Search

Natchaya Vanwong,1,2 Sayanit Tipnoppanon,1 Chalitpon Na Nakorn,3 Pornpen Srisawasdi,4 Punyanuch Rodcharoen,4 Sadeep Medhasi,5 Pajaree Chariyavilaskul,2,6,7 Sarawut Siwamogsatham,2,8,9 Yongkasem Vorasettakarnkij,2,9 Chonlaphat Sukasem10– 12 1Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand; 2Cardiovascular Precision Medicine Research Group, Special Task Force of Activating Research (STAR), Chulalongkorn University, Bangkok, Thailand; 3Department of Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Prince of Songkla University, Songkhla, Thailand; 4Division of Clinical Chemistry, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 5Department of Transfusion Medicine and Clinical Microbiology, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, Thailand; 6Department of Pharmacology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; 7Clinical Pharmacokinetics and Pharmacogenomics Research Unit, Chulalongkorn University, Bangkok, Thailand; 8Chula Clinical Research Center, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; 9Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand; 10Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 11Laboratory for Pharmacogenomics, Somdech Phra Debaratana Medical Center (SDMC), Ramathibodi Hospital, Bangkok, Thailand; 12Pharmacogenomics and Precision Medicine, The Preventive Genomics & Family Check-up Services Center, Bumrungrad International Hospital, Bangkok, ThailandCorrespondence: Chonlaphat Sukasem, Division of Pharmacogenetics and Personalized Medicine, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand, Tel +66-2-200-4331, Fax +66-2-200-4332, Email chon

Pornpen Srisawasdi,1 Punyanuch Rodcharoen,1 Somlak Vanavanan,1 Anchalee Chittamma,1 Chonlaphat Sukasem,2 Chalitpon Na nakorn,2 Charungthai Dejthevaporn,3 Martin H Kroll4 1Division of Clinical Chemistry, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 2Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 3Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 4Quest Diagnostics, Secaucus, NJ 07094, United States of AmericaCorrespondence: Pornpen Srisawasdi Division of Clinical Chemistry, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Rama VI Road, Ratchathewi, Bangkok 10400, ThailandTel +66-2-201-0008Fax +66-2-354-7266Email srisawasdip@yahoo.comObjective: Patients treated with statins for dyslipidemia may still have a residual risk of atherosclerotic cardiovascular disease (ASCVD). To determine whether genetic variants in the cholesteryl ester transport protein (CETP), rs3764261 (C>A), rs708272 (G>A), and rs12149545 (G>A) affect ASCVD risk, we studied the association of these variants with dyslipidemia in statin-treated patients.Patients and Methods: We included 299 adult Thai patients treated with a statin (95 men and 204 women). Genotyping was performed by conducting a TaqMan real-time polymerase chain reaction-based analysis. We used logistic regression models adjusted for potential confounders of age, body mass index, blood pressure, insulin resistance, and statin dosage to analyze the association between CETP variants and atherogenic lipoprotein patterns.Results: CETP polymorphisms of rs3764261 and rs708272, but not rs12149545, were significantly associated with high-density lipoprotein cholesterol (HDL-C), apoA-I, triglycerides, very low-density lipoprotein (VLDL)-C, and large LDL (LDL1-C) levels as well

Apichaya Puangpetch,1 Pornpen Srisawasdi,2 Weerapon Unaharassamee,3 Napa Jiratjintana,3 Somlak Vanavanan,2 Suweejuk Punprasit,2 Chalitpon Na Nakorn,1 Chonlaphat Sukasem,1 Martin H Kroll41Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 2Division of Clinical Chemistry, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 3Department of Psychiatry, Somdet Chaopraya Institute of Psychiatry, Bangkok, Thailand; 4Quest Diagnostics, Secaucus, NJ 07094, USAObjective: To determine whether genetic polymorphisms related to pharmacodynamics with metabolic adverse effects, namely leptin promoter (LEP) rs7799039, leptin receptor rs1137101, dopamine D2 rs4436578, serotonin 5-HT2A rs6313, and serotonin 5-HT2C rs518147 and rs12836771, are associated with hyperglycemia induced by risperidone or clozapine in adult Thai patients with psychosis.Methods: A total of 180 patients treated with risperidone-based (n=130) or clozapine-based (n=50) regimens were included in this study. Blood samples were analyzed for genotyping of the candidate genes and biochemical testing. Genotyping was performed by conducting a TaqMan real-time polymerase chain reaction-based analysis.Results: The prevalence of hyperglycemia was higher in patients receiving clozapine (64.0%) than in those receiving risperidone (30.8%). Among the candidate genes, only the LEP rs7799039 polymorphism demonstrated a significant association with hyperglycemia (χ2=9.879, P=0.008) in patients treated with risperidone; patients with the AA genotype had the highest risk (41.1%), followed by those with AG (20.8%) and GG (0%) genotypes. Using the recessive genetic model (AA vs AG + GG), the odds ratio and 95% CI were 3.28 and 1.44 −7.50, respectively. None of the genes were associated with hyperglycemia in patients treated with clozapine. A binary logis

Somlak Vanavanan,1 Pornpen Srisawasdi,1 Mana Rochanawutanon,2 Nalinee Kumproa,1 Khanat Kruthkul,3 Martin H Kroll4 1Division of Clinical Chemistry, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 2National Healthcare Systems, Bangkok, Thailand; 3Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 4Quest Diagnostics, Madison, NJ, USA Background: Body mass index (BMI) and percentage of body fat (PBF) are used to measure obesity; however, their performance in identifying cardiometabolic risk in Southeast Asians is unclear. Generally, Asian women have higher PBF and lower BMI than do men and other ethnic populations. This study was conducted to address whether a discord exists between these measures in predicting obesity-related cardiometabolic risk in a Thai population and to test whether associations between the measures and risk factors for cardiovascular disease have a sex-specific inclination.Methods: A total of 234 (76 men and 158 women) outpatients were recruited. BMI obesity cutoff points were ≥25.0 and ≥27.0 kg/m2 and PBF cutoff points were ≥35.0% and ≥25.0% for women and men, respectively. Blood samples were analyzed for total cholesterol, triglycerides, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, lipoprotein subclasses, apolipoprotein A-I, apolipoprotein B, glucose, hemoglobin A1c, insulin, high-sensitive C-reactive protein (hsCRP), adiponectin, leptin, and 25-hydroxyvitamin D.Results: Twenty-five percent of participants classified as normal-BMI had excessive fat, whereas 9% classified as normal-PBF had excessive BMI. Good relationships were found between BMI and PBF using sex stratification (R2 >0.5). The prevalence of metabolic syndrome was markedly increased in overweight and/or excess body fat groups compared with lean group. Logistic regression analyses showed that BMI was the be

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 child