1 Platelet aggregation responses to 5-HT and adenosine diphosphate were examined in a population of eighteen patients treated with fluphenazine decanoate for longer than one year.2 5-HT induced aggregation was enhanced in ten subjects. This enhancement was similar to that previously described in patients receiving chlorpromazine. 3 Patients who showed enhanced 5-HT induced aggregation showed less rateable psychopathology and less extrapyramidal side-effects than patients who did not show enhancement. 4 These findings suggest that platelet aggregation responses could be used to identify patients who could be safely withdrawn from long-term neuroleptic therapy.
Radcliffe Infirmary, Oxford OX2 6HE 1 The effects of treatment with a range of neuroleptic drugs on 5-hydroxytryptamine (5-HT) induced platelet aggregation in vivo were examined in a group of recently admitted psychiatric patients and in a larger group of chronic schizophrenic patients. 2 Five of seven recently admitted patients treated with chlorpromazine showed enhanced aggregation. Four of seven patients treated with fluphenazine, flupenthixol, trifluoperazine and haloperidol showed enhancement. 3 Enhanced aggregation responses were observed in only 20% of chronic schizophrenic patients being treated with a neuroleptic drug. 4 The relationship between changes in platelet aggregation and clinical changes in recently admitted patients was variable and platelet aggregation responses were not predictive ofresponse to treatment. 5 Chronic schizophrenic patients with enhanced aggregation showed significant week to week variation in platelet aggregation response. Variability of responses was not related to the drug used or to the dose administered. There was some evidence that higher plasma concentrations of neuroleptic drugs were associated with enhanced platelet aggregation responses.6 'Treatment with neuroleptic drugs leads to enhancement of platelet aggregation responses induced by 5-HT. The frequency and reliability with which such responses can be elicited is unpredictable and the value ofplatelet aggregation responses as an empirical guide to treatmentwith neuroleptic drugs is therefore open to question.
Nineteen patients with acute psychoses, the majority schizophrenics, were studied in the course of chlorpromazine (CPZ) treatment. Plasma levels of the drug, plasma prolactin (PRL), extrapyramidal side-effects (EPS) and changes in mental state were monitored weekly, as in our earlier study. The results confirm some of our previous findings: (a) plasma CPZ levels vary widely among patients and correlate poorly with daily doses of CPZ; (b) increased plasma PRL is associated with higher plasma CPZ levels and is more common among the patients who develop EPS; and (c) none of these three variables differ between groups of patients with good and poor treatment outcome. However we did not confirm our previous finding of a significant association between EPS and higher plasma CPZ, nor did we find that the ratio of CPZ-sulphoxide to CPZ differed between the improved patients and the rest.
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