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

Sahin 2014.

Methods A study of methylphenidate use for 2 months
Participants Number of patients screened: not stated
Number of participants included: 30
Number of participants followed up: 30
Number of withdrawals: 0
Diagnosis of ADHD: DSM‐IV (subtype: combined (46.7%), hyperactive‐impulsive (10%), inattentive (43.3%))
Age: mean 9.54 (SD 2.83), range 6‐18 years old
IQ: > 70
Sex: 24 males, 6 females
Methylphenidate‐naïve: 100%
Ethnicity: not stated
Country: Turkey
Comorbidity: disruptive behaviour disorder (DBD): 17, anxiety disorder: 5, learning disability: 3, enuresis/encopresis: 3, tic disorder: 2
Comedication: none
Sociodemographics: not stated
Inclusion criteria
  1. Children and adolescents aged 6‐18 years who were to receive sustained release methylphenidate for DSM‐IV diagnosed ADHD


Exclusion criteria
  1. Previously received methylphenidate

  2. Used any other psychotropic drug for more than 7 days

  3. Used any drug within the last 1 month

  4. Any systemic or metabolic disease, mood disorder, extensive developmental disorder, psychotic disorder, substance abuse, progressive neurological disease, visual and/or auditory disability, or mental retardation (IQ < 70)

Interventions Methylphenidate type: osmotic release oral system (OROS)
Mean methylphenidate dosage: 0.70 (SD 0.20) mg/kg/day (0.64 (SD 0.16) mg/kg/day in the 1st month and 0.76 (SD 0.25) mg/kg/day in the 2nd month)
Administration schedule: not stated
Duration of intervention: 2 months
Treatment compliance: 100%
Outcomes Non‐serious adverse events:
  1. Barkley Side Effects Rating Scale after 2 months of treatment

  2. Height and weight measured pre‐ and post‐treatment

Notes Sample calculation: no
Ethics approval: yes
Funding: sponsored by Ondokuz Mayis University project number PYO.TIP.1904.12.013.
Vested interests/authors' affiliations: none of the authors report conflicts of interest
Key conclusions of the study authors: leptin and brain‐derived neurotrophic factor (BDNF) were not associated with poor appetite and/or weight loss due to methylphenidate treatment. However, ghrelin and adiponectin might be biomolecules that play a role in underlying neurobiological mechanisms of methylphenidate‐related appetite or weight loss.
Exclusion of methylphenidate non‐responders/children who have previously experienced adverse events on methylphenidate: no