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Apeldoorn, Netherlands

Roke Y.,z Central Psychiatric Center | Van Harten P.N.,z Central Psychiatric Center | Van Harten P.N.,Maastricht University | Buitelaar J.K.,Radboud University Nijmegen | And 5 more authors.
Hormone Research in Paediatrics | Year: 2012

Aims: This cross-sectional study investigates the effect of antipsychotic (AP)-induced hyperprolactinemia on testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), inhibin B, and puberty in boys with mainly autism spectrum disorders (ASD). Method: One hundred and four physically healthy 10-to 19-year-old boys with ASD or disruptive behavior disorder (DBD) were recruited between October 2006 and November 2009. Fifty-six adolescents had been treated with AP for >16 months; 48 had never been exposed to AP. Morning non-fasting levels of serum prolactin, testosterone, LH, FSH and inhibin B were obtained and Tanner pubertal stage was determined. Patients with hyperprolactinemia (n = 28) were compared to those without hyperprolactinemia (n = 76) using non-parametric or parametric tests, as appropriate. Results: Patients with AP-induced hyperprolactinemia had significantly lower testosterone levels with adjustment for age (p = 0.035) compared to patients without hyperprolactinemia and without AP treatment. The difference was not significant within the AP-treated group, and the level of testosterone was within the reference range compared to age-and gender-matched normative data. There was no between-group difference for LH, FSH, inhibin B or Tanner stages. Conclusion: AP-induced hyperprolactinemia is related to significantly lower testosterone levels in pubertal boys with ASD and DBD. © 2012 S. Karger AG, Basel. Source


Roke Y.,z Central Psychiatric Center | Van Harten P.N.,z Central Psychiatric Center | Van Harten P.N.,Maastricht University | Buitelaar J.K.,Radboud University Nijmegen | And 6 more authors.
European Journal of Endocrinology | Year: 2012

Objective: To investigate the long-term effects of antipsychotic (AP) treatment and AP-induced hyperprolactinemia on bone mineral density (BMD) and body composition in male adolescents with autism spectrum disorders (ASDs) and/or disruptive behavior disorder (DBD). Design: Physically healthy 10- to 20-year-old boys with ASD and/or DBD, chronically treated (n=56; mean 52 months, range 16-126 months) or not treated (n=47) with an AP, were recruited to this observational study. Prolactin levels and biochemical bone parameters were measured and BMD of the lumbar spine and total body, and body composition were assessed by dual-energy X-ray absorptiometry, and volumetric BMD of the lumbar spine calculated. Group differences were tested with Student's t-test, χ2 test, Fisher exact test, and logistic regression analysis. Results: Forty-nine percent of the boys treated with an AP had hyperprolactinemia. The mean volumetric lumbar spine BMD z-score was lower (P=0.043), the total percentage of body fat z-score was higher (P=0.042), and biochemical bone marker carboxyterminal cross-linking telopeptide of bone collagen was lower in the AP-treated boys with hyperprolactinemia than in the AP-treated boys without hyperprolactinemia. Seven to 11% of the hyperprolactinemic boys had low BMD. The mean lumbar spine and total body BMD z-scores and body composition were similar in the boys who were or were not treated with an AP. The total study population had a lower mean lean tissue mass (mean z-score -0.37, P=0.004) and a higher percentage of total body fat (mean z-score 1.16, P < 0.001) than healthy controls (normative data); biochemical bone parameters were within normal limits. Conclusion: AP-induced hyperprolactinemia in boys with ASD or DBD may have a negative effect on lumbar spine BMD. Longitudinal studies are needed to confirm this finding and further disentangle the effects of the disorder, lifestyle, treatment, and hyperprolactinemia. © 2012 European Society of Endocrinology. Source

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