than 1-2 years after the onset of SRC developed recurrence. Anemia preceded allograft SRC in two cases, pericardial effusion in one, and skin tightening in two others. UNOS data (October 1987-July 2004) documented 260 transplants performed for the renal diagnosis of scleroderma, with a 5-year graft survival rate of 56.7%. The risk for allograft SRC recurrence appears to correlate with early native renal function loss following the onset of SRC. Recurrent SRC in the allograft may be heralded by multiple clinical markers known to be predictive of severe scleroderma, including progression of diffuse skin thickening, new-onset anemia and cardiac complications.

Topics: Anemia; Arterioles; Autoimmune Diseases; Disease Progression; Edema; Female; Fibrin; Graft Rejection; Graft Survival; Humans; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Glomerulus; Kidney Transplantation; Kidney Tubules; Leukocytes, Mononuclear; Lymphocytes; Middle Aged; Pericardial Effusion; PubMed; Recurrence; Renal Dialysis; Risk Factors; Scleroderma, Systemic; Skin; Thrombosis; Time Factors; Transplantation, Homologous

From a registry of 136 patients undergoing pericardiocentesis, 14 patients with autoimmune and 15 patients with neoplastic effusions were selected. All underwent pericardioscopy, epicardial and pericardial biopsy with histologic, immunohistologic, and polymerase chain reaction/or in situ hybridization analysis for microbial DNAs and RNA. Pericardioscopy identified neoplastic effusions by the high occurrence of protrusions. Fibrin threads and layers and neovascularization were found in both groups. For identification of the inflammatory and neoplastic process, the combined analysis of the cytology of the effusion and epicardial biopsy evaluation proved to be most important. Epicardial biopsy demonstrated a slightly higher sensitivity for identifying neoplastic disorders in the pericardium than cytology alone. Pericardial biopsy was inconclusive. Intrapericardial administration of 1 g of crystalloid triamcinolone in autoreactive pericarditis prevented recurrence in 13 of the 14 cases after 3 months and in 12 of the 14 cases after 1 year. In neoplastic effusion, intrapericardial administration of 50 mg cis-platin for 24 h prevented recurrence of a hemodynamically relevant effusion after 3 months in all, and after 6-12 months in 14 of 15 patients. Mortality in neoplastic effusion due to noncardiac tumor progression was 47 and 80%, respectively, after 3 and 6 months, as can be expected in endstage neoplastic disease. This pilot study demonstrates that local drug application is feasible, life-saving, and well tolerated by the patients. It opens perspectives for local drug application in other cardiac disorders as well.

Topics: Adolescent; Adult; Aged; Anti-Inflammatory Agents; Antineoplastic Agents; Autoimmune Diseases; Bacterial Infections; Biopsy; Cisplatin; Endoscopy; Female; Fibrin; Glucocorticoids; Humans; Male; Middle Aged; Neoplasms; Neovascularization, Pathologic; Paracentesis; Pericardial Effusion; Pericarditis; Pericardium; Pilot Projects; Sensitivity and Specificity; Survival Rate; Triamcinolone