Metabolic Brain Disease | 2019

Prolactin, flupenthixol decanoate and first episode schizophrenia – clinical and laboratory correlates

 
 
 
 
 

Abstract


First-episode psychosis (FEP) patients are more sensitive to neuroleptic side-effects such as hyperprolactinemia. We examined the prolactin levels of previously minimally treated patients with first episode schizophrenia over their first year of treatment with flupenthixol decanoate and the relationship between prolactin levels, gender and clinical features of schizophrenia. Prolactin levels were assessed at three monthly intervals in 126 patients with first-episode schizophrenia in a single-site study conducted over 12 months during treatment with flupenthixol decanoate according to a fixed protocol. The mean prolactin level for the total sample was 11.91 ng/ml (standard deviation [SD]15.52) at baseline. Women had higher levels of prolactin than men at month 3, 6 and 12, reaching statistical significance at month 12 (p\u2009=\u20090.02). At 12 months more women than men had hyperprolactinemia (defined as more than 20 ng/ml for males, and as more than 25 ng/ml for females (p\u2009=\u20090.007). Using a mixed effect model, there was a significant association between prolactin change scores over 12 months and gender (p\u2009=\u20090.025) as well as Positive and Negative Syndrome Scale (PANSS) total scores (p\u2009=\u20090.001). In addition female gender (p\u2009=\u20090.04) and age (p\u2009=\u20090.02) correlated with the risk of hyperprolactinemia as categorical variable. In this study treatment with flupenthixol decanoate was associated with relatively low levels of hyperprolactinemia, likely owing to flupenthixol’s relatively atypical mode of action, as well as to the low doses used in our study. We found an inverse correlation between total PANSS scores and prolactin levels, which could support the suggested theory of prolactin having antipsychotic properties. Our study confirms the importance of gender on the prolactin raising effects of antipsychotic treatment.

Volume 34
Pages 1679 - 1687
DOI 10.1007/s11011-019-00474-5
Language English
Journal Metabolic Brain Disease

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