Blood microparticles (MPs) in sickle cell disease (SCD) are reportedly derived only from erythrocytes and platelets. Yet in SCD, endothelial cells and monocytes are activated and abnormally express tissue factor (TF). Thus, sickle blood might contain TF-positive MPs derived from these cells. With the use of flow cytometry to enumerate and characterize MPs, we found total MPs to be elevated in crisis (P ؍ .0001) and steady state (P ؍ .02) in subjects with sickle cell disease versus control subjects. These MPs were derived from erythrocytes, platelets, monocytes, and endothelial cells. Erythrocytederived MPs were elevated in sickle crisis (P ؍ .0001) and steady state (P ؍ .02) versus control subjects, as were monocytederived MPs (P ؍ .0004 and P ؍ .009, respectively). Endothelial and plateletderived MPs were elevated in sickle crisis versus control subjects. Total TF-positive MPs were elevated in sickle crisis versus steady state (P ؍ .004) and control subjects (P < .0001) and were derived from both monocytes and endothelial cells. Sickle MPs shortened plasma-clotting time compared with control MPs, and a TF antibody partially inhibited this procoagulant activity. Markers of coagulation were elevated in patients with sickle cell disease versus control subjects and correlated with total MPs and TF-positive MPs (P < .01 for both). These data support the concept that SCD is an inflammatory state with monocyte and endothelial activation and abnormal TF activity.
Among patients treated in an anticoagulation clinic, INR values of >5 were most common during the first 12 weeks of combined therapy with amiodarone and warfarin and necessitated reduction in warfarin dosage. No other notable changes in INR or amiodarone or warfarin dosage occurred throughout the remainder of the 80-week study period.
Central nervous system (CNS) lesions in newly diagnosed, advanced Hodgkin's disease (HD) commonly suggest intracranial involvement with HD. However, occasionally this could be the result of a CNS infection. We report a case of concurrent CNS tuberculosis in a patient with stage III E HD the first reported in the English literature. Management of this case and the literature pertaining to infectious complications of HD are reviewed.
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