Dahl S G
Clin Pharmacokinet. 1986 Jan-Feb;11(1):36-61. doi: 10.2165/00003088-198611010-00003.
The steady-state plasma concentrations of antipsychotic drugs show large interpatient variations but remain relatively stable from day to day in each individual patient. Monitoring of antipsychotic drug concentrations in plasma might be of value provided the patients are treated with only 1 antipsychotic drug. Some studies have reported a relationship between therapeutic response and serum antipsychotic drug 'concentrations' as measured using the radioreceptor assay (RRA) method, which measures dopamine receptor-blocking activity in plasma. Most studies, however, have failed to demonstrate such a relationship, and the RRA does not seem to provide the generally useful tool for plasma concentration monitoring of antipsychotic drugs that was hoped for initially. A lack of correlation between dopamine receptor-blocking activity in plasma and therapeutic response may be due to differences in the blood-brain distribution of both antipsychotic drugs and their active metabolites. Chemical assay methods (e.g. GLC and HPLC) have been used in studies which examined the relationships between therapeutic response and antipsychotic drug concentrations in red blood cells and in plasma. It seems that for these drugs, measuring red blood cell concentrations does not offer any significant advantage over measuring plasma concentrations. Reasonably controlled studies of plasma concentration-response relationships using randomly allocated, fixed dosages of chlorpromazine, fluphenazine, haloperidol, perphenazine, sulpiride, thioridazine and thiothixene have been published but often involve relatively few patients. A correlation between therapeutic response and plasma concentrations of thioridazine and its metabolites has not been demonstrated, and plasma level monitoring of thioridazine and its metabolites therefore appears to have no clinical value. Clinical behavioural deterioration concomitant with high plasma concentrations of chlorpromazine and haloperidol have been reported. A dosage reduction might be considered after 2 to 4 weeks' treatment in non-responders who have plasma chlorpromazine concentrations above 100 to 150 micrograms/L or plasma haloperidol concentrations above 20 to 30 micrograms/L. Non-responders and good responders to chlorpromazine treatment, however, have plasma drug concentrations in the same range, and a therapeutic range of plasma chlorpromazine levels has not been defined. Therapeutic plasma haloperidol concentrations (i.e. 'window') in the range of 5 to 20 micrograms/L have been reported by some investigators, but others have found no such relationship.(ABSTRACT TRUNCATED AT 400 WORDS)
抗精神病药物的稳态血浆浓度在患者之间存在很大差异,但在每个患者中每天相对稳定。如果患者仅接受一种抗精神病药物治疗,监测血浆中抗精神病药物浓度可能有价值。一些研究报告了使用放射受体测定法(RRA)测量的治疗反应与血清抗精神病药物“浓度”之间的关系,该方法测量血浆中的多巴胺受体阻断活性。然而,大多数研究未能证明这种关系,而且RRA似乎并未提供最初所期望的用于抗精神病药物血浆浓度监测的普遍有用工具。血浆中多巴胺受体阻断活性与治疗反应之间缺乏相关性可能是由于抗精神病药物及其活性代谢物在血脑分布上的差异。化学分析方法(如气相色谱法和高效液相色谱法)已用于研究治疗反应与红细胞和血浆中抗精神病药物浓度之间的关系。对于这些药物,测量红细胞浓度似乎并不比测量血浆浓度具有任何显著优势。已经发表了使用随机分配的固定剂量的氯丙嗪、氟奋乃静、氟哌啶醇、奋乃静、舒必利、硫利达嗪和替沃噻吨进行的血浆浓度-反应关系的合理对照研究,但通常涉及的患者相对较少。硫利达嗪及其代谢物的治疗反应与血浆浓度之间的相关性尚未得到证实,因此硫利达嗪及其代谢物的血浆水平监测似乎没有临床价值。已经报告了血浆中氯丙嗪和氟哌啶醇浓度高时伴随的临床行为恶化。对于血浆氯丙嗪浓度高于100至150微克/升或血浆氟哌啶醇浓度高于20至30微克/升的无反应者,在治疗2至4周后可考虑减少剂量。然而,氯丙嗪治疗的无反应者和良好反应者的血浆药物浓度在相同范围内,并且尚未确定氯丙嗪血浆水平的治疗范围。一些研究人员报告了治疗性血浆氟哌啶醇浓度(即“窗口”)在5至20微克/升范围内,但其他人未发现这种关系。(摘要截短为400字)