BRIEF REPORTS: PDF OnlyLack of association in Japanese patients between neuroleptic malignant syndrome and a debrisoquine 4-hydroxylase genotype with low enzyme activityKawanishi, Chiakia; Furuno, Takua; Onishi, Hidekia; Sugiyama, Naoyaa; Suzuki, Kyokoa; Matsumura, Takehikoa; Ishigami, Tomoakib; Kosaka, KenjibAuthor Information aDepartment of Psychiatry, Yokohama City University School of Medicine andbThe Second Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan Correspondence to Chiaki Kawanishi, M.D., Ph.D., Department of Psychiatry, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan. Received 27 April 2000; accepted 26 September 2000 Psychiatric Genetics: September 2000 - Volume 10 - Issue 3 - p 145-147 Buy Abstract Decreased activity of debrisoquine 4-hydroxylase (CYP2D6), which participates in hepatic metabolism of several frequently used neuroleptics and antidepressants, is inherited as an autosomal recessive trait through polymorphic CYP2D6 gene alleles. In eastern Orientals, a C → T substitution at nucleotide 188 (Pro34Ser) is primarily responsible for decreased ability to metabolize CYP2D6 substrates. We therefore studied a possible association between neuroleptic malignant syndrome (NMS) and the C188T mutation. We examined the frequency of the C188T mutation by polymerase chain reaction and restriction fragment length polymorphism analysis in 36 Japanese patients previously diagnosed with NMS and 107 neuroleptic-treated schizophrenic patients with no NMS history. The C188T allele frequency was 0.417 in NMS patients and 0.463 in patients without NMS. No significant allele or genotype associations were observed. We cannot conclude that low CYP2D6 activity genotype causes susceptibility to NMS in Japanese patients. © 2000 Lippincott Williams & Wilkins, Inc.