Hong 2012.

Methods	An 8‐week open‐label trial to investigate the independent and interaction effects of DAT1, DRD4,ADRA2A and NET1 on treatment response to methylphenidate in ADHD
Participants	Number of participants screened: not stated Number of participants included: 112 Number of participants followed up: 103 Number of withdrawals: 9 Diagnosis of ADHD: DSM‐IV (subtype: combined (69, 61.6%), hyperactive‐impulsive (6, 5.4%), inattentive (29, 25.9%), not otherwise specified (8, 7.1%)) Age: mean 9.1 (SD 2.1) years IQ: 107.4 SD 13.7 Sex: not stated Methylphenidate‐naïve: 100% Ethnicity: Asian Country: South Korea Comorbidity: ODD (15, 13.4%), anxiety disorder (12, 10.7%), enuresis (5, 4.5%) Comedication: not stated Sociodemographics: not stated Inclusion criteria Children diagnosed with ADHD according to DSM‐IV criteria Stimulant‐naïve Exclusion criteria IQ < 70 Currently diagnosed with tic disorder, OCD, language disorder, learning disorder, convulsive disorder Past and/or ongoing history of pervasive developmental disorder, schizophrenia, bipolar disorder, brain damage
Interventions	Methylphenidate type: immediate release and extended release Mean methylphenidate dosage: 19.8 SD 8.2 mg/day (initial dose) and 29.1 SD 11.6 mg/day (final dose) Administration schedule: not stated Duration of intervention: 8 weeks Treatment compliance: 1 participant's parents were anxious about their child taking psychiatric medication, this participant discontinued prematurely
Outcomes	ADHD‐RS (ADHD Rating Scale‐IV) which consists of 18 items, each item is rated from 0 (never or rarely) to 3 (very often). Rated by parents before and after 8 weeks of treatment The study design did not include collection of side‐effect profiles, so possible reasons for dropping out were not systematically assessed Non‐serious adverse events: 2 of the 9 dropouts experienced loss of appetite after methylphenidate medication, and 1 also complained about insufficient effect. Another participant was documented to experience insomnia, and described to be hyperactive at the last visit before dropping out. The remaining dropouts are not accounted for
Notes	Sample calculation: none Ethics approval: institutional review board for human subjects at the Seoul National University Hospital Funding: Supported by the Jun Sang‐Bae Child and Adolescent Psychiatry Research Fund of the Korean Neuropsychiatric Association in 2009 Vested interests/authors' affiliations: no conflicts of interest or financial ties Key conclusions of the study authors: genetic determinants of methylphenidate response consist of both the dopaminergic and noradrenergic gene polymorphisms, and efforts to predict response to methylphenidate should cover these 2 catecholaminergic systems and their multifaceted aspects of their interactions as well Exclusion of methylphenidate non‐responders/children who have previously experienced adverse events on methylphenidate: all participants were methylphenidate‐naïve