Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pleural diseases. 157 32

Rates of bacteremia among hospitalized patients with central venous catheters range up to 21%. Few data exist for home intravenous therapy (IVT). We studied 300 patients from two hospital-based home IVT services in 29 months. Diagnoses included 92 cases of osteomyelitis, 33 of pneumonia, 35 of malnutrition, 26 of chronic pain, and 114 of other diseases. Peripheral IVT was given to 97 patients. Mean age was 39.4 years (range, 0.3-98). Hickman, Infuse-A-Port, Broviac, Arrow triple lumen, Hohn, and peripherally inserted central catheters (PICC) were used for a mean of 44 days. Six bacteremias (one death) (2%, 4.6/10,000 catheter days), two subclavian thromboses, 13 catheter site infections, and one additional death occurred. PICC experience included 76 patients, mean age 46 years (range, 4-76), primarily with infections, chronic pain, or dehydration. Mean duration of therapy was 24 days (0-67) and was completed in 51 patients; others completed therapy with standard peripheral catheters a mean of 6 days later. Complications included 17 obstructions by clot, 11 cases of phlebitis, six catheter fractures, five punctures, two accidental removals, and one infiltration. Liquid silicone repaired holes; urokinase opened clots. Successful completion of therapy was more common in the second year, 88% versus 57%. Despite more complications, patients, home IVT nurses, and physicians preferred PICCs. We conclude that home IVT is safe via many means of access, with fewer infections than with hospital care. Such infections may be termed "nosohusial."
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PMID:Infectious complications among patients receiving home intravenous therapy with peripheral, central, or peripherally placed central venous catheters. 192 99

The potential importance of pleural fibrin deposition in the pathogenesis of pleural injury is supported by both clinical and experimental observations. We hypothesized that the local equilibrium between procoagulant and fibrinolytic activities is disrupted to favor fibrin deposition in exudative pleuritis. To test this hypothesis, we characterized procoagulant and fibrinolytic activities in pleural exudates from patients with pneumonia, lung cancer, or empyema and transudates from patients with congestive heart failure. Procoagulant activity was generally increased in exudative processes and was due mainly to tissue factor. All effusions contained antithrombin III and inhibited factor Xa and thrombin, but endogenous prothrombinase or thrombin activities were variably detected. Pleural fluid fibrinolytic activity was increased in congestive heart failure and was due to both tissue plasminogen activator and urokinase. Depressed fibrinolytic activity was found in pleural exudates despite increased concentrations of plasminogen, mainly glu-1-plasminogen, and was due to inhibition of plasminogen activation by plasminogen activator inhibitors 1 and 2 and of plasmin, in part by alpha 2-antiplasmin. Concentrations of PAI-1 in exudative pleural fluids were increased up to 913-fold, compared with normal pooled plasma. Exudative pleural effusions are characterized by increased procoagulant and depressed fibrinolytic activity, favoring fibrin deposition in the pleural space. The balance of these activities is reversed and favors fibrin clearance in congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities of pathways of fibrin turnover in the human pleural space. 206 28

Urokinase type plasminogen activator (u-PA) was purified from three different chest fluids obtained from patients with liver cirrhosis and pleuritis, aplastic anemia and pneumonia, and lung tumor, and the relationship between molecular weight and plasminogen activator (PA) activity was examined by zymography. The molecular weights of u-PAs from the chest fluids were 200 Kd, 150-180 Kd, 95 Kd, 55 Kd, 44 Kd, 33 Kd and 14 Kd, and PA activity was observed at molecular weights of 95 Kd, 55 Kd and 33 Kd. Fibrin binding of u-PA was observed at molecular weights of 55 Kd and 33 Kd.
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PMID:Properties of urokinase type-plasminogen activator found in chest fluid. 210 19

The surgical indication for spontaneous cerebellar hemorrhage is not as controversial as the operative management of intracranial hemorrhage. Timing of the operation is crucial: intervening too early can produce an additional strain on the patient and an increased risk, while waiting too long to evacuate the hematoma can be fatal. This dilemma may be a factor in the relatively high mortality and morbidity rates following both operative and conservative treatment that have been reported in the literature (42.5% and 30%, respectively). In long-term studies on 14 patients, the authors have shown that stereotactic puncture and fibrinolysis for cerebellar hemorrhage is a valuable alternative to treatments used currently. The method consists of computerized tomography (CT)-guided stereotactic puncture and partial evacuation of the hematoma. After fibrinolysis with urokinase, the residual hematoma can be completely evacuated via a catheter introduced into the cavity of the hematoma. Only one of the 14 patients died in the direct postoperative phase; the remaining patients were enjoying a good to very good quality of life 6 months after the acute event. Two patients subsequently died as a result of pneumonia and cerebral infarction, respectively; both conditions were unrelated to the hemorrhage. The authors conclude that the CT-guided stereotactic method is simple, effective, and safe, and can be applied to patients of any age.
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PMID:CT-guided stereotactic fibrinolysis of spontaneous and hypertensive cerebellar hemorrhage: long-term results. 219 40

Urokinase receptors on lymphocytes described in the paper link immune system of the body with fibrinolytic one, play a biological role in sano-++- and pathogenesis in aggravation of chronic purulent bronchitis, of focal and croupous pneumonia. A correlation between the trend in the expression of urokinase receptors on lymphocytes and changes in activity of plasminogen activator in the blood and urine was established: the more the expression, the more the activity. The method can serve a criterion of the treatment effectiveness+ in nonspecific inflammatory bronchial and pulmonary diseases and be helpful in designing methods of their treatment improvement.
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PMID:[Regulation of fibrinolysis by lymphocytes in inflammatory diseases of the bronchopulmonary system]. 256 May 7

Recognizing the confirmed efficacy of urokinase as a thrombolytic and proteolytic agent, we assess its usefulness in the treatment of multiloculated pleural effusion, empyema and hematoma as a substitute of other more invasive procedures. Treatment with urokinase was applied in 18 consecutive cases. Inclusion criteria were a well-placed thoracic probe that did not drain and a radiological image showing occupation. Patients were excluded if they had bronchial fistulas or hemothorax of less than 7 days duration. Effusion in the included cases had developed after pneumonia, after surgery or after trauma. Treatment lasted 3 to 4 days ant was considered effective or not based on the volume of liquid drained and on radiological evidence of change. The amount of liquid drained was highly variable (mean 1,282 and S.D. 1,224; range 100-3,975). Radiological change was considered completely satisfactory in 10 cases, with 6 patients continuing to show occupation of the costophrenic sinus with no clinical repercussions. Two patients died of causes unrelated to administration of the drug. There were two mild relapses that did not require a second round of treatment with urokinase. Patients were followed for a least 30 days after discharge and no new recurrences were detected. We have found urokinase to be a useful fibrinolytic agent for treating multiloculated effusion. Contraindications are few and therefore urokinase should be considered the first-choice treatment to be applied before other more invasive measures are taken.
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PMID:[Usefulness of urokinase in multilocular pleural effusion]. 770 89

A 44-year-old Japanese man having aplastic anemia (AA)-paroxyamal nocturnal hemoglobinuria (PNH) syndrome was referred to our hospital because of purpuras due to thrombocytopenia in July 1994. He suffered from pneumonia after admission, complicated with cerebral, splenic, and left renal infarction. Pulmonary infaction was also confirmed by perfusion lung scan. He had a plasma plasminogen (PLG) functional activity of 54.4% with a normal level of PLG antigen. The gel isoelectrofocusing pattern of the plasminogen derived from the patient showed 10 normal bands and 10 additional doublet bands with slightly higher isoelectric points than the normal components. Abnormal PLG is converted by urokinase to an inactive two-chain plasmin molecule. These findings were similar to those of a case with dysplasminogenemia (PLG Tochigi) reported by Aoki et al. He was given warfarin for the prevention of thrombosis in December 1994. As of October 1995, these was no recurrence of thrombosis. The cause of thrombosis in the present case have been the association with PNH, predisposition to PLG Tochigi, or the complication of pneumonia. This is the first report of AA/PNH syndrome associated with dysplasminogenemia.
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PMID:[Thrombotic complication in the course of aplastic anemia-paroxysmal nocturnal hemoglobinuria syndrome; possible involvement of dysplasminogenemia (plasminogen Tochigi) in the pathogenesis of thrombosis]. 872 51

Urokinase-type plasminogen activator (u-PA) is known to be secreted by malignant cells during proliferation and migration, and is associated with tumour cell invasion and metastasis. This study was undertaken to evaluate whether u-PA is significantly increased in carcinomatous pleural fluids compared to those due to other aetiologies, and to identify the cells in the pleural space that are involved in its accumulation. Using an enzyme-linked immunosorbent assay, we quantified u-PA in the pleural fluid specimens of 40 patients with carcinomatous pleuritis, 18 with tuberculosis, 18 with parapneumonic pleuritis and 11 with congestive heart failure (CHF). The level of u-PA was elevated in carcinomatous pleural fluid compared with the level in transudative pleural fluid from patients with CHF (p<0.0001). The levels of u-PA were not statistically different between patients with cancer and tuberculosis, or between patients with cancer and pneumonia. The levels of u-PA in patients who did not respond to chemical pleurodesis were significantly higher than those who had complete response (p=0.0001). In immunocytochemical and immunoblotting studies, cancer cells in pleural fluids as well as mesothelial cells contained u-PA. u-PA was detected in the culture supernatants of viable pleural cells in the majority of patients with carcinomatous pleuritis. Our results suggest that local release of urokinase-type plasminogen activator by viable cells, including cancer cells and mesothelial cells, may affect the levels of urokinase-type plasminogen activator in pleural fluids.
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PMID:Urokinase-type plasminogen activator in carcinomatous pleural fluid. 923 Feb 48

Pneumonia is the most common serious complication of varicella infection in adults. A variety of thrombotic complications including purpura fulminans and disseminated intravascular coagulation have been reported in children with varicella but not in adults. Two men with varicella pneumonia who had profound lower extremity ischemia caused by thrombosis of the profunda femoris and tibial arteries are reported. Both patients had free protein S deficiency and vascular thrombosis in association with varicella pneumonia without overt evidence of disseminated intravascular coagulation or purpura fulminans. Antiphospholipid immunoglobulin G and immunoglobulin M antibodies were present in one, whereas the other had evidence of the lupus anticoagulant. The proposed pathogenesis and management options including intraarterial thrombolytic therapy with urokinase and the need for long-term anticoagulation are discussed.
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PMID:Spontaneous tibial artery thrombosis associated with varicella pneumonia and free protein S deficiency. 954 47


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