title: Bone mineral density in male adolescents with autism spectrum disorders and disruptive behavior disorder with or without antipsychotic treatment.
abstract: 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).
  
  
  METHODS
  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, χ(2) 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: GGz Central Psychiatric Centre, PO Box 3051, 3800 DB Amersfoort, The Netherlands. y.roke@ggzcentraal.nl
authors.forename: Yvette
authors.initials: Y
authors.lastname: Roke
authors.forename: Peter N
authors.initials: PN
authors.lastname: van Harten
authors.forename: Jan K
authors.initials: JK
authors.lastname: Buitelaar
authors.forename: Diederik E
authors.initials: DE
authors.lastname: Tenback
authors.forename: Lorentz G B A
authors.initials: LG
authors.lastname: Quekel
authors.forename: Yolanda B
authors.initials: YB
authors.lastname: de Rijke
authors.forename: Annemieke M
authors.initials: AM
authors.lastname: Boot
mesh_terms: D015502:Absorptiometry, Photon; D000293:Adolescent; D014150:Antipsychotic Agents / Q000009:adverse effects* / Q000627:therapeutic use*; D019958:Attention Deficit and Disruptive Behavior Disorders / Q000188:drug therapy*; D015519:Bone Density / Q000187:drug effects*; D002648:Child; D002659:Child Development Disorders, Pervasive / Q000188:drug therapy*; D006801:Humans; D006966:Hyperprolactinemia / Q000139:chemically induced / Q000378:metabolism; D008297:Male
chemical_list: D014150:Antipsychotic Agents