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. 2018 May 10;2018(5):CD012069. doi: 10.1002/14651858.CD012069.pub2

Wang 2011.

Methods
  1. An observational, 24‐week, prospective, non‐randomised study of methylphenidate treatment

  2. A 24‐week cross‐sectional study

Participants Number of participants screened: not stated
Number of participants included: 50
Number of participants followed up: 30
Number of withdrawals: 20
Diagnosis of ADHD: DSM‐IV diagnosis (subtype: combined (48%), hyperactive‐impulsive (22%), inattentive (30%))
Age: mean 7.56, range 6‐12 years old
IQ: above 70
Sex: 40 males, 10 females
Methylphenidate‐naïve: not stated
Ethnicity: not stated
Country: Taiwan
Comorbidity: none
Comedication: none
Sociodemographics: not stated
Inclusion criteria
  1. Age between 6 and 12 years

  2. ADHD according to DSM‐IV

  3. Newly diagnosed or had not taken medication for ADHD during the previous 6 months or more


Exclusion criteria
  1. History of major physical or psychiatric diseases (such as pervasive developmental disorder, oppositional defiant disorder, conduct disorder, bipolar disorder, depressive disorder, anxiety disorder, psychotic disorder, or substance use disorder)

Interventions Methylphenidate type: not stated
Methylphenidate dosage: 5‐15 mg/day
Mean methylphenidate dosage: 10.62 mg/daily at 1 month, 14.15 mg/daily at 3 months and 12.84 mg/daily at 6 months.
Administration schedule: not stated
Duration of intervention: 24 weeks
Treatment compliance: the drug compliance at each visit was confirmed to the reports of patients' parents and the remnant drug
Outcomes Non‐serious adverse events
No reporting of adverse events
3 patients discontinued prematurely due to decreased appetite and weight loss
Notes Sample calculation: no
Ethics approval: approved by the Institutional Review Board of Chang Gung Memorial Hospital
Funding: the study was funded by the Chang‐Gung Memorial Hospital Research Project
Vested interests/authors' affiliations: the authors have no conflicts of interest to declare
Key conclusions of the study authors: DHEA (dehydroepiandrosterone), but not the cortisol basal level, may be a biological laboratory marker for ADHD, particularly for performance on the CPT. Both the causal relationship between DHEA and ADHD and the role of DHEA in treating ADHD require further investigation
Supplemental information received through personal email correspondence with the authors in December 2013 (Wang 2013 [pers comm])