精神分裂症患者血清催乳素对电抽搐治疗的反应

对20例女性精神分裂症患者进行ECT-1前30分钟与后5、15、30和60分钟的血清催乳素(PRL)水平测定,其中10例做了ECT-6的复查。结果,ECT-1后PRL水平迅速显著升高,15分钟达最高峰。提示ECT具有急性抗多巴胺和神经阻滞剂样作用。ECT-6前的PRL基础水平较ECT-1前显著升高,ECT-6后PRL的释放较ECT-1显著下降,表明在多次ECT后异常的多巴胺代谢得到了纠正。     

精神分裂症患者血清催乳素和生长激素水平与奎硫平、氟哌啶醇治疗关系的对照研究

目的研究精神分裂症患者血清催乳素(PRL)、生长激素(GH)的基础水平与正常人的差异,以及奎硫平、氟哌啶醇治疗前后PRL、GH的变化。方法采用放射免疫法检测126例精神分裂症患者(包括奎硫平组62例和氟哌啶醇组64例)治疗前和治疗8周后PRL、GH水平,观察这2种药物对PRL、GH的影响及比较两者的差异,并与65名健康者进行对照分析。结果 126例精神分裂症患者的基础PRL、GH水平与对照组比较无显著性差异(P>0．05),奎硫平组治疗后PRL和GH均无显著改变(P>0．05)。氟哌啶醇组治疗后PRL值为(96．20±41．12)μg/L,较治疗前的(20．39±11．26)μg/L显著升高(P<0．01),女性升高更明显,为男性的 2．6倍。氟哌啶醇组治疗后GH值为(1．72±1．32)μg/L,较治疗前的(2．41±11．26)μg/L显著降低(P<0．01)。结论奎硫平治疗精神分裂症患者,对PRL及GH无明显影响,更适合生长期的青少年患者和药物性溢乳、乳房发育患者。     

抗精神病药对老年精神分裂症患者血清催乳素的影响

目的：探讨几种抗精神病药对老年精神分裂症患者血清催乳素（PRL）的影响。方法：随机选取抗精神病药治疗老年精神分裂症患者121例,分别在治疗前后测定血清PRL水平。结果：患者经舒必利、奋乃静、氟哌啶醇和利培酮治疗后血清PRL明显升高,各药物之间以及治疗前后比较差异均有显著性（F=15．95,P〈0．01）。PRL水平的升高与药物剂量呈正相关。氯氮平对PRL水平影响不明显。结论：典型和非典型抗精神病药对老年精神分裂症患者血清PRL水平的影响同样明显,强弱的顺序依次是舒必利、奋乃静、氟哌啶醇和利培酮。     

精神分裂症患者电抽搐治疗前后脑脊液催乳素水平的改变

目的　探讨精神分裂症患者脑脊液催乳素 (PRL)水平及治疗前后的变化。方法　电抽搐治疗 (ECT)精神分裂症 ;在治疗前后用放射免疫分析法测定患者脑脊液PRL含量 ,简明精神病评定量表 (BPRS)评定。结果　精神分裂症患者ECT前脑脊液PRL测定均值 (0 98±0 32 )ng/mL ,女略高于男 (P >0 0 5) ;患者ECT后脑脊液PRL水平 [(1 .41± 0 .47)ng/mL]显著升高 (P <0 0 1 ) ,女性明显高于男性 (P <0 0 5)。结论　提示ECT具有抗DA能神经阻滞剂样作用 ;ECT后PRL释放值有性别差异。     

丛集性头痛患者内分泌功能的检测

目的 通过检测丛集性头痛（CH）患者的内分泌功能探讨CH的发病机制。方法 采用放射免疫分析法检测了26例CH患者（CH组）在丛集期和缓解期血清睾酮（T）、雌二醇（E2）、催乳激素（PRL）以及生长激素（GH）水平,并与25例正常对照者（NC组）及18例偏头痛患者（MC组）进行比较。结果 （1）CH患者在丛集期血清T、GH、E2、PRL水平较NC组和MC组明显降低。其中男性患者血清T、E2、PRL水平与NC组和MC组比较具有高度显著性差异（P＜0．01）;女性患者血清T、E2、PRL水平及所有患者血清GH水平与NC组和MC比较有显著差异（＜0．05）。（2）CH患者缓解期血清T、GH、E2、PRL水平与NC组和MC组比较,差异不明显（P＞0．05）。（3）CH患者丛集期与缓解期血清T、GH、E2、PRL水平比较,差异不明显（P＞0．05）。结论 CH丛集期内分泌功能明显降低,结合临床特点,提示下丘脑功能改变作为起步机制在丛集性头痛发作中起重要作用。     

肢端肥大症诊治规范(草案)

3.多巴胺受体激动剂多巴胺受体激动剂可以使部分肢大症患者的血清GH水平降低和症状改善。常用的多巴胺受体激动剂包括麦角衍生物溴隐亭、cabergoline等和非麦角衍生物如喹高利特等。这类药物在GH水平轻中度升高的患者中,有10%～20%的患者GH和IGH-1水平降至满意水平,其剂量是治疗PRL瘤的2-4倍。目前国内仅有第一代多巴胺受体激动剂溴隐亭,国内使用该药降低GH水平至满意水平的很少。     

四种非典型抗精神病药对血清催乳素和血脂的影响

目的探讨四种非典型抗精神病药对精神分裂症患者血脂和血清催乳素（PRL）的影响,以及血清PRL水平与药物疗效的关系。方法118例精神分裂症患者分为4组,分别予以喹硫平（29例）、氯氮平（30例）、奥氮平（30例）和利培酮（29例）治疗12周。于治疗前及治疗4、8及12周末予以阳性与阴性症状量表（PANSS）评定,测定血总胆固醇（TC）、甘油三脂（TG）高密度脂蛋白（HDL）、低密度脂蛋白（LDL）、阿朴脂蛋白A—I（ApoA-1）、阿朴脂蛋白-B（Apo—B）及血清PRL浓度。结果（1）喹硫平组TG、HDL在12周末有显著升高（P〈0．05）,氯氮平组Apo—B在4、12周末有显著升高（P〈0．05）、LDL在8、12周末有显著升高（P〈0．05）,利培酮组除TG外其余血脂指标在8、12周末有显著升高（P〈0．05）,奥氮平组TG、HDL、LDL、ApoA-1、Apo—B在12周末有显著升高（P〈0．05）,TC在8与12周有显著升高（P〈0．05）。（2）利培酮组治疗8、12周后血清PRL明显升高（P〈0．01）。（3）氯氮平组和利培酮组PANSS一般病理分的减分率分别与PRL、LDL有显著相关;氯氮平组PRL与LDL有显著相关。结论利培酮、奥氮平、喹硫平和氯氮平均影响血脂代谢;氯氮平疗效与血清催乳素及LDL有关,利培酮疗效与LDL有关。     

氨磺必利致精神分裂症患者显著泌乳素升高的影响因素研究

目的:探讨精神分裂症患者氨磺必利治疗后血清泌乳素(PRL)升高的影响因素。方法:给予48例精神分裂症患者氨磺必利治疗8周;在基线、治疗后4及8周时检测血清PRL水平及氨磺必利血药浓度。以治疗8周时血清PRL 1 600 m IU/L为界,将入组者分为显著PRL升高组和非显著PRL升高组,比较两组人口学及临床资料,分析氨磺必利治疗后血清PRL升高的影响因素。结果:治疗8周后24例归入显著PRL升高组,24例归入非显著PRL升高组。与非显著PRL升高组比较,显著PRL升高组的氨磺必利剂量更大、女性及基线时PRL水平高于正常的比例更高(P0.05或P0.01)。回归分析显示,女性的OR值为13.933(95%CI=2.636~73.648,P0.05),基线PRL高于正常的OR值为5.728(95%CI:1.142~28.741,P0.01)。结论:女性及基线时PRL水平高于正常是精神分裂症患者使用氨磺必利后显著PRL升高的危险因素。     

精神分裂症患者催乳素对胰岛素昏迷治疗的反应

对12例精神分裂症患者测定了第2与30次胰岛素昏迷治疗中的血清催乳素(PRL)水平。发现在注射胰岛素后PRL水平逐渐升高,昏迷期达最高峰,清醒后开始下降。在多次胰岛素昏迷治疗后PRL反应降低,作者认为胰岛素昏迷治疗同样也具有一种抗多巴胺能和神经阻滞剂样的作用。     

帕利哌酮缓释片对催乳素及糖脂代谢的影响

目的：探讨帕利哌酮缓释片治疗精神分裂症患者前后催乳素（PRL）及糖脂水平的变化。方法：47例精神分裂症患者接受帕利哌酮缓释片治疗8周。于治疗前和治疗4、8周抽取空腹血测定PRL、胰岛素（INS）、血糖（FBS）、三酰甘油（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL）、低密度脂蛋白胆固醇（LDL）、载脂蛋白A1（ApoA1）、载脂蛋白B（ApoB）水平,同时测量患者腹围及体质量变化。结果：治疗4周和8周,男性患者PRL水平由治疗前（31.53±19.27）ng/ml分别升高至（42.24±18.45）ng/ml和（40.47±26.53）ng/ml（P〈0.01）;女性患者PRL水平由（78.13±48.70）ng/ml分别升高至（138.38±58.92）ng/ml和（135.12±56.47）ng/ml（P〈0.01）;以女性患者PRL水平较男性患者升高显著（P〈0.01）。PRL水平与帕利哌酮缓释片剂量相关性无统计学意义（P均〉0.05）。比较治疗前和治疗4、8周后FBS、INS、TG、TC、HDL、LDL、ApoA1、ApoB水平及患者腹围、体质量的变化,差异均无统计学意义（P均〉0.05）。结论：帕利哌酮缓释片可明显升高血清PRL水平,以女性患者升高显著,而对糖脂代谢的影响较小。     

Hormone response to repeated electroconvulsive therapy: effects of naloxone

Plasma prolactin (PRL), cortisol, and growth hormone (GH) were measured before, and at 15-min intervals for 1 hr after, electroconvulsive therapy (ECT). This was repeated over a series of 6 consecutive treatments for each of 12 depressed drug-free inpatients. Patients received naloxone, 2 mg or 20 mg, by intravenous infusion before the third and fifth treatment. ECT was consistently followed by a release of PRL and cortisol, although two patterns of PRL response could be distinguished. In eight patients, the PRL response did not change significantly with repeated ECT, whereas in four patients, the plasma PRL increased tenfold after the first treatment and decreased after each successive treatment. The GH level varied widely, with no evidence of a reliable response to ECT. Opiate receptor blockade with low- or high-dose naloxone did not alter the release of PRL or cortisol after ECT. These findings demonstrate a reliable PRL and cortisol response to ECT, but do not support a role for endogenous opiates in these hormonal changes.     

Prolactin and thyrotropin in serum during electroconvulsive therapy in patients with major depressive illness

Thirty-three patients with major depressive illness received electroconvulsive therapy (ECT), and serum prolactin (PRL) and thyrotropin (TSH) levels were measured 30 min before and 1, 5, 15, 30, and 60 min after the treatment. There was a threefold increase in PRL levels with a maximum after 15 min. The TSH plasma levels rose significantly with a maximum at 30 min after ECT. No change in PRL and TSH concentrations was seen in control experiments when the patients received anaesthesia only. In 15 patients the hormone levels were studied both during the first and sixth (last) ECT. The PRL and TSH levels were significantly higher following the first as compared to the sixth ECT. Patients on phenothiazines had higher PRL and lower TSH levels than those on other drugs or without medication, but there was no significant difference in the mean increment by ECT. Dopamine depresses PRL and TSH secretion. The diminished hormone release after a series of ECT may be explained by ECT-induced increase of postsynaptic dopamine receptor function leading to inhibition of PRL and TSH release from the pituitary gland.     

Growth hormone and somatomedin serum levels in patients with major depressive illness undergoing electroconvulsive therapy

Thirty-three patients with major depressive illness received electroconvulsive therapy (ECT), and serum growth hormone (GH) levels were measured 30, min before and 1, 5, 15, 30 and 60 min after treatment. Six of the patients were studied 2 days before the first ECT (ECT-1) while receiving anaesthesia only. The anaesthesia given appeared to depress GH levels, which were significantly lower at 1 and 5 min after ECT than before treatment. When ECT was given there was a recovery of the GH level at 60 min, indicating a stimulatory effect of ECT on GH secretion. In 26 of the patients also investigated during the sixth and last ECT (ECT-6) in a series, no such recovery was observed. This may be due to changes in the sensitivity of intracerebral monoaminergic receptors in neurons controlling GH secretion from the pituitary gland. Since inhibition of GH secretion is mediated via beta-adrenergic pathways, the depression of GH secretion may be due to ECT-induced supersensitivity of postsynaptic beta-adrenergic receptors. In 27 of the patients serum somatomedin A, measured by radioreceptorassay (SMA-RRA), was analysed before ECT-1 and in 19 patients before ECT-6. In seven subjects the SMA-RRA was measured 30 min before and 1, 5, 15, 30, and 60 min after ECT-1. SMA-RRA levels were mainly within the normal range for age and did not change during ECT. No difference in SMA-RRA levels was observed before ECT-1 and ECT-6. This indicates that, although abnormalities in the GH-response to challenge stimuli have been reported in adults with major depressive disorder, their GH production is normal.     

Effects of single and repeated electroconvulsive therapy sessions on plasma ACTH, prolactin, growth hormone and cortisol concentrations.

To study the effects of electroconvulsive therapy (ECT) on hormone release, we measured circulating concentrations of adrenocorticotropic hormone (ACTH), prolactin (PRL), growth hormone (GH) and cortisol (CORT) immediately before and at 2 min, 5 min, 15 min, and 30 min following ECT. Compared to pre-ECT concentrations, there were significant increases in post-ECT plasma ACTH, PRL and CORT. GH did not change consistently. No significant difference between unilateral and bilateral ECT was observed. Compared to the first ECT, repeated treatments were associated with a significant decrease in the magnitude of hormone surge. These hormonal changes induced by ECT may reflect changes at the neurotransmitter level.     

Predictors for improvement after electroconvulsive therapy in parkinsonian patients with on-off symptoms

Summary The antiparkinsonian effect of electroconvulsive therapy (ECT) was investigated in nine parkinsonian patients with on-off phenomena. The patients were maintained on previously adjusted doses of antiparkinsonian drugs during and after ECT. Parkinsonian as well as mental symptoms were rated before and after treatment.Basal serum levels of prolactin (PRL) and growth hormone (GH) as well as apomorphine induced changes (0.24 mg i.v.) in these levels were investigated three days before start of treatment.Marked improvement of parkinsonian symptoms was seen in five patients. Two further patients showed slight improvement. The improvement persisted for 2–41 weeks. Improvement after ECT was found to correlate with age at the time of treatment and with duration of L-dopa therapy as well as the estimated life-dose of L-dopa. No correlation was found between improvement of parkinsonian symptoms and either scores of mental depression before treatment, basal serum levels of GH and PRL or apomorphine induced changes in these hormone levels. The investigation indicates that ECT is a valuable adjuvant in the treatment of a selected group of parkinsonian patients with on-off phenomena. Furthermore, the results support our earlier proposal that ECT increases the responsiveness in postsynaptic dopamine sensitive structures.     

Changes in growth hormone and prolactin release after superior cervical ganglionectomy of rats

Superior cervical ganglionectomy (SCG X) decreased significantly serum growth hormone (GH) levels in rats 14-96 h after surgery, during and immediately after anterograde degeneration of regional sympathetic terminals. At later times (up to 28 days after SCG X) an increase in serum GH was observed. SCG X augments prolactin (PRL) release, but only at the earliest time examined (14 h after surgery). Injection of the alpha-adrenoceptor blocker, phenoxybenzamine, but not of the beta-blocker, propranolol, negated the depression in serum GH found in SCG X rats 14 h after surgery, without affecting PRL release.     

Increased serum cortisol and growth hormone levels in earthquake survivors with PTSD or subclinical PTSD

Alteration of neuroendocrine systems has been demonstrated to be involved in the pathology of posttraumatic stress disorder (PTSD). Three months after an earthquake in Northern China, cortisol, growth hormone (GH) and prolactin (PRL) levels were assessed in 34 earthquake survivors with PTSD (according to DSM-IV criteria), 30 earthquake survivors with subclinical PTSD and 34 normal controls. Only earthquake survivors diagnosed with PTSD had significantly higher serum GH levels. Also, we found that earthquake survivors (either with PTSD or subclinical PTSD) had significantly higher serum cortisol levels. We concluded that PTSD might be associated with an increased level of serum GH and traumatic survivors might be associated with a higher level of serum cortisol.     

The effects of chronic naloxone on pituitary hormone secretion in female rats

The effects of a sustained-release implant for naloxone (NAL) on serum concentrations of prolactin (PRL), immunoreactive beta-endorphin (IR-beta-ENDO), growth hormone (GH) and thyroid stimulating hormone (TSH) were evaluated in ovariectomized female rats. After 9 days of exposure to NAL, serum levels of none of these 4 pituitary hormones were altered. However, the NAL implant antagonized the stimulatory effects of morphine (15 and 30 mg/kg body weight) on PRL and IR-beta-ENDO secretion, enhanced the stimulatory effects of morphine on GH secretion, and had no effect on morphine-induced suppression of TSH secretion. These results indicate that while chronic NAL exposure does not, by itself, persistently alter pituitary hormone secretion, it differentially effects the response of these hormones to morphine exposure. These data suggest that chronic treatment with narcotic antagonists may invoke differential compensatory mechanisms to maintain normal hormone secretion.     

Effect of apomorphine on growth hormone and prolactin secretion in schizophrenic patients, with or without oral dyskinesia, withdrawn from chronic neuroleptic therapy.

Serum growth hormone (GH) and prolactin (PRL) concentrations were measured after administration of the dopamine receptor agonist, apomorphine HC1 (0.75 mg subcutaneously), to 17 chronic schizophrenic patients, four of whom had an oral dyskinesia, who were withdrawn from chronic neuroleptic therapy for periods of two to 15 weeks, and in 21 control subjects (normal volunteers or physically healthy alcoholics not exposed to neuroleptics). Six of the schizophrenic patients, but none of the controls, had raised baseline levels of GH (greater than 6 ng/ml). After apomorphine all controls showed an increase in serum GH with a peak concentration of 9 ng/ml or more, whereas eight subjects withdrawn from neuroleptics showed an inadequate response (peak less than 6 ng/ml) and in two others an inadequate response was obtained on one of two trials. The peak GH concentration was significantly less after apomorphine in patients withdrawn from neuroleptics (11.90 +/- 3.19 ng/ml) compared with controls (20.80 +/- 2.11 ng/ml) (P less than 0.05). Among patients withdrawn from neuroleptics, those with an oral dyskinesia had significantly lower peak GH concentration 2.46 +/- 0.93 ng/ml) after apomorphine compared with those without (14.85 +/- 3.83 ng/ml) (P less than 0.05). There were no differences in serum PRL concentrations, before or after apomorphine administration, between patients withdrawn from neuroleptics and controls. In uncontrolled observations none of the four patients with an oral dyskinesia showed any worsening of the movement disorder after apomorphine. These data provide no evidence for supersensitivity of dopamine receptors in chronic schizophrenic patients withdrawn from chronic neuroleptic therapy.