warfarin has been researched along with Sarcoidosis* in 6 studies
6 other study(ies) available for warfarin and Sarcoidosis
Article | Year |
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Surgical removal of a left ventricular thrombus associated with cardiac sarcoidosis.
We report successful surgical management of a 31-year-old man with a left ventricular thrombus following heart failure due to cardiac sarcoidosis. Preoperative echocardiography showed diffuse hypokinesis and a mobile ball-like thrombus in the left ventricle. Computed tomography revealed a left ventricular tumor and bilateral hilar lymphadenopathy, while MRI of the brain showed small infarctions in the occipital lobe. Postoperative pathologic examination of a specimen from the left ventricular free wall and a mediastinal lymph node revealed non-caseating granulomas consistent with cardiac sarcoidosis. The patient was referred to a cardiologist for further treatment with prednisolone. This is a rare case of surgical removal of a left ventricular ball-like thrombus in a patient with cardiac sarcoidosis. Topics: Adult; Anticoagulants; Cardiomyopathies; Cerebral Infarction; Glucocorticoids; Heart Diseases; Heart Failure; Heart Ventricles; Humans; Lymphatic Diseases; Magnetic Resonance Imaging; Male; Occipital Lobe; Prednisolone; Sarcoidosis; Thrombectomy; Thrombosis; Tomography, X-Ray Computed; Treatment Outcome; Warfarin | 2008 |
A case of renal sarcoidosis with complement activation via the lectin pathway.
A 57-year-old woman with pulmonary sarcoidosis was admitted to the hospital because of an elevation of serum creatinine and blood urea nitrogen. On admission, the laboratory data suggested interstitial nephritis without proteinuria and hematuria, whereas a renal biopsy showed granulomatous interstitial nephritis and mild mesangial proliferative glomerulonephritis. Immunoglobulin and C1q deposits were negative, but mannose-binding lectin, C3, C4d, and C5b-9 deposits were marked in the glomerular mesangial areas. The lectin pathway of complement activation may have contributed to the development of glomerular injury in this patient. DNA of Propionibacterium acnes , which is now strongly suspected as the pathogen of sarcoidosis, was detected in the patient's glomerular mesangial cells; tubular epithelial cells, which were involved in granulomatous inflammation; and mononuclear cells in epithelioid granulomas by in situ hybridization. These findings may add new insights to the pathogenesis of renal sarcoidosis, including its relation to infection, because mannose-binding lectin plays a crucial role in the host defense against various pathogens. From this case of renal sarcoidosis, it is hypothesized that P acnes may be involved in pathogenesis of granulomatous interstitial nephritis and that it plays a role in glomerular complement activation via the lectin pathway. Topics: Anti-Inflammatory Agents; Anticoagulants; Complement Activation; Complement C3; Complement C4b; Complement Membrane Attack Complex; DNA, Bacterial; Drug Therapy, Combination; Female; Glomerular Mesangium; Glomerulonephritis, Membranoproliferative; Gram-Positive Bacterial Infections; Heparin; Histiocytosis, Langerhans-Cell; Humans; Lung; Lung Diseases, Interstitial; Mannose-Binding Lectin; Methylprednisolone; Middle Aged; Nephritis, Interstitial; Peptide Fragments; Prednisone; Propionibacterium acnes; Sarcoidosis; Warfarin | 2005 |
Warfarin therapy complicated by recurrent hemobilia in a patient with sarcoidosis.
Topics: Anticoagulants; Biopsy, Needle; Cholangiography; Cholecystectomy, Laparoscopic; Endoscopy, Gastrointestinal; Fatal Outcome; Female; Follow-Up Studies; Heart Failure; Hemobilia; Humans; Middle Aged; Recurrence; Sarcoidosis; Warfarin | 1997 |
Human alveolar macrophages synthesize factor VII in vitro. Possible role in interstitial lung disease.
Both fibrin and tissue macrophages are prominent in the histopathology of chronic inflammatory pulmonary disease. We therefore examined the procoagulant activity of freshly lavaged human alveolar macrophages in vitro. Intact macrophages (5 X 10(5) cells) from 13 healthy volunteers promoted clotting of whole plasma in a mean of 65 s. Macrophage procoagulant activity was at least partially independent of exogenous Factor VII as judged by a mean clotting time of 99 s in Factor VII-deficient plasma and by neutralization of procoagulant activity by an antibody to Factor VII. Immunoprecipitation of extracts of macrophages metabolically labeled with [35S]methionine by Factor VII antibody and analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed a labeled protein consistent in size with the known molecular weight of blood Factor VII, 48,000. The addition of 50 micrograms of unlabeled, purified Factor VII blocked recovery of the 48,000-mol wt protein. In addition, supernatants of cultured macrophages from six normal volunteers had Factor X-activating activity that was suppressed an average of 71% after culture in the presence of 50 microM coumadin or entirely by the Factor VII antibody indicating that Factor VII synthesized by the cell was biologically active. Endotoxin in vitro induced increases in cellular tissue factor but had no consistent effect on macrophage Factor VII activity. We also examined the tissue factor and Factor VII activities of freshly lavaged alveolar cells from nine subjects with clinical and/or histologic evidence of sarcoidosis. Four of the nine subjects expressed increased tissue factor and seven of nine had increased Factor VII activity over the normal range (P less than 0.01). We estimate the mean Factor VII associated with the cells of sarcoid patients to be 4.7 ng/10(6) cells (range 0.4-20) as compared to a mean of 0.74 ng/10(6) cells (range 0.2-2) for that of normal subjects. Along with previous data showing synthesis of plasminogen activator, these findings indicate that human alveolar macrophages normally synthesize and express measurable amounts of the initial enzymes of proteolytic reactions regulating both fibrin deposition and fibrin resorption. Abnormalities in Factor VII activity in a small group of patients with sarcoidosis raise the possibility that modulation of fibrin turnover by macrophages may contribute to the pathology of this and perhaps other interstitial lung diseases. Topics: Blood Coagulation; Cells, Cultured; Endotoxins; Factor VII; Factor X; Humans; Lung Diseases; Macrophages; Pulmonary Alveoli; Sarcoidosis; Warfarin | 1985 |
Anticoagulant treatment in sarcoidosis.
The treatment of sarcoidosis has so far been disappointing. This paper presents a patient in whom persistent disappearance of the pulmonary infiltrations was observed during anticoagulant treatment for venous thrombosis. A possible mechanism for a beneficial effect of anticoagulant treatment in sarcoidosis is discussed. Topics: Adult; Female; Heparin; Humans; Radiography; Sarcoidosis; Warfarin | 1977 |
Sarcoidosis and amyloidosis.
Topics: Acute Kidney Injury; Adult; Aluminum Hydroxide; Amyloidosis; Barbiturates; Calcium; Cortisone; Humans; Magnesium; Male; Parasympatholytics; Phosphorus; Prednisone; Sarcoidosis; Splenectomy; Warfarin | 1971 |