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1.
目的:了解重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(益赛普)对类风湿关节炎(RA)患者血清自身抗体的影响。方法:选取24例处于活动期的RA患者,年龄28~56岁,其中女19例,男5例,病程0.5~3年。益赛普25mg皮下注射,每周2次,共治疗12周。在益赛普治疗前、后抽取患者血清,分别检测血清中类风湿因子(RF)、抗核抗体(ANA)、抗ENA抗体、抗双链DNA(ds-DNA)抗体、抗组蛋白抗体、抗心磷脂抗体(aCL)、抗中性粒细胞胞浆抗体(ANCA)等自身抗体。结果:益赛普治疗12周后,RF水平较治疗前明显下降(P<0.01);治疗后ANA、抗dsDNA抗体及抗组蛋白抗体阳性率较治疗前明显升高(P<0.05);而治疗前、后抗ENA抗体、aCL、ANCA的阳性率变化无显著性,24例RA患者中无一例出现系统性红斑狼疮样综合征。结论:RA患者使用益赛普治疗后可以出现自身抗体的变化,但没有发现患者出现系统性红斑狼疮样综合征。  相似文献   

2.
类风湿关节炎(RA)是一个累及周围关节为主的多系统性炎症性的自身免疫病。RA患者的滑膜液中肿瘤坏死因子(TNF-α)呈高水平与滑膜炎和骨侵蚀水平密切相关。传统治疗RA常用非甾体抗炎药、激素、甲氨蝶呤等,其治疗作用有的只能一时改善症状,而不能阻止病情发展和恶化,有的对身体的多个系统可造成不同程度的损害,且起效慢。重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhTNFR:FC)是全人肿瘤坏死因子,它通过全新靶向治疗影响RA发病机制中的关键环节,其作用机制为竞争性与血中TNF-α结合,阻断它和细胞表面TNF受体结合,早期应用可阻止关节破坏,[第一段]  相似文献   

3.
目的评估重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhTNFR∶Fc)治疗类风湿关节炎的临床疗效及安全性。方法将符合诊断标准的30例类风湿关节炎患者随机分为治疗组和对照组各15例。治疗组采用rhTNFR∶Fc 50 mg皮下注射,1次/周,同时口服甲氨蝶呤片10 mg,1次/周;对照组口服甲氨蝶呤片10 mg,1次/周。两组均连续用药12周。观察治疗前后临床、实验室指标的变化及不良反应。结果患者压痛关节数、肿胀关节数,疼痛VAS评分、晨僵、患者对疾病总体状况的VAS评分、医生对疾病总体状况的VAS评分,HAQ得分、ESR和CRP水平治疗前两组间差异均无统计学意义(P均〉0.05);治疗后均较基线有明显改善(P均〈0.05);治疗后4、8、12周随访时,试验组上述各项评价指标均优于对照组(P均〈0.05)。两组各出现4例不良反应,主要包括注射部位反应、皮疹、感染、转氨酶升高、胃肠道反应等,均经处理后缓解。结论 rhTNFR∶Fc联合甲氨蝶呤片治疗类风湿关节炎起效快,疗效好,具有较好的安全性和患者可耐受性。  相似文献   

4.
目的探讨重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhTNFR:Fc)治疗活动期类风湿关节炎(RA)的有效性及安全性。方法将2011年9月-2013年1月收治的86例活动期RA患者随机分为治疗组43例和对照组43例,其中治疗组采用皮下注射rhTNFR:Fc 25 mg,2次/周,口服甲氨蝶呤(MTX)10 mg,1次/周;对照组则给予口服MTX10 mg,1次/周,口服羟氯喹100 mg,2次/d,口服来氟米特10 mg,1次/d;疗程12周。疗效评价采用美国风湿病学会(ACR)20、50、70疗效评定标准。结果治疗4、8、12周时,治疗组ACR20、50、70有效率均高于对照组,差异有统计学意义(P〈0.05);两组在治疗12周后晨僵时间、关节压痛数、关节肿胀数、红细胞沉降率、C反应蛋白、血小板、类风湿因子、关节功能指标均较治疗前有明显改善,且治疗组优于对照组,差异有统计学意义(P〈0.05);两组药物之间不良反应发生率差异无统计学意义(P〉0.05)。结论 rhTNFR:Fc用于治疗活动性RA起效快,具有良好的有效性及安全性。  相似文献   

5.
目的探讨注射用重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白联合甲氨蝶呤治疗类风湿关节炎的临床效果。方法选取2017年1月至2018年12月西安市第五医院收治的136例类风湿关节炎患者作为研究对象,按照随机数字表法将其分为试验组与对照组,各68例。两组患者均采用醋氯芬酸进行常规治疗,在此基础上,对照组采用甲氨蝶呤+硫酸羟氯喹治疗,试验组采用甲氨蝶呤+注射用重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白治疗。比较两组患者治疗3、6个月后的治疗总有效率、治疗前、后的机体关节症状严重程度、血清相关细胞因子水平及不良反应发生情况。结果治疗3、6个月后,试验组的治疗总有效率均显著高于对照组(P<0.05)。治疗后,两组的DAS28评分均显著降低,且试验组低于对照组(P<0.05)。治疗后,两组的血清COX-2、TNF-α、IL-6、M-CSF水平均降低,且试验组低于对照组(P<0.05)。两组的不良反应总发生率比较,差异无统计学意义(P>0.05)。结论注射用重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白联合甲氨蝶呤治疗类风湿关节炎临床效果显著,可加快关节症状改善,减轻机体炎性反应,促进患者恢复,且可有效保证治疗安全性。  相似文献   

6.
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8.
目的 研究注射用重组人肿瘤坏死因子受体-抗体融合蛋白依那西普(Etanercept,ETA)治疗类风湿关节炎(rheumatoid arthritis,RA)的疗效及安全性.方法 65例患者以抽签方式随机分为试验组(31例)和对照组(34例).试验组每周1次口服空白模拟甲氨蝶呤10 mg或来氟米特片20 mg/a,同时每周2次皮下注射ETA 25 mg;对照组每周1次口服甲氨蝶呤10 mg或来氟米特片20mg/d,同时每周2次皮下注射空白模拟ETA 25 mg,疗程3月.疗效评价采用美国风湿病学会(ACR)疗效评定标准.结果 试验组治疗后的类风湿因子滴度(RF)、血沉(ESR)、c反应蛋白(CRP)水平及DAS28评分明显低于对照组(P<0.05),达到ACR50及ACR70的患者试验组均明显高于对照组(P=0.02,P<0.001).两组不良反应发生率差异无统计学意义.结论 ETA用于治疗RA具有良好的安全性和显著的疗效.  相似文献   

9.
目的:探讨重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rh TNFR:Fc)对油酸致大鼠急性肺损伤的保护作用。方法:72只SD大鼠随机分为生理盐水组(对照组)、油酸组(OA组)和rh TNFR:Fc干预组,分为0.5、2、4、6 h亚组;OA组:尾静脉注射油酸0.04 m L/kg造成急性肺损伤,采集外周血、支气管肺泡灌洗液(BALF)及肺组织标本。rh TNFR:Fc干预组:第1、4天皮下注射rh TNFR:FC 0.6 mg/只,第7天注射油酸0.04 m L/kg,采集标本。对照组:尾静脉注射等量生理盐水并收集标本。肺组织HE染色,测定血清肿瘤坏死因子-α(TNF-α)含量、BALF多形核白细胞(PMN)计数;计算肺组织湿/干质量比、肺泡通透指数(LPI)。结果:OA组显微镜下肺间质充血、水肿,大量炎性细胞浸润,rh TNFR:Fc组肺损伤介于OA组和对照组之间;OA组大鼠血清TNF-α含量、BALF中PMN百分比、肺湿/干质量比、LPI均显著高于rh TNFR:Fc干预组和对照组(P<0.05)。结论:rh TNFR:Fc通过中和TNF-α,降低TNF-α生物活性,减少肺组织液渗出,对油酸引起的大鼠急性肺损伤有一定的保护作用。  相似文献   

10.
张程  陈平  蔡珊  吴杰  陈剑波 《医学临床研究》2007,24(4):532-534,537
[目的]探讨重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白(rhTNFR:Fc)对慢性阻塞性肺疾病(COPD)大鼠营养状态的影响.[方法]48只大鼠随机分为4组:正常对照组、COPD组、rhTNFR:Fc干预组和干预对照组.单纯吸烟法建立COPD模型,后3组烟雾暴露达1个月时,干预组给予rhTNFR:Fc进行干预,干预对照组给予空白对照制剂.熏烟80 d称重后,处理所有大鼠.正常对照组、COPD组肺组织切片行HE染色观察形态学改变,定量测定肺平均内衬间隔(MLI)、平均肺泡数(MAN).以酶联免疫吸附法(ELISA)测定各组血清中的TNF-α浓度.使用自动生化分析仪测定各组大鼠血清白蛋白含量.[结果]①COPD组肺MLI高于正常对照组,MAN低于正常对照组(P<0.05).②COPD组血清TNF-α浓度高于正常对照组和rhTNFR:Fc干预组(P<0.05),和干预对照组比较差异无显著性(P>0.05).③COPD组体重较正常对照组、rhTNFR:Fc干预组体重降低,差异有显著性统计学意义(P<0.01).rhTNFR:Fc干预组体重与干预对照组体重比较,差异有显著性统计学意义(P<0.01).④COPD组血清白蛋白较正常对照组降低(P<0.05),但与rhTNFR:Fc干预组和干预对照组比较差异无显著性统计学意义(P>0.05).⑤(COPD组 干预对照组)大鼠血清TNF-α浓度与体重呈负相关(r =-0.75,P<0.05),与血清白蛋白浓度呈负相关(r =-0.73,P<0.05).[结论]rhTNFR:Fc可降低COPD大鼠血清TNF-α水平;rhTNFR:Fc可能对改善其营养状态具有一定作用.  相似文献   

11.

Background

Anti–tumor necrosis factor agents (anti-TNFs) have changed the course of rheumatoid arthritis (RA) for more than a decade. Use of these medications often results in remission, or at least low disease activity (LDA), but at a substantial cost. It has been postulated that discontinuation of these medications among patients with RA in remission or LDA may be possible without an associated increase in RA disease activity.

Objective

The goal of this systematic literature review was to summarize published articles regarding discontinuation of anti-TNFs in patients with RA.

Methods

A systematic literature review was conducted to identify English-language articles indexed in PubMed from July 1999 through June 2013 reporting results regarding anti-TNF discontinuation in patients with RA. Study designs included observational longitudinal studies and clinical trials. Outcomes had to include 1 of the following: time to flare after anti-TNF discontinuation, failure to remain in remission, or proportion of patients in LDA or remission at the end of the study.

Results

Ten studies examined discontinuation of anti-TNF therapies in RA. Inclusion criteria varied significantly across studies in terms of disease activity status (remission or LDA) and duration of this disease status (1 year or 1 month) before discontinuation being attempted. Results from larger studies (eg, >100 patients) suggest that the proportion of patients who discontinued anti-TNF and did not have an increase in disease activity ranged from 24% to 81%. In 3 studies that evaluated durability of LDA or remission after anti-TNF discontinuation, the mean time to relapse varied from 15 weeks to 17 months. In studies that analyzed radiographic data, once therapies were reinitiated after an increase in disease activity was detected, patients generally did not experience progression in structural damage.

Conclusions

Discontinuation of anti-TNF therapy is achievable for many RA patients who start in clinical remission or LDA. However, heterogeneous inclusion criteria and highly variable outcome definitions across studies make it difficult to efficiently summarize the literature on this topic or to conduct a meta-analysis. There is a lack of evidence regarding how to best predict which patients have the greatest likelihood of continuing to do well after discontinuation of anti-TNF therapy.  相似文献   

12.
目的 研究新型重组人肿瘤坏死因子(new recombinant human tumor necrosis Factor,nrhTNF)对小鼠肝损伤的机理。方法 小鼠尾静脉注射原型TNF和nrhTNF,检测血清天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、肝脏指数,并用硫代巴比妥酸(TBA)测定肝组织中丙二醛(MDA)含量,同时测定超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH—Px)活性。结果 小鼠尾静脉注射原型TNF和nrhTNF8h后,血清ALT、AST活性显著升高(P〈0.05),肝脏指数和MDA含量也明显增加(P〈0.05),而SOD活性下降(P〈0.05),但GSH—Px活性未见明显改变(P〉0.05)。结论 nrhTNF低、中剂量对小鼠肝毒性较低;高剂量则较高,但比原型TNF相比肝毒性较低;高剂量nrhTNF所致肝损伤与其诱发自由基引起的脂质过氧化有关。  相似文献   

13.

Introduction

The purpose of this study was to evaluate clinical outcomes and drug/administration costs of treatment with tumor necrosis factor inhibitor (TNFi) agents in US veterans with rheumatoid arthritis (RA) initiating TNFi therapy. The analysis compared patients initiating and continuing a single TNFi with patients who subsequently switched to a different TNFi.

Methods

Data from patients enrolled in the Veterans Affairs Rheumatoid Arthritis (VARA) registry who initiated treatment with adalimumab, etanercept, or infliximab from 2003 to 2010 were analyzed. Outcomes included duration of therapy, Disease Activity Score based on 28 joints (DAS28), and direct drug and drug administration costs.

Results

Of 563 eligible patients, 262 initiated a single TNFi therapy, 142 restarted their initial TNFi after a ≥90-day gap in treatment (interrupted therapy), and 159 switched to a different TNFi. Patients who switched had higher mean DAS28 before starting TNFi therapy than patients with single or interrupted therapy: 5.3 vs 4.5 or 4.6, respectively. Mean duration of the first course was 34.3 months for single therapy, 18.3 months for interrupted therapy, and 17.7 months for switched therapy. Mean post-treatment DAS28 was highest for patients who switched TNFi. Mean annualized costs for first course were $13,800 for single therapy, $13,200 for interrupted therapy, and $14,200 for switched therapy; mean annualized costs for second course were $12,800 for interrupted therapy and $15,100 for switched therapy.

Conclusion

Patients who switched TNFi had higher pre-treatment DAS28 and higher overall costs than patients who received the same TNFi as either single or interrupted therapy.

Funding

This research was funded by Immunex Corp., a fully owned subsidiary of Amgen Inc., and by VA HSR&D Grant SHP 08-172.
  相似文献   

14.

Introduction

Dose escalation with tumor necrosis factor (TNF)-blockers is poorly characterized in pharmacy benefit management (PBM) settings.

Methods

This retrospective study used integrated pharmacy and medical claims from the PBM Medco to characterize dose escalation among rheumatoid arthritis (RA) patients treated with etanercept and adalimumab. Data from adults with RA with pharmacy claims for etanercept or adalimumab between 1/1/2007 and 12/31/2009 and continuous enrollment for ≥6 months before and ≥12 months after first (index) pharmacy claim were analyzed. “New” patients had no claim for TNF-blocker in the 6 months prior to receipt of their index TNF-blocker; otherwise, they were classified as “continuing” patients. Endpoints included 12-month persistence and duration on index medication and dose escalation. Dose escalation (allowed per adalimumab label but not for etanercept) in patients’ persistent ≥12 months was estimated using five methods: (1) average weekly dose ≥110% of recommended label dose; (2) average subsequent dose ≥130% of starting dose; (3) last dose ≥110% of starting dose; (4) ≥2 consecutive instances of dose ≥130% of starting dose; and (5) any instance where dose increase connoted an additional syringe/vial use.

Results

Data from 1,260 patients on etanercept and 852 patients on adalimumab were analyzed; 45.3 and 45.9% of new patients on etanercept and adalimumab, respectively, and 60.5 and 60.8% of continuing patients had ≥12 months persistence on index medication. Across all five methods used to estimate dose escalation, patients receiving etanercept had significantly lower rates of dose escalation (P < 0.001) than patients receiving adalimumab. For new patients, rates of dose escalation were 0.4–1.2% for etanercept and 8.3–14.1% for adalimumab. For continuing patients, rates ranged from 1.1 to 2.9% for etanercept and 7.0–28.3% for adalimumab.

Conclusions

New and continuing patients from this PBM database on etanercept had significantly lower rates of dose escalation than patients on adalimumab.  相似文献   

15.

Introduction

To examine treatment persistence and clinical outcomes associated with switching from a tumor necrosis factor inhibitor (TNFi) to a medication with a new mechanism of action (MOA) (abatacept, anakinra, rituximab, tocilizumab, or tofacitinib) versus cycling to another TNFi (adalimumab, certolizumab pegol, etanercept, golimumab, or infliximab) among patients with rheumatoid arthritis.

Methods

This retrospective, longitudinal study included patients with rheumatoid arthritis in the JointMan® US clinical database who received a TNFi in April 2010 or later and either cycled to a TNFi or switched to a new MOA therapy by March 2015. Cox proportional hazards models were used for time to non-persistence (switching or discontinuing). An ordinary least squares regression model compared 1-year reduction from baseline for the Clinical Disease Activity Index (CDAI).

Results

There were 332 (54.2%) TNFi cyclers and 281 (45.8%) new MOA switchers. During a median follow-up of 29.9 months, treatment persistence was 36.7% overall. Compared with new MOA switchers, TNFi cyclers were 51% more likely to be non-persistent (adjusted hazard ratio, 1.511; 95% CI 1.196, 1.908), driven by a higher likelihood of switching again (adjusted hazard ratio, 2.016; 95% CI 1.428, 2.847). Clinical outcomes were evaluable for 239 (53.3%) TNFi cyclers and 209 (46.7%) new MOA switchers. One-year mean reduction in CDAI from baseline to end of follow-up was significantly higher for new MOA switchers than TNFi cyclers (?7.54 vs. ?4.81; P = 0.037), but the difference was not statistically significant after adjustment for baseline CDAI (?6.39 vs. ?5.83; P = 0.607).

Conclusion

In this study, TNFi cycling was common in clinical practice, but switching to a new MOA DMARD was associated with significantly better treatment persistence and a trend toward greater CDAI reduction that was not significant after adjustment for baseline disease activity.

Funding

Sanofi and Regeneron Pharmaceuticals.
  相似文献   

16.
目的 分析类风湿关节炎(RA)患者血清胆固醇酯转运蛋白(CETP)水平及对脂质紊乱的影响.方法 ELISA法测定RA患者(41例)血清CETP浓度,并与52例年龄、性别匹配的健康人作对照.结果 RA组CETP浓度较对照组显著增加(3.15±2.04 mg/L vs. 2.26±1.86 mg/L,P<0.05).总胆固醇(TC)、三酰甘油(TG) 、低密度脂蛋白胆固醇(LDL-C)等致动脉粥样硬化的血脂和脂蛋白水平也明显升高.结论 RA患者血清CETP水平显著升高,高水平CETP可能是致RA高血脂的原因之一.  相似文献   

17.
本研究探讨脐血单个核细胞(mononuclear cells,MNC)中基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)的活性表达,重组人肿瘤坏死因子-α(recombinant human tumor necrosis factor alpha,rh—TNF—α)对脐血MNCMMP-9活性和细胞体外迁移能力中的作用及二者之间的关系。采用明胶酶谱技术检测脐血MNC中MMP-9的活性。通过微孔细胞迁移实验检测脐血MNC的体外迁移能力,并以不同浓度的rh—TNF-α对脐血MNC进行干预,检测rh—TNF—α对MMP-9活性和细胞体外迁移的作用。结果表明:脐血MNC经无血清培养24和48小时后,均可检测出MMP-9活性,细胞相对迁移率分别为(1.371±0.011)%和(1.384±0.014)%,两者间无统计学差异。大剂量TNF-α(500U/ml)作用可致细胞死亡;小剂量TNF-α(〈200U/ml)可以上调脐血MNCMMP-9表达,且随着TNF—α剂量增加MMP-9表达增强。小剂量TNF—α(〈200U/ml)可提高脐血单个核细胞的体外迁移率,且与剂量呈正相关。结论:小剂量TNF-α可上调脐血MNCMMP-9活性,提高脐血MNC的体外迁移能力,此作用可能加速脐血移植后细胞归巢,促进脐血移植后的造血重建。  相似文献   

18.
目的:观察老年类风湿关节炎(senile rheumatoid arthritis,SRA)患者的蛋白质代谢变化及分析其相关因素。方法:随机选取40例RA患者(老年组占14例,中青年组26例)和20例健康人对照组,并测定其血前白蛋白(PA)、白蛋白(ALB)、白蛋白/球蛋白(A/G)、载脂蛋白A1(Apo-A1)、载脂蛋白B(Apo-B)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)等,分析不同年龄段患者测定各指标变化及其与临床症状、活动性指标、生活质量、焦虑自评量表(SAS)、抑郁自评量表(SDS)标准分及类风湿性关节炎活动度评分表(DAS-28)等的相关性。结果:①与健康对照者相比,老年RA患者PA、总蛋白(TP)、ALB、HDL、Apo-A1、Apo-B、调节性T细胞(Treg)水平显著下降(P〈0.05);与中青年RA患者相比,老年RA患者PA、TP、GLO、HDL、Apo-A1、Treg水平都有不同程度的下降(P〈0.05)。②PA、TP与红细胞(RBC)、血红蛋白(HB)、Fe、CD4+T呈明显正相关(P〈0.05);TP与血沉(ESR)呈明显负相关(P〈0.05);GLO与白细胞(WBC)、补体3(C3)呈明显正相关(P〈0.05);A/G与IgA、C3、ESR呈明显负相关(P〈0.05);LDL、Apo-A1与CD4+T呈明显正相关(P〈0.01)。③PA与DAS-28、SAS呈明显负相关(P〈0.05);GLO与15m步行时间、食欲减退、食后腹胀呈明显负相关(P〈0.05);A/G与15m步行时间、食欲减退、食后腹胀呈明显正相关(P〈0.05);HDL与食后腹胀呈明显负相关(P〈0.01);LDL与皮下结节呈明显负相关(P〈0.05);Apo-A1与晨僵时间、关节重着、中医证候总分呈明显负相关(P〈0.05);APO-B与皮下结节、SAS、SDS呈明显负相关(P〈0.05);APOA1/B与大便稀溏、关节重着呈明显负相关(P〈0.05)。结论:与健康对照者及中青年RA患者相比,老年性RA患者存在蛋白质代谢的异常,主要表现为PA、TP、ALB、HDL、Apo-A1、APO-B等指标水平明显下降,其变化与RA炎性活动、贫血状况及生理功能等密切相关,亦与Treg有一定的关联。  相似文献   

19.
呼芳  孙江艳 《医学临床研究》2016,(12):2360-2363
[目的]探讨动机性访谈对类风湿关节炎(Rheumatoid arthritis,RA)患者功能锻炼效果的影响.[方法]选取2014年10月至2015年12月在本院接受治疗的RA患者148例,采取随机数表法分成对照组和干预组.对照组患者接受常规复诊指导、日常健康教育、出院康复训练指导和建立随访电子档案按计划随访;干预组在对照组的基础上增加动机性访谈,评估并比较出院时和出院6个月后两组患者的晨僵时间、疼痛评分、日常活动能力影响评分和患者依从性.[结果]两组患者出院时的晨僵时间、疼痛评分、日常活动能力影响评分及依从性评分比较无统计学意义(P>0.05),出院6个月后干预组患者晨僵时间、疼痛评分、日常活动能力影响评分均明显低于对照组患者,依从性评分显著高于对照组,其差异有统计学意义(P<0.05).[结论]动机性访谈对RA患者功能锻炼效果显著,具有重要的临床应用价值.  相似文献   

20.
生长激素对急性期脑出血患者蛋白质代谢的作用   总被引:1,自引:0,他引:1  
目的:研究生长激素对急性期脑出血患者蛋白质合成及分解代谢的作用。方法:选择有低蛋白血症的急性期脑出血患者30例,随机分为3组:A组10例,采取能全力(TPN)+重组人生长激素(rhGH)治疗;B组10例,采用TPN治疗;C组10例,采用普通饮食治疗。治疗前、治疗后第8天分别测定血清白蛋白和24 h尿氮、氮平衡。结果:A组患者治疗后血清白蛋白和氮平衡明显升高(P<0.01),24 h尿氮明显降低(P<0.01)。结论:生长激素加用TPN治疗可以明显地促进蛋白质合成、抑制蛋白质分解,改善脑出血患者的营养状态。  相似文献   

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