For instance, it has been estimated that acute (i.e. ≤12 weeks) better treatment with risperidone in children and adolescents is associated with an average increase in inhibitor 17-AAG prolactin concentration of nearly 21 ng/ml compared with placebo [Pringsheim et al. 2011]. With prolactin reference values typically ranging from 3 to

25 ng/ml, such an increase is substantial, placing many individuals above the upper limit Inhibitors,research,lifescience,medical of normal. Similarly, compared with placebo, treatment for 3 and 6 weeks with olanzapine was associated with a nearly 31-fold increase in the risk of hyperprolactinemia, although the magnitude of the elevation is smaller than that observed with risperidone [Tohen et al. 2007; Kryzhanovskaya et al. 2009; Pringsheim et al. 2011]. Quetiapine has also been associated Inhibitors,research,lifescience,medical with hyperprolactinemia while ziprasidone

and clozapine tend to be prolactin sparing [Roke et al. 2009]. In contrast, aripiprazole reduces prolactin concentration below normal in nearly two-thirds of treated children, likely due to its partial dopamine agonist activity [Safer et al. 2013]. Of note, changes in prolactin concentration have been observed during AP treatment across a variety Inhibitors,research,lifescience,medical of psychiatric disorders [Roke et al. 2009; Pringsheim et al. 2011]. Over more extended periods of exposure, prolactin concentration decreases although

hyperprolactinemia persists in a substantial number of individuals [Findling et al. 2003; Calarge et al. 2009b; Kryzhanovskaya et al. 2009]. For example, between 30 and 50% of children Inhibitors,research,lifescience,medical and adolescents treated with risperidone continue to exhibit this side effect [Findling et al. 2003; Calarge et al. 2009b]. Hyperprolactinemia is also common during long-term Inhibitors,research,lifescience,medical treatment with typical APs as well as with olanzapine [Kryzhanovskaya et al. 2009; Roke et al. 2009]. In order to explore the tolerability of risperidone during long-term treatment in children and adolescents, Calarge and colleagues recruited Cilengitide 7–17 year-old patients who had received risperidone for at least 6 months [Calarge et al. 2009b, 2010]. At study enrollment, psychotropic polypharmacy was allowed but treatment with APs other than risperidone led to study exclusion. A morning fasting blood sample was used to measure prolactin and sex hormones. Nearly 3 years after the onset of risperidone treatment, hyperprolactinemia was present in 50% of the participants. Older age, more advanced pubertal development, and a higher oral dose of risperidone were associated with higher prolactin concentrations whereas treatment with psychostimulants, which potentiates dopaminergic signaling, lowered prolactin [Calarge et al. 2009b].