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Yaowaluck Hongkaew,1,2 Nattawat Ngamsamut,3 Apichaya Puangpetch,1,2 Natchaya Vanwong,1,2 Pornpen Srisawasdi,4 Montri Chamnanphon,1,2 Bhunnada Chamkrachchangpada,3 Teerarat Tan-kam,3 Penkhae Limsila,3 Chonlaphat Sukasem1,2 1Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine, 2Laboratory for Pharmacogenomics, Somdech Phra Debaratana Medical Center (SDMC), Ramathibodi Hospital, Mahidol University, 3Yuwaprasart Waithayopathum Child and Adolescent Psychiatric Hospital, Department of Mental Health Services, Ministry of Public Health, 4Division of Clinical Chemistry, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Abstract: Hyperprolactinemia is a common adverse effect observed in children with autism spectrum disorder (ASD) during pharmacotherapy with risperidone. The main aim of this study was to investigate important clinical factors influencing the prolactin response in risperidone-treated Thai ASD. A total of 147 children and adolescents (127 males and 20 females) aged 3–19 years with ASD received risperidone treatment (0.10–6.00 mg/day) for up to 158 weeks. Prolactin levels were measured by chemiluminescence immunoassay. The clinical data of patients collected from medical records – age, weight, height, body mass index, dose of risperidone, duration of treatment, and drug-use pattern – were recorded. Hyperprolactinemia was observed in 66 of 147 (44.90%) subjects. Median prolactin level at the high doses (24.00, interquartile range [IQR] 14.30–29.20) of risperidone was significantly found to be higher than at the recommended (16.20, IQR 10.65–22.30) and low (11.70, IQR 7.51–16.50) doses of risperidone. There was no relationship between prolactin levels and duration of risperidone treatment. Dose-dependence is identified as a main factor associated with hyperprolactinemia in Thai children and adolescents with ASD treated with risperidone. This study suggests that risperidone treatment causes prolactin elevations and the effects of risperidone on prolactin are probably dose-related in pediatric patients. Keywords: prolactin level, risperidone, autism spectrum disorders, Thai, hyperprolactinemia

Teerarat Tan-kam,1 Chutamanee Suthisisang,2 Chosita Pavasuthipaisit,1 Penkhae Limsila,1 Apichaya Puangpetch,3 Chonlaphat Sukasem31Yuwaprasart Waithayopathum Child and Adolescent Psychiatric Hospital, Department of Mental Health Services, Ministry of Public Health, 2Department of Pharmacology, Faculty of Pharmacy, Mahidol University, 3Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, ThailandAbstract: This case report highlights the importance of pharmacogenetic testing in the treatment of attention deficit hyperactive disorder (ADHD). A 6-year-old boy diagnosed with ADHD was prescribed methylphenidate 5 mg twice daily (7 am and noon) and the family was compliant with administration of this medication. On the first day of treatment, the patient had an adverse reaction, becoming disobedient, more mischievous, erratic, resistant to discipline, would not go to sleep until midnight, and had a poor appetite. The All-In-One PGX (All-In-One Pharmacogenetics for Antipsychotics test for CYP2D6, CYP2C19, and CYP2C9) was performed using microarray-based and real-time polymerase chain reaction techniques. The genotype of our patient was identified to be CYP2D6*2/*10, with isoforms of the enzyme consistent with a predicted cytochrome P450 2D6 intermediate metabolizer phenotype. Consequently, the physician adjusted the methylphenidate dose to 2.5 mg once daily in the morning. At this dosage, the patient had a good response without any further adverse reactions. Pharmacogenetic testing should be included in the management plan for ADHD. In this case, cooperation between the medical team and the patients' relatives was key to successful treatment.Keywords: attention deficit hyperactive disorder, pharmacogenomics, CYP2D6, adverse drug reactions, dose adjustment, intermediate metabolizer