Dervieux T, Médard Y, Verpillat P, Guigonis V, Duval M, Lescoeur B, Suciu S, Vilmer E, Jacqz-Aigrain E
Service de Pharmacologie Pédiatrique et Pharmacogénétique, Hôpital Robert Debré, Paris, France.
Leukemia. 2001 Nov;15(11):1706-12. doi: 10.1038/sj.leu.2402259.
6-Mercaptopurine (6-MP) is metabolized by thiopurine S-methyltransferase (TPMT), an enzyme subject to genetic polymorphism. We investigated the relationships between the TPMT locus (TPMT activity and genotype) and the pharmacological response to 6-MP during maintenance therapy of 78 children with acute lymphoblastic leukemia (ALL). For each patient, 6-MP dosage, leukocyte counts and occurrence of infectious episodes were monitored on an 8 week basis. Higher 6-MP dosage was associated with higher TPMT activity (P = 0.03) and higher average leukocyte counts (P < 0.01). Eight patients (10%) carrying a TPMT mutant genotype (one homozygous and seven heterozygous) received lower 6-MP doses (average: 48 vs 65 mg/m2/day; P = 0.02) and had on average lower leukocyte counts (2834 vs 3398 cells/mm3; P = 0.003) than patients carrying the wild-type TPMT genotype. Higher occurrence of infectious episodes graded 2 or 3 was correlated with higher 6-MP dosage (P < 0.01) but no difference was observed between TPMT mutants and TPMT wild-type patients. Patients who received 6-MP dosage above the group median (62 mg/m2/day) or having a TPMT activity above the group median (21.5 nmol/h/ml) had a higher percentage of 8 week periods with infectious episodes requiring treatment (34% vs 17% and 33% vs 19%, respectively) than those with 6-MP dose or TPMT activity below the group median (P < 0.01). In the last 25 patients enrolled in the study, steady-state erythrocyte thioguanine nucleotide (TGN) concentrations were associated with lower leukocyte counts (P= 0.01) but not with a higher occurrence of infectious episodes. In contrast, higher steady-state erythrocyte methylmercaptopurine nucleotide (MeMPN) concentrations were associated with higher 6-MP dosage (P< 0.01) and higher occurrence of infectious episodes (P < 0.001). In conclusion, during maintenance therapy of ALL, children with higher TPMT activity receive a higher 6-MP dosage and may have infectious episodes caused by metabolism of 6-MP into methylmercaptopurine nucleotides.
6-巯基嘌呤(6-MP)由硫嘌呤S-甲基转移酶(TPMT)代谢,该酶存在基因多态性。我们研究了78例急性淋巴细胞白血病(ALL)患儿维持治疗期间TPMT基因座(TPMT活性和基因型)与对6-MP的药理反应之间的关系。对每位患者,每8周监测一次6-MP剂量、白细胞计数和感染性发作情况。较高的6-MP剂量与较高的TPMT活性(P = 0.03)和较高的平均白细胞计数(P < 0.01)相关。8例(10%)携带TPMT突变基因型(1例纯合子和7例杂合子)的患者接受的6-MP剂量较低(平均:48 vs 65 mg/m2/天;P = 0.02),平均白细胞计数也较低(2834 vs 3398个细胞/mm3;P = 0.003),低于携带野生型TPMT基因型的患者。2级或3级感染性发作的发生率较高与较高的6-MP剂量相关(P < 0.01),但TPMT突变型患者和TPMT野生型患者之间未观察到差异。接受的6-MP剂量高于组中位数(62 mg/m2/天)或TPMT活性高于组中位数(21.5 nmol/h/ml)的患者,需要治疗的感染性发作的8周时间段百分比更高(分别为34% vs 17%和33% vs 19%),高于6-MP剂量或TPMT活性低于组中位数的患者(P < 0.01)。在研究中最后纳入的25例患者中,稳态红细胞硫鸟嘌呤核苷酸(TGN)浓度与较低的白细胞计数相关(P = 0.01),但与感染性发作的较高发生率无关。相反,较高的稳态红细胞甲基巯基嘌呤核苷酸(MeMPN)浓度与较高的6-MP剂量相关(P < 0.01)和感染性发作的较高发生率相关(P < 0.