The relationship of prolactin to tardive dyskinesia and psychosis in treatment-resistant schizophrenia

Prolactin (PRL) has been considered a putative measure of central D2 blockade. It was reported to be inversely correlated with tardive dyskinesia (TD), presumably due to greater D2 blockade. Also, prolactin elevation correlated with treatment response to typical neuroleptics in acutely ill patients. However, studies on acute, treatment-responsive patients may not be replicated in chronic, treatment-resistant patients. We studied 29 patients (M = 15, F = 14) with DSM III-R schizophrenia, who went through 4 weeks of a typical neuroleptic (10 mg haloperidol) (HLP), followed by 16 weeks of clozapine (CLZ) in randomized doses of 100, 300 & 600mg. The means of age, age of onset & duration of illness were 45.6, 19.6 and 26.03 respectively. In the HLP phase, PRL showed no correlation with TD, measured by ADRS (M: r = −0.15, p = 0.5; F: r0.14, p = 0.6). Also, severity of psychosis, measured by BPRS did not correlate with PRL (M: r = −0.02, p = 0.9; F: r = 0.14, p = 0.6). In the CLZ phase, change in BPRS scores at 16 weeks, did not correlate with change in prolactin levels (M: r = 0.11, p = 0.6; F:−0.09, p = 0.7). There was no relationship between PRL change and improvement in BPRS even after retrospectively categorizing patients into ‘improvers’ and ‘non-improvers’, based on CGI. This chronic population had a long history of neuroleptic treatment with poor response. In keeping with the reported accommodation of PRL on chronic treatment, most patients did not show elevated levels. The overall treatment response to clozapine was low. Prolactin may not be a useful guide in treatment-resistant schizophrenia, with reference to TD or psychosis.