Dextran as a modulator of immune and coagulation activities in trauma patients.
Low Mr dextran has been utilized as a prophylactic therapy in treatment of coagulopathy. There is evidence that monocyte dysfunctions are important contributors to hypercoagulability episodes, as well as to immunoincompetence post-trauma. Dextran is a known monocyte modulator. Consequently, we evaluated the efficacy of dextran infusion in moderating immune dysfunction, monocyte aberrations, and hypercoagulability episodes. Twenty-eight trauma patients were randomly divided into two groups. One group of 15 received dextran at 1 g/kg wt/24 hr for 5 days in addition to standard resuscitation and treatment. The control or nontreated patient group received only standard treatment. Trauma patients in the two groups were retrospectively matched by injury severity score (ISS) to ensure comparability. Blood samples were collected daily for some studies and at 3-day intervals for other assays. In vivo coagulation status was evaluated by assessing the changes in intravascular fibrinopeptide A (FPA). Immune reactivity to the mitogen phytohemagglutinin (PHA) was also evaluated. Both monocyte production of plasminogen activator (PA) and monocyte production of procoagulant activity (PCA) have been shown to correspond to and be augmented by monocyte-T lymphocyte interactions. Consequently, monocyte production of plasminogen activator and procoagulant activity were assessed as measures of monocyte immune activity as well as indicators of monocyte function in controlling the balance between fibrinolysis and coagulation. Only patients with ISS of greater than 25 experienced significant immune, coagulation, or monocyte aberrations. Of those having an injury severity score (ISS) score of 25-35, all of the control and two of the dextran patients had significant perturbations in their immune and monocyte functions.(ABSTRACT TRUNCATED AT 250 WORDS)
Miller
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Lim
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D001777:Blood Coagulation; D003911:Dextrans / Q000627:therapeutic use*; D004903:Erythrocyte Aggregation / Q000209:etiology; D006801:Humans; D007111:Immunity, Cellular; D007167:Immunotherapy; D008938:Mitosis / Q000187:drug effects; D009000:Monocytes / Q000502:physiology*; D009113:Muramidase / Q000096:biosynthesis; D010835:Phytohemagglutinins / Q000494:pharmacology; D010960:Plasminogen Activators / Q000096:biosynthesis; D014947:Wounds and Injuries / Q000628:therapy*
D003911:Dextrans; D010835:Phytohemagglutinins; D009113:Muramidase; D010960:Plasminogen Activators