96例活体肾移植患者免疫抑制剂应用情况分析

目的:了解我院活体肾移植患者住院期间免疫抑制剂的应用情况。方法:回顾性调查我院2005～2007年活体肾移植患者病历96份,分别对免疫抑制剂品种、相关费用及不良反应情况进行统计、分析。结果:活体肾移植患者平均住院费用为48385.85元,免疫抑制剂平均费用为17364.46元;术后急性排斥反应发生率为5.74%,免疫抑制剂相关不良反应发生率为54.17%。结论:活体肾移植具有排斥反应小、花费少的特点。今后应就活体肾移植患者如何降低免疫抑制剂用量,减少诱导免疫耐受治疗,施行环孢素撤除治疗等展开深入研究。     

肾移植患者服免疫抑制剂的指导及护理

同种异体肾移植,是治疗终末期肾衰的有效方法;也是提高这类患者生活质量的主要手段。然而,肾移植术后患者要长期服用免疫抑制剂。如何正确指导患者合理应用免疫抑制剂,对肾移植的人和肾长期存活十分重要。免疫抑制剂药物在肾移植术后治疗的种类为抗代谢剂:如硫唑噤呤;激素:强的松;其它:环孢霉素     

双环醇防治肾移植术后药物性肝损害的疗效观察

目的双环醇防治肾移植术后药物性肝损害的疗效观察。方法选择我院42例肾移植术后患者,治疗组22例,术后用药为免疫抑制剂联合双环醇片,对照组20例,用药为单纯免疫抑制剂抗排斥治疗,观察患者在术后4周内的症状和体征,包括乏力、食欲不振、黄疸、肝区痛、肝肿大等及肝肾功能情况。结果两组患者术后药物性肝损害发生率分别为：治疗组18.18%,对照组40%,两组比较差异有统计学意义。术后4周治疗组ALT、AST显著低于对照组水平。结论研究表明口服双环醇片75mg/d可有效防治环孢素药物性肝损害,不仅有利于改善患者的生活质量,而且也有益于保证免疫抑制剂的治疗效果。     

肾移植术后肺部感染的诊断与治疗

目的探讨肾移植术后合并肺部感染的诊断与治疗。方法对23例肾移植术后肺部感染患者的临床资料进行回顾性分析。结果21例存活,2例死亡,未发生明显不良反应及移植肾排斥反应。结论对于肾移植术后肺部感染患者,要给予高度重视和及早救治,综合治疗是基础,较大剂量糖皮质激素的应用和调整免疫抑制剂的用量．是治疗的关键．     

彩色多普勒超声在肾移植术后并发症诊断中的应用进展

肾移植是终末期肾病最理想的治疗方法。随着肾移植外科技术的改进和新型免疫抑制剂在临床的应用,肾移植患者的生存率已明显提高。但随着肾移植手术的普遍开展,术后并发症     

儿童肾移植术后肺炎的诊治体会并文献复习

目的探讨儿童肾移植术后肺炎的治疗方案。方法对15例儿童肾移植术后肺炎临床资料进行回顾性分析,归纳总结减少或撤除免疫抑制剂、抗感染、抗病毒、激素、有创通气等综合治疗方案,并对近年国内外相关文献进行分析总结。结果儿童肾移植术后肺炎以发热为首发症状,仅53.3%患者有呼吸道症状,痰、咽拭子培养、BAL检出率低(40%),经治疗,治愈13例,死亡2例,2例行有创通气。结论儿童肾移植术后肺炎,起病隐匿,病情进展快,尽早诊断,减少或撤除免疫抑制剂、抗感染、抗病毒、激素、有创通气等综合治疗是成功的关键。     

运用微粒子酶免疫分析法监测肾移植患者雷帕霉素实时治疗窗

目的:实时监测肾移植患者的雷帕霉素血药浓度,研究肾移植患者术后不同时期雷帕霉素治疗窗浓度范围,从而有效指导肾移植患者的合理用药,提高肾移植患者的术后长期存活率及生活质量。方法:采用微粒子酶免疫分析法测定本院64例肾移植患者术后不同时期雷帕霉素血药浓度,同时测定患者肝肾功能,评价疗效。结果:雷帕霉素治疗窗浓度范围术后1个月内为10.0～12.0ng·mL-1,第2～4个月为7.0～10.0ng·mL-1,第5个月以后为4.0～7.0ng·mL-1,上述浓度范围既能达到满意的免疫抑制效果,又能减少雷帕霉素的副作用。结论:雷帕霉素可作为肾植移术后的新型免疫抑制剂,术后治疗窗浓度随时间的延长而改变。微粒子酶免疫分析法可有效地监测患者雷帕霉素的血药浓度,为指导患者的临床用药提供了有价值的参考。     

肾移植术后的药学监护实践

目的:确保肾移植术后患者用药安全、有效、经济.方法:通过治疗药物监测、为患者建立药历、进行疗效评价和做好咨询等方法对肾移植术后患者实施药学监护.结果:通过药学监护,明显提高了肾移植术后患者用药的安全性、有效性、经济性,改善了患者的生活质量.结论:对肾移植术后患者实施药学监护十分必要,具有重要意义.     

肾移植术后肺部感染的药学监护

目的:提高肾移植术后肺部感染患者的药物治疗效果。方法:明确病原体,予以抗细菌、抗真菌及抗病毒等治疗,调整免疫抑制剂用药方案,适时应用糖皮质激素,并给予全身支持治疗。结果与结论:通过药学监护,制定安全、有效、经济的药疗方案,可有效降低肾移植术后患者的病死率。     

他克莫司在932例肾移植患者中的应用评价

目的 :评价他克莫司 (FK506)用于肾移植患者免疫抑制治疗的效果与安全性。方法 :对肾移植术后应用FK506的932例患者的资料进行回顾性分析。结果 :肾移植术后即应用FK506的547例患者 ,急性排斥反应发生率低 ;由环孢素A (CsA)改用FK506的385例患者 ,大部分排斥反应缓解 ,肝功能改善。FK506的主要不良反应有血糖升高和神经系统毒性。结论 :FK506是一种强效免疫抑制剂 ,还可用于CsA不能逆转排斥反应的挽救治疗。     

新生儿缺氧缺血性脑病的CT表现与病理对比分析

目的探讨新生儿缺氧缺血性脑病CT的诊断及与病理关系。方法对165例临床诊断为HIE患儿进行CT检查。结合病理进行CT对比分析。结果165例HIE患儿中，轻度83例，占50％，中度62例，占38％，重度20例，占12％。合并蛛网膜下腔出血30例，脑室内出血5例，硬膜下血肿2例。结论CT检查能明确诊断及HIE患儿的脑损伤情况和颅内出血情况．为临床治疗提供积极作用。     

The functional ratio of chymase and angiotensin converting enzyme in angiotensin I-induced vascular contraction in monkeys, dogs and rats

Recently, a chymase-dependent angiotensin (Ang) II-forming pathway was found in human cardiovascular tissues, and the significance of this pathway in the pathogenesis of some cardiovascular diseases was suggested. The present study examined the ratio of angiotensin converting enzyme (ACE) to chymase-dependent Ang II formation in various isolated vessels from monkeys, dogs and rats. In all of the examined vessels, the addition of KCl at a concentration of 50 mM could induce a maximal contraction. Except for monkey coronary artery and rat renal and femoral artery, the addition of Ang I could induce transitory contractions, whereas the force of contractions in these vessels was quite different. The sensitivity to Ang II in these vessels was similar to that for Ang I. In monkey gastroepiploic and mesenteric arteries, about 70% of the Ang I-induced contraction was suppressed by chymase inhibition, while it was suppressed about 50% in monkey renal, femoral and carotid arteries. In dog renal arteries, about 65% of the Ang I-induced contraction was suppressed by chymase inhibition, while it was suppressed by about 30% in other dog arteries. In contrast, in all rat arteries, Ang I-induced contractions were completely suppressed by treatment with ACE inhibitor alone. We concluded that regional differences in the response to Ang I exist in vascular tissues, and the ratio of ACE- to chymase-dependent Ang II formation is different in the various vessels.     

Comparative study of coronary vasodilator and cardiac effects of nitrendipine by use of isolated, blood-perfused dog heart preparations

The coronary vasodilator and cardiac effects of 3-ethyl-5-methyl-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl) -3,5-pyridinedicarboxylate (nitrendipine, Bay e 5009) were compared in isolated, blood-perfused sinoatrial (SA) node, atrioventricular (AV) node and papillary muscle preparations of dogs with i.a. administration. In all preparations nitrendipine increased (coronary) blood flow. In SA node preparations nitrendipine reduced sinus rate but the reduction remained only about 13% of the basal value even at the highest dose. The dose estimated to produce a 15% (nearly a half maximum) decrease in sinus rate was about 8 times the dose which doubled coronary blood flow. In AV node preparations nitrendipine prolonged AV conduction time when injected into the artery supplying the AV node but the prolongation remained only about 12% of the basal value even at the highest dose. The dose estimated to produce a 15% (nearly a half maximum) increase in AV conduction time was about 11 times the dose which doubled coronary blood flow. When injected into the artery supplying the His-Purkinje ventricular system of AV node preparations, nitrendipine was entirely ineffective on AV conduction. In paced papillary muscle preparations nitrendipine reduced force of contraction. The reduction, however, remained less than 50% of the basal value even at the highest dose. The dose estimated to reduce force of contraction by half was about 11 times the dose which doubled coronary blood flow. Nitrendipine was entirely ineffective on ventricular beating rate of spontaneously beating papillary muscle preparations. These results indicate that nitrendipine is highly vasoselective, and warrant its high efficacy as an antianginal drug.     

Disposition of azapropazone in chronic renal and hepatic failure

Summary The disposition of azapropazone 600 mg i.v. was investigated in 6 healthy subjects, 13 patients with cirrhosis and 8 patients with renal failure. In healthy subjects the elimination half-life was 12.2±2.1 h (mean ± SD), the volume of distribution 10.6±3.31 and the total clearance was 597±135 ml·h^–1. Renal clearance accounted for about 62% of the total clearance. The free fraction of azapropazone in the plasma was 0.0045±0.0006. The patients with cirrhosis were divided into Group I with modest and Group II with severe impairment of liver function. In Group I the total clearance of azapropazone was not significantly different from that in healthy subjects. There was a 2.5-fold increase in its free fraction in plasma, and a reduction in the free drug clearance to about half that in healthy subjects. In Group II patients total clearance was reduced to about 20% of normal. This was partly due to reduced non-renal clearance but mainly to impaired renal clearance of azapropazone. The diminished renal clearance was considered at least in part to represent a drug-induced impairment of renal function, as there was a concomitant reduction in creatinine clearance. The free fraction of azapropazone in the plasma was markedly enhanced (>0.02), and simultaneously, free drug clearance was drastically reduced, to about 2% of that in healthy subjects. In patients with renal failure the total clearance was diminished, depending on the degree of impairment of kidney function. Anephric patients were estimated to have about one third of the total clearance in normal subjects. The free fraction of azapropazone in the plasma was increased in 4 of the 8 patients. It is concluded that patients with cirrhosis and modest impairment of liver function may require about half the normal dose of azapropazone, since free drug clearance is reduced by about 50%. Patients with severe impairment of liver function are expected to be highly susceptible to dose-related side effects, since the pronounced increase in the free fraction in plasma and the decreases in renal and non-renal clearance lead to marked reduction in free drug clearance and so to accumulation of free drug in the body. In patients with renal failure the dose of azapropazone should be reduced according to the degree of impairment of kidney function and plasma protein binding of the drug.     

Olanzapine for injection: new formulation. No advantage in agitated patients

(1) The intramuscular neuroleptic of choice for the treatment of agitated schizophrenic patients and patients with acute mania is haloperidol, at a dose of 5 mg. Olanzapine is now marketed in France for hospital use in both these indications. (2) In two comparative trials in patients with schizophrenia, olanzapine 10 mg was shown to be no better than haloperidol 7.5 mg (a high dose). Control of agitation was satisfactory in three-quarters of patients after a single injection of either neuroleptic. (3) Olanzapine has not been compared with other neuroleptics in the treatment of acute mania. In one trial, olanzapine acted faster than lorazepam for injection (used at a rather low dose). (4) In one trial, patients given olanzapine had a lower incidence of acute dystonia and extrapyramidal symptoms (about 1%) than patients given haloperidol (about 6-7%), but the haloperidol dose (7.5 mg) was higher than recommended in the SPC (5 mg). The incidence of postural hypotension was significantly higher among patients given olanzapine (about 12%) compared with haloperidol (about 3%). (5) In practice, haloperidol remains the intramuscular neuroleptic of choice for the treatment of agitated patients with schizophrenia or acute mania.     

Studies of the kinetics and metabolism of 17 beta-heptanoyl-17 alpha-ethinyl-4-oestren-3-one-7-3H (norethisterone enanthate) in humans following intramuscular injection.

The kinetics and metabolism of 17 beta-heptanoyl-17 alpha-ethinyl-4-oestren-3-one-7-3H (7-3H-norethisterone enanthate, NET-En) after i.m. injection in two female subjects is described. 177.4 mg and 174.5 mg NET-En were injected. Maximum 3H-activity in plasma was reached 8 to 14 days after the injection. In terms of NET-En it amounted to 70-100 mug/100 ml. Maximum NET concentration was reached on the 4th to 8th day and amounted to about 1 mug/100 ml. After 4 weeks NET concentration was still about 0.05 to 0.1 mug/100 ml and even after 6 weeks NET was still detectable in plasma. In 14 days the two subjects excreted about 13% of the administered dose in the urine and about 15% and 21%, respectively, in the faeces. On the basis of a rough calculation, the subjects eliminated about 60% and 55% of the radioactivity with urine and faeces within 42 days.     

Consumers' understanding and concerns about bovine spongiform encephalopathy (BSE): comparison among Canadian, American, and Japanese consumers

In spite of much analysis of the impact of bovine spongiform encephalopathy (BSE) on consumer perceptions and meat purchases, there has been little explicit analysis of the level of BSE knowledge. In this study the role of knowledge about BSE was examined in Canada, the United States, and Japan. In addition, the level of knowledge was linked to human health concerns regarding BSE and whether there is agreement with paying a premium for beef with BSE animal tests. From a public policy perspective, understanding whether higher or lower knowledge is linked to public concern and desire for market intervention might help in the design of risk communication in any future animal disease outbreak. Should lack of knowledge about the disease be related to a public desire for market intervention (animal testing, for example), then an increase in detailed information about how humans might contract the disease might change public pressure for intervention. As compared to U.S. and Canadian respondents, Japanese respondents are more knowledgeable regarding the ways in which humans might be exposed to the human variant of BSE (variant Creutzfeldt-Jakob disease, vCJD) and are more concerned about the disease. However, U.S. respondents are more willing to pay a premium for beef tested to ensure that it will not result in vCJD. Japanese respondents who are more knowledgeable about BSE are more concerned about the risk of BSE to human health. In Canada, subjects who are more knowledgeable about the ways in which humans attain vCJD are less concerned about the risk of BSE to human health. Knowledge of the ways in which humans develop vCJD does not significantly influence concerns about the risk of BSE to human health in the United States or willingness to pay for BSE-tested beef in any of the three countries. The links between knowledge and concerns about BSE and between knowledge and agreement with paying premiums for BSE-tested beef were estimated for each country using ordered probit regressions.     

Recovery of noradrenaline in adrenergic axons of rat sciatic nerves after reserpine treatment

The recovery of noradrenaline in adrenergic axons of the rat sciatic nerve after a single dose of reserpine (10 mg/kg i.p.) has been studied in unligated nerves and nerves ligated for 6 h. In unligated nerves the recovery at 24 h after reserpine was about 14% of normal. The noradrenaline content then slowly rose to reach about normal concentrations 6–7 days after reserpine injection. In nerves ligated 6 h before death, about 8·0 ng of noradrenaline accumulated proximal to the ligation in normal animals. At 6 and 12 h after reserpine about 4% of normal amounts of noradrenaline were found. Thereafter the amount of accumulated noradrenaline rapidly increased to about normal levels on day 2 after reserpine. At this time the content in unligated nerves was only about 45% of normal unligated nerve. On days 3–5 after reserpine, supranormal accumulations of noradrenaline were found (statistically highly significant), having a maximum at day 4 of about 145% of normal. At this time the noradrenaline content in unligated nerve was only about 80% of normal. The results may indicate an increased synthesis and increased rate of downtransport of amine storage granules during the early recovery phase after reserpine. This phenomenon may be part of a feed-back mechanism operating after depletion of the transmitter in the nerve terminals.     

The disposition and metabolism of durene (1,2,4,5-tetramethylbenzene) in rats

The organ and tissue distribution, excretion and metabolism of [3H]1,2,4,5-tetramethylbenzene ([3H]durene) in male Wistar albino rats were investigated following a single i.p. administration (40 mg/kg) and within 9 days after five daily repeated administrations. Urine proved to be the main route of tritium excretion. Within the first 24 h after a single administration 69% of the radioactivity was excreted in the urine and only 9% in the feces. The highest level of tritium binding was found in the fat tissue, liver, kidneys and adrenal glands. The accumulation of tritium in the plasma proceeded with a kinetic constant of 0.49 h(-1), whereas the half-life of radioactivity decay amounted to about 6.3 h. In erythrocytes, the tritium level was found to be about three times lower than in blood plasma. The total amount eliminated during the 9 days following repeated administration was about 94% of the five doses given. The highest level of tritium was found in fat tissue and adrenal glands, followed by the liver, kidneys, sciatic nerve and muscle. A gradual decline in tritium levels was observed during the following 4 days in most tissues to reach about 2% of the dose given. The main urinary metabolites resulting from the administration of durene were 2,4,5-trimethylbenzyl alcohol (about 22%), 4,5-dimethyl-1,2-benzdialdehyde (about 19%), 2,4,5-trimethylbenzaldehyde (about 19%) and 2,4,5-trimethylbenzoic acid (about 16%). The oxygen-containing metabolites accounted for almost 80%, whereas sulphur-containing metabolites accounted for approximately 10% of the products of biotransformation. In conclusion, most of the durene administered has a relatively rapid turnover rate, with minor levels retained in the tissues for longer time periods.     

Neuromuscular blocking and ganglion blocking activities of some acetylcholine antagonists in the cat

The potencies of tubocurarine, gallamine, pancuronium, benzoquinonium, hexamethonium and mecamylamine in blocking neuromuscular transmission in the soleus muscle, and in blocking contractions of the nictitating membrane evoked by preganglionic sympathetic stimulation have been compared in cats under chloralose anaesthesia. On a molar basis, pancuronium was about 8 times and benzoquinonium about 2·5 times more potent than tubocurarine in blocking the soleus muscle; gallamine was less than half as potent, mecamylamine about 128 times and hexamethonium about 380 times less potent. In blocking the superior cervical ganglion, mecamylamine was about 17 times more, tubocurarine was about 5 times more and pancuronium about twice as potent as hexamethonium. Benzoquinonium was about half as potent as hexamethonium, and gallamine about 5 times less potent. The results emphasize that the shorter distance between charged centres, as in hexamethonium, reduces affinity for muscle receptors but does not necessarily enhance affinity for ganglion receptors, and from the point of view of deductions concerning the configuration of the ganglionic receptor, the ganglion blocking potencies of some neuromuscular blocking drugs should be taken into account.