Happe Svenja, Tings Tobias, Helmschmied Kathrin, Neubert Karin, Wuttke Wolfgang, Paulus Walter, Trenkwalder Claudia
Department of Clinical Neurophysiology, University of Göttingen, Germany.
Mov Disord. 2004 Dec;19(12):1511-5. doi: 10.1002/mds.20244.
Challenge with low-dose apomorphine causes a significant rise in growth hormone (GH) in patients with Parkinson's disease (PD) compared to controls and patients with multiple system atrophy (MSA) who have not previously received dopaminergic treatment. To date, it has not been demonstrated whether an apomorphine-induced rise in GH can still be detected in PD patients who are currently treated with levodopa. We investigated whether an ongoing treatment with levodopa influences the GH response to subcutaneously applied low-dose apomorphine in PD patients. We studied 44 patients with idiopathic PD using the low-dose apomorphine test. Twenty-three patients were under treatment with levodopa and 21 patients were without any dopaminergic therapy. GH and cortisol levels were analyzed at time of injection and 45 minutes and 60 minutes after subcutaneous apomorphine injection. Forty-five minutes after apomorphine injection, there was no significant difference between the mean rise in plasma GH in untreated PD patients compared with levodopa-treated patients (P = 0.235). There was no increase of cortisol levels in each treatment group. Age, sex, duration, and severity of the disease did not show a covariate effect with GH levels. A small group of PD patients (n = 8) treated with dopamine agonists and a small group of patients with MSA (n = 5) as well as patients with vascular parkinsonism (n = 5) did not show any increase of GH. Our data suggest that the apomorphine-induced rise in GH does not depend on previous levodopa treatment in PD patients but, as expected, is blocked by dopamine agonists and is not present in patients with other than idiopathic parkinsonian syndrome. Thus, the low-dose apomorphine test may also be a useful biological marker in the early differential diagnosis of PD patients who have already received levodopa treatment.
与对照组以及未接受过多巴胺能治疗的多系统萎缩(MSA)患者相比,低剂量阿扑吗啡激发试验可使帕金森病(PD)患者的生长激素(GH)显著升高。迄今为止,尚未证实目前正在接受左旋多巴治疗的PD患者是否仍能检测到阿扑吗啡诱导的GH升高。我们研究了左旋多巴的持续治疗是否会影响PD患者皮下应用低剂量阿扑吗啡后的GH反应。我们使用低剂量阿扑吗啡试验研究了44例特发性PD患者。23例患者正在接受左旋多巴治疗,21例患者未接受任何多巴胺能治疗。在注射时以及皮下注射阿扑吗啡后45分钟和60分钟分析GH和皮质醇水平。阿扑吗啡注射后45分钟,未治疗的PD患者与左旋多巴治疗的患者血浆GH的平均升高之间无显著差异(P = 0.235)。每个治疗组的皮质醇水平均未升高。年龄、性别、病程和疾病严重程度与GH水平均无协变量效应。一小群接受多巴胺激动剂治疗的PD患者(n = 8)、一小群MSA患者(n = 5)以及血管性帕金森综合征患者(n = 5)均未出现GH升高。我们的数据表明,阿扑吗啡诱导的GH升高不依赖于PD患者先前的左旋多巴治疗,但正如预期的那样,会被多巴胺激动剂阻断,并且在非特发性帕金森综合征患者中不存在。因此,低剂量阿扑吗啡试验也可能是已接受左旋多巴治疗的PD患者早期鉴别诊断的有用生物学标志物。