warfarin has been researched along with Immunologic-Deficiency-Syndromes* in 3 studies
1 review(s) available for warfarin and Immunologic-Deficiency-Syndromes
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Macrophage procoagulants.
From the preceding exposition it is now clear that the regulation of monocyte/macrophage PCA is dependent upon a complex network of interacting pathways, some of which amplify the response of the monocyte/macrophage, while others inhibit. In all probability many more will emerge. The construct illustrated in Figure 3, therefore, is a simplified view of the two major stimulatory pathways: the T cell-dependent pathway, activated by immune recognition and mediated by lymphokine(s); and the T cell-independent pathway, activated by direct perturbation of monocytes by such stimuli as LPS. At least 2 or 3 different PCAs can be expressed by monocyte/macrophages from different species, depending upon the anatomic site of the origin of the cell and the types of stimuli imposed. Inhibition of PCA expression is accomplished by at least one set of regulatory lipoproteins, and other inhibitory loops may be found. The result of these multiple interactions is the deposition of fibrin on the cell surface or in the surrounding milieu. It is our belief that this close relationship between coagulation reactions and inflammatory reactions, resulting in fibrin deposition, represents a fundamental host defense designed to delimit the inflammatory response. Nevertheless, the precise role of monocyte procoagulants in vivo remains unclear. A number of potential mechanisms exist for activation of coagulation in both inflammatory and neoplastic disorders, and the finding of enhanced monocyte procoagulant activity by no means establishes its importance in physiologic or, pathosphysiologic responses in vivo. Further studies, possibly with agents capable of specific inhibition of monocyte procoagulants in vivo, will be necessary to define the precise importance of these procoagulants in clinical disorders. Topics: Animals; Anti-Inflammatory Agents; Antigens; Blood Coagulation; Blood Coagulation Factors; Cell Line; Factor V; Factor VII; Factor X; Factor Xa; Fibrin; Fibrin Fibrinogen Degradation Products; Guinea Pigs; Humans; Hypersensitivity, Delayed; Immunologic Deficiency Syndromes; Infections; Inflammation; Lipopolysaccharides; Macrophages; Mice; Monocytes; Neoplasms; Neutrophils; Rabbits; Rats; T-Lymphocytes; Thromboembolism; Thromboplastin; Warfarin | 1984 |
2 other study(ies) available for warfarin and Immunologic-Deficiency-Syndromes
Article | Year |
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Consensus conference. Fresh-frozen plasma. Indications and risks.
Topics: Blood Coagulation Disorders; Blood Preservation; Blood Transfusion; Freezing; Humans; Immunologic Deficiency Syndromes; National Institutes of Health (U.S.); Plasma; Research; Risk; Technology Assessment, Biomedical; Transfusion Reaction; United States; Warfarin | 1985 |
Procainamide-induced SLE and lymphoreticular disorders.
A 56-year-old male patient diagnosed as a case of procainamide-induced systemic lupus erythematosus (SLE) was found to have a lymphoproliferative disorder at postmortem examination.Contrary to other immune disorders, the association of SLE with neoplasia is a rare occurrence. The present case raises the question of whether a relationship exists between the lupus diathesis and lymphoreticular neoplasia. The study of the incidence of neoplasia in families of patients with SLE may prove helpful in establishing this relationship. Topics: Aortic Diseases; Autopsy; Blindness; Bone Marrow; Digoxin; Drug Therapy, Combination; Heart Diseases; Heparin; Humans; Immunologic Deficiency Syndromes; Kidney; Lupus Erythematosus, Systemic; Lymph Nodes; Lymphoma; Male; Middle Aged; Procainamide; Quinidine; Retinal Artery; Spleen; Thromboembolism; Warfarin | 1974 |