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To assess whether therapy with two widely used antidepressants influences platelet counts.
Subjects and methods
In 90 patients hospitalized for treatment of a major depressive episode according to DSM-IV, platelet counts were performed after a 6 d antidepressant-free run-in period and again after 35 d of active standardized treatment with amitriptyline (n = 40) or paroxetine (n = 50).
Results
There was a trend for platelet counts to increase during treatment with amitriptyline (from 245.5 ± 68.6 to 256.8 ± 69 cells × 109 L-1, P < 0.06); no change was observed during treatment with paroxetine (from 232.6 ± 58.3 to 234.6 ± 68.9 cells × 109 L-1, n.s).
Conclusions
Treatment with amitriptyline tends to be associated with elevated platelet counts. The cause for this increase is not known, but may be relevant in terms of patients’ long-term thromboembolic risk.
The changes in the coagulation system in normal pregnancy are consistent with a continuing low grade process of coagulant activity. Using electron microscopy, fibrin deposition can be demonstrated in the intervillous space of the placenta and in the walls of the spiral arteries supplying the placenta. Normal pregnancy is accompanied by dramatic changes in the coagulation and fibrinolytic systems, with a marked increase in some of the procoagulant factors, particularly fibrinogen, and suppression of fibrinolysis. Certain disease states specific to pregnancy have profound effects on platelet consumption, lifespan and function. A fall in the platelet count may precede any detectable rise in serum fibrin degradation products (FDP) in women subsequently developing pre-eclampsia. The most common platelet abnormality encountered in clinical practice is thrombocytopenia. During healthy pregnancy there is little change in antithrombin level but there is some decrease at parturition and an increase in the puerperium.
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