Chronic malignant pleural exudation is generally characterized by little or no fibrin deposition. However, during induced inflammation, fibrin deposition concomitant with cessation of exudation is seen. To judge the involvement of the fibrinolytic system in this process, concentrations of fibrinolytic factors were followed in 10 patients during treatment by quinacrine instillation and tube drainage. Plasminogen and alpha-2-antiplasmin were found in low concentrations and did not show significant changes during treatment. The plasminogen activator inhibitor PAI-1, which plays an important role in the regulation of fibrinolysis, was also studied during treatment. Before treatment the concentration of PAI-1 was 21.7 +/- 12.0 (mean +/- SD) AU/ml and it increased to 86.9 +/- 25.9 AU/ml 6 h after quinacrine instillation. D-dimer, a product of the lysis of fibrin, was found in high concentrations before treatment (62.7 +/- 25.5 micrograms/ml) and in low concentrations 6 h after treatment (12.2 +/- 7.9 micrograms/ml). Thus, it was possible to demonstrate that the fibrinolytic system is activated during chronic malignant pleural exudation and, furthermore, that the activity decreases during induced inflammation.
We sought to determine the incidence rate of carpal tunnel syndrome in the general population. Using three different case definitions, we conducted a prospective study to ascertain by medical record review all cases of incident disease in a defined population during a 2-year period. Newly diagnosed probable or definite carpal tunnel syndrome (N = 309) occurred at a rate of 3.46 cases per 1,000 person-years (95% confidence interval = 3.07-3.84). The incidence rate in our study was 3.5 times higher than the rate 20 years ago in a Minnesota city. The rate difference probably results from a combination of reasons, including a true rise in incidence.
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