急性心肌梗塞早期康复运动耐量与心率变异性分析

目的 :探讨急性心肌梗塞 (AMI)患者早期运动康复对运动耐量的影响以及心率变异性的变化。方法 :对 35例 AMI患者出院前行活动平板运动试验和心率变异性测定 ,其中 2 0例 AMI患者进行了两周运动康复程序治疗。结果 :康复组平均运动耐量为 5.3± 2 .5METs,未康复组为 2 .87± 0 .83METs,两组间有显著差异 (P<0 .0 1)。 35例 AMI患者心率变异性较正常对照组明显降低 ,AMI康复组的心率变异较非康复组有明显的改善。结论 :早期运动康复治疗可增加 AMI患者运动耐量 ,明显改善其心率变异性 ,并可能降低 AMI死亡率 ,改善其预后     

冠状动脉造影评价静脉溶栓治疗急性心肌梗塞100例临床疗效

目的　我院自 1 994年 3月至 1 997年 6月对 1 0 0例急性心肌梗塞 (AMI)病人应用国产尿激酶 (UK)和德国链激酶 (SK)静脉溶栓治疗 ,以冠状动脉造影结果评价其疗效及安全性。结果发现 :UK和SK血管开通率分别为 60 8%及 63 0 % ,5周死亡率分别为 8 6%及 7 4 % ,严重出血并发症分别为1 85%及 2 1 7% ,均无统计学意义。 1 0例加大UK剂量至 2 0 0万U ,并不增加血管开通率反而增加出血并发症。临床观察证明UK和SK用于静脉溶栓治疗AMI是安全有效的。两者均能明显降低AMI的死亡率 ,来自溶栓治疗的严重并发症也是罕见的。     

两周康复程序在急性心肌梗塞早期康复治疗中的可行性

目的 :探索两周康复程序对急性心肌梗塞的早期康复治疗的可行性。方法 :根据个体化及活动量循序递增的原则 ,对 4 2例无严重并发症的急性心肌梗塞患者进行 2周康复程序的康复治疗 ,包括饮食指导、戒烟、适量运动及处理应激的训练等。结果 :所有患者均顺利完成 2周康复程序的治疗 ,门诊随访 1～ 5个月 ,所有患者均能生活自理 ,半数以上的患者能坚持参加步行锻炼和家务劳动。结论 :急性心肌梗塞早期康复治疗的 2周康复程序是切实可行和安全有效的     

急性心肌梗塞早期左心室容积参数与收缩功能关系的研究

目的 :研究急性心肌梗塞早期左心室收缩末容积、左心室舒张末容积、每搏搏出量及左心室射血分数改变特点及其相互关系和意义。　　方法 :首次急性心肌梗塞患者 37例为患者全组 ,平均年龄 6 1.2± 10 .0岁 ,平均发病时间 6 .6± 5 .8小时 ,其中前壁组 2 2例 ,下壁组 15例 ,另设正常对照组 11例。采用双探头门控单光子发射计算机断层摄影系统采集心肌显像资料 ,由计算机内已设程序自动计算左心室射血分数及各容积参数。　　结果 :1左心室舒张末容积 :患者全组为 110 .0± 45 .2 ml,其中前壁组和下壁组分别为 12 5 .4± 43.9ml和 87.9±38.3ml,正常对照组为 74.7± 12 .2 ml,患者全组与正常对照组、下壁组和前壁组间均差异显著 (P<0 .0 5 )。 2左心室收缩末容积 :正常对照组 ,患者全组 ,前壁组和下壁组分别为 2 5 .3± 5 .8ml,6 4.0± 35 .9ml,79.0± 33.7ml和 42 .0±2 7.3ml。正常对照组与患者全组之间差异十分显著 (P<0 .0 0 1) ,前壁组与下壁组之间差异显著 (P<0 .0 1)。 3每搏搏出量 :正常对照组 ,患者全组 ,前壁组和下壁组四者两两之间均无差异。 4左心室射血分数 :患者全组显著低于正常对照组(0 .6 6± 0 .0 5比 0 .45± 0 .13,P<0 .0 0 1) ,前壁组低于下壁组 (0 .38± 0 .0 8比 0 .5 5± 0 .11,P<0     

介入、溶栓及常规方法治疗急性心肌梗死的疗效比较

20 0 0年 6月至 2 0 0 3年 6月 ,我院收治急性心肌梗死(AMI)患者 118例 ,分别采用介入、溶栓及常规治疗。现对各种方法的疗效报告如下。临床资料 :118例 AMI患者中 ,男 78例 ,女 4 0例 ;年龄(5 6± 10 )岁。随机分为三组 ,A组 4 2例 ,B组 4 3例 ,C组 33例。三组患者平均年龄、治疗距发病的平均时间、心肌梗死和危险因素 (糖尿病、高血压、吸烟、血脂 )均无显著性差异 (P<0 .0 5 )。治疗方法 :B组用国产尿激酶 (UK) 15 0万～ 2 0 0万 U或重组链激酶 (r- SK ) 15 0万 U治疗 ,A组采用冠状动脉介入(PCI)治疗 ,C组采用常规治疗。三组患…     

急性心梗两周康复程序的疗效观察及分析

目的:探讨两周康复程序对急性心肌梗塞(AMI)患者运动能力、心功能恢复、心理状态的影响。方法:98例AMI患者,分成康复组50例、对照组48例,两组均常规药物治疗,康复组在药物治疗的基础上加两周康复程序,对两组的运动能力即代谢当量(METS)值、心肌酶、左室射血分数(LVEF)、E峰与A峰比值(E/A)进行对比分析。结果:康复组运动能力[(2.91±0.72)METS∶(2.57±0.63)METS]、6 min步行距离[(258.9±22.59)m∶(226.17±17.03)m],LVEF[(56.4±6.25)%∶(50.4±6.84)%]、E/A1(40例∶29例)、抑郁[(1.5±0.6)∶(2.0±0.5)]、焦虑[(1.4±0.7)∶(1.9±0.8)]较对照组明显改善(P均0.05)。结论:两周康复程序增加急性心肌梗塞患者运动能力,减轻焦虑、抑郁症状,提高生活质量,值得推广。     

纳洛酮试验在急性脑梗死溶栓治疗前的应用价值探讨

目的　探讨纳洛酮试验在急性脑梗死溶栓治疗前的应用价值。方法　 33例急性脑梗死患者溶栓治疗前进行纳洛酮试验 ,观察静脉溶栓前后神经功能变化 ,同时观察颅内出血的副作用。结果　纳洛酮试验神经功能缺损评分减少 8分的 2 5例为A组 ,减少不足 8分或评分增加的 8例为B组 ,A组神经功能缺损评分溶栓治疗前(2 4 6 0± 5 2 0 )分 ,治疗后 (5 10± 3 2 0 )分 (P <0 0 1) ,而B组溶栓治疗前 (2 3 90± 4 2 0 )分 ,治疗后 (18 70± 6 2 0 )分 (P >0 0 5 ) ;A组发生颅内出血 1例 ,B组发生 3例 (P <0 0 1)。结论　纳洛酮试验阳性患者溶栓治疗疗效好 ,且颅内出血机率小 ,在溶栓治疗前纳洛酮试验能起到初步筛选病例的作用     

rt-PA静脉溶栓治疗在高龄急性心肌梗死患者中的近期疗效研究

目的　探讨静脉溶栓治疗对高龄 (70岁以上 )急性心肌梗死 (AMI)患者的疗效。　方法　对比分析用重组组织型纤溶酶原激活剂 (rt PA) 5 0mg静脉溶栓治疗与非溶栓治疗的高龄AMI患者各 86例住院期间临床疗效。　结果　溶栓组住院期间 4周内病死率 1 2 8%(1 1 86 )明显低于非溶栓组 31 4%(2 7 86 ) (P <0 0 5 ) ,心绞痛、心力衰竭、严重心律失常、心源性休克的发生率明显低于非溶栓组 (P <0 0 5 )。冠脉造影 ,TIMI分级 ,溶栓组梗死相关血管 (IRA)开通率为 6 5 0 %(5 6 86 ) ,距发病溶栓时间 6小时以内IRA开通率为 80 4%(45 5 6 ) ,非溶栓组开通率仅32 %,溶栓病人未发生颅内出血及过敏反应。　结论　提示用rt PA静脉溶栓治疗高龄AMI患者为一种安全有效的方法 ,并有利于AMI的近期预后改善。     

58例急性心肌梗塞早期室颤电除颤后静脉溶栓的疗效

目的:探讨电除颤成功的早期急性心肌梗塞(AMI)患者静脉溶栓治疗的疗效。方法:58例AMI早期(2 h 内)室颤患者采用非同步电击除颤法复律成功后,随机应用尿激酶或重组组织型纤维蛋白溶酶原激活剂静脉溶栓,观察其再通率,并发症,2周内死亡率,并于2周后进行心功能评估。结果:血管再通率81％,无严重并发症,无1例死亡,心功能评估满意。结论:AMI早期(2 h内)室颤患者在复苏成功后迅速进行静脉溶栓治疗安全、有效。     

急性心肌梗塞溶栓治疗期间血浆D-二聚体的动态变化及其临床意义

目的 :探讨血浆 D-二聚体对评价溶栓治疗急性心肌梗塞 (AMI)的价值及意义。　　方法 :2 9例 AMI患者分为溶栓组 (n=2 1) ,未溶栓组 (n=8) ;溶栓组根据溶栓治疗后冠状动脉 (冠脉 )是否开通又分为溶栓再通组 (n=12 ) ,溶栓未通组 (n=9) ;采用酶联免疫吸附试验 (EL ISA)法检测血浆 D-二聚体的水平 ,并与正常对照组 (n=2 0 )进行比较。　　结果 :AMI未溶栓组血浆 D-二聚体较正常对照组显著升高 (P<0 .0 5 ) ;溶栓组血浆 D-二聚体较未溶栓组显著升高(P<0 .0 5 ) ,溶栓后血浆 D-二聚体较溶栓前显著升高 (P<0 .0 1) ,于溶栓后 6小时达高峰 ;溶栓再通组血浆 D-二聚体较溶栓未通组显著升高 ,溶栓前及溶栓后 6小时两组比较有极显著统计学意义 (P<0 .0 1)。　　结论 :AMI早期已有纤溶系统亢进 ,应用溶栓药后进一步激活纤溶系统而发挥作用 ,且以溶栓再通组更显著。     

Quadruple,sequential, and concomitant first-line therapies for H. pylori eradication: a prospective,randomized study

BackgroundCurrent Italian guidelines recommend 10-day bismuth-based or bismuth-free (sequential and concomitant) regimens for first-line H. pylori eradication. However, comparison among these regimens is lacking in our country.AimTo perform a ‘head-to-head’ comparison among these three therapies as first-line treatment for H. pylori eradication in clinical practice.MethodsThis was a prospective, open-label randomized study enrolling consecutive patients diagnosed with H. pylori infection never previously treated. Patients were randomized to receive one of the following 10-day therapies: (a) Bismuth-based therapy: esomeprazole 20 mg b.i.d and Pylera 3 tablets q.i.d; (b) Concomitant therapy: esomeprazole 20 mg plus amoxicyllin 1,000 mg, clarithromycin 500 mg and tinidazole 500 mg (all b.i.d.), and (c) Sequential therapy: esomeprazole 20 mg plus amoxicyllin 1,000 mg for 5 days followed by esomeprazole 20 mg plus clarithromycin 500 mg and tinidazole 500 mg for 5 days (all b.i.d). H. pylori eradication was assessed by using UBT 4-6 weeks after the end of therapy.ResultsOverall, 187 patients were enrolled. The eradication rates achieved with Pylera, concomitant and sequential were 85.2%, 95.2%, and 93.6%, respectively, at intention to treat, and 94.5%, 96.7%, and 95.1% at per protocol analyses, without a statistically significant difference. The incidence of severe side-effects was higher with the bismuth-based therapy than with the two bismuth-free regimens (9.8% vs 1.6%; p = 0.046).ConclusionsBismuth-based and bismuth-free therapies are equally effective for first-line H. pylori eradication. However, bismuth therapy was more frequently interrupted for side-effects than bismuth-free therapies.     

Mutant KRAS is a druggable target for pancreatic cancer

Pancreatic ductal adenocarcinoma (PDA) represents an unmet therapeutic challenge. PDA is addicted to the activity of the mutated KRAS oncogene which is considered so far an undruggable therapeutic target. We propose an approach to target KRAS effectively in patients using RNA interference. To meet this challenge, we have developed a local prolonged siRNA delivery system (Local Drug EluteR, LODER) shedding siRNA against the mutated KRAS (siG12D LODER). The siG12D LODER was assessed for its structural, release, and delivery properties in vitro and in vivo. The effect of the siG12D LODER on tumor growth was assessed in s.c. and orthotopic mouse models. KRAS silencing effect was further assessed on the KRAS downstream signaling pathway. The LODER-encapsulated siRNA was stable and active in vivo for 155 d. Treatment of PDA cells with siG12D LODER resulted in a significant decrease in KRAS levels, leading to inhibition of proliferation and epithelial–mesenchymal transition. In vivo, siG12D LODER impeded the growth of human pancreatic tumor cells and prolonged mouse survival. We report a reproducible and safe delivery platform based on a miniature biodegradable polymeric matrix, for the controlled and prolonged delivery of siRNA. This technology provides the following advantages: (i) siRNA is protected from degradation; (ii) the siRNA is slowly released locally within the tumor for prolonged periods; and (iii) the siG12D LODER elicits a therapeutic effect, thereby demonstrating that mutated KRAS is indeed a druggable target.Pancreatic cancer is an aggressive disease that develops in a relatively symptom-free manner and in most cases, is already advanced at the time of diagnosis (1). It has one of the highest fatality rates of all cancers and is one of the leading causes of cancer-related deaths in the Western world (1, 2). Pancreatic ductal adenocarcinoma (PDA) is the most common pancreatic neoplasm, responsible for 95% of pancreatic cancer cases (3). Genetic alterations in the KRAS signaling pathway are involved in over 90% of pancreatic cancer cases (4–6). KRAS mutations were shown to be an early event in the development of pancreatic cancer (5, 7, 8).The most common KRAS mutation of the human pancreas adenocarcinoma is a gain-of-function substitution mutation of glycine at codon 12 to aspartate (G12D) (5, 9–11). Moreover, PDA cancer cell growth was shown to be dependent on the activity of the mutated KRAS (5, 11) and accordingly, silencing KRAS has proven effective in controlling pancreatic cell line proliferation (12). Here, we aimed to harness the advantages of siRNA technology as a therapeutic modality for pancreatic cancer.Parenteral controlled drug delivery systems are used to improve and advance the therapeutic effects of drug treatments by providing optimized local drug concentrations over prolonged periods of time, reduction of side effects, and cost reduction (13). A prominent method of controlling the release rate of a drug in a pharmaceutical dosage is to embed the active agent within a polymeric matrix (14, 15). The polymer must be biocompatible, and in the case of parenteral administration, preferably biodegradable, to avoid the need to remove empty remnants.In the present study, we exploited the slow-release characteristics of the biodegradable polymer matrix, which we named local drug eluter (LODER) for the treatment of solid tumors.     

Mapping the molecular determinants of BRAF oncogene dependence in human lung cancer

Oncogenic mutations in the BRAF kinase occur in 6–8% of nonsmall cell lung cancers (NSCLCs), accounting for more than 90,000 deaths annually worldwide. The biological and clinical relevance of these BRAF mutations in NSCLC is incompletely understood. Here we demonstrate that human NSCLC cells with BRAF^V600E, but not other BRAF mutations, initially are sensitive to BRAF-inhibitor treatment. However, these BRAF^V600E NSCLC cells rapidly acquire resistance to BRAF inhibition through at least one of two discrete molecular mechanisms: (i) loss of full-length BRAF^V600E coupled with expression of an aberrant form of BRAF^V600E that retains RAF pathway dependence or (ii) constitutive autocrine EGF receptor (EGFR) signaling driven by c-Jun–mediated EGFR ligand expression. BRAF^V600E cells with EGFR-driven resistance are characterized by hyperphosphorylated protein kinase AKT, a biomarker we validated in BRAF inhibitor-resistant NSCLC clinical specimens. These data reveal the multifaceted molecular mechanisms by which NSCLCs establish and regulate BRAF oncogene dependence, provide insights into BRAF–EGFR signaling crosstalk, and uncover mechanism-based strategies to optimize clinical responses to BRAF oncogene inhibition.The discovery of genetic alterations that drive tumor growth in a wide variety of tumor types and the development of targeted therapies acting against these oncogenic drivers have revolutionized the management of many cancer patients (1). Paradigmatic examples of the successful use of oncogene-targeted therapy include the identification and treatment of patients who have EGF receptor (EGFR)-mutant and ALK fusion-positive lung cancer with the tyrosine kinase inhibitors erlotinib and crizotinib, respectively, and of patients who have BRAF^V600E-melanoma with the selective BRAF kinase inhibitor vemurafenib. The clinical success of driver oncogene-targeted therapy arises because of tumor cell oncogene dependence that is established during tumorigenesis, but the mechanistic basis of this dependence remains incompletely understood. Filling this knowledge gap is critical, because the clinical success of driver oncogene-targeted therapies is limited by the almost inevitable escape from oncogene dependence and drug resistance that occur in patients with solid tumors, including lung cancer, the leading cause of cancer mortality worldwide (2, 3). The identification of the signaling events driving resistance provides insights into the molecular mechanisms underlying oncogene dependence and a rationale for mechanism-based polytherapy strategies to subvert resistance in patients (2, 4, 5).The BRAF gene is mutated in ∼7% of human cancers, including melanoma, colorectal, papillary thyroid, and NSCLC (6, 7). The BRAF^V600E variant is the most frequent mutant allele and has been used to match patients genetically to BRAF-inhibitor therapy. The clinical success and approval of the BRAF inhibitors vemurafenib and dabrafenib in BRAF^V600E melanoma have provided a rationale for testing BRAF inhibition in nonmelanoma patients whose tumors harbor BRAF mutations (8–10). The success of such efforts has been limited, with either BRAF-inhibitor treatment or downstream MAPK blockade failing to produce the desired clinical activity in patients with colorectal and thyroid cancers harboring BRAF^V600E; in both cases the failure is caused by intrinsic resistance (11–13). These observations indicate that tumor cell oncogene dependence is context specific and underscore the need to define the molecular events that regulate oncogene dependence in each tumor type to optimize clinical responses.Somatic mutations in BRAF (both V600E and non-V600E variants) are found in 6–8% of NSCLCs, accounting for more than 90,000 deaths annually worldwide. BRAF-mutant NSCLCs frequently harbor the V600E allele (∼55%); additional highly recurrent activating BRAF variants reported in NSCLC include G469A (∼35%) and D594G (∼10%) (14–17). The sensitivity of NSCLC cells across the spectrum of BRAF mutant alleles to BRAF-inhibitor treatment has not been characterized. Despite this uncertainty regarding allelotype specificity, the clinical efficacy of BRAF-inhibitor treatment in BRAF^V600E-melanoma has prompted a clinical trial testing the efficacy of BRAF-inhibitor treatment in patients with BRAF^V600E NSCLC. Given the emerging biological and clinical importance of mutant BRAF and the success (and limitations) of other oncogene-targeted therapies, including EGFR and ALK kinase inhibitors, in NSCLC patients, we sought to define the molecular basis of BRAF oncogene dependence in NSCLC. We investigated and uncovered critical events driving response and resistance to BRAF-inhibitor treatment in models of human BRAF-mutant NSCLC. Our findings provide insight into the regulation of BRAF oncogene dependence and reveal rational strategies for immediate clinical use to enhance patients’ responses to BRAF inhibitors.     

Eradication of Helicobacter pylori infection

Eradication of Helicobacter pylori infection has become an important issue recently, because this bacterial species cluster can cause many gastrointestinal diseases. Elevated antibiotic resistance is related to an increasing failure rate of H. pylori eradication. Standard triple therapy is still the first-line therapy; however, according to the Maastricht IV Consensus Report, it should be abandoned in areas of high clarithromycin resistance. Alternative first-line therapies include bismuth-containing quadruple therapy, sequential, concomitant, and hybrid therapies. Quinolone-based triple therapy may be considered as first-line therapy in areas of clarithromycin resistance >15–20% and quinolone resistance <10%. Unique second-line therapy is still unclear, and bismuth-containing quadruple therapy or levofloxacin-based triple therapy can be used as rescue treatment. Third-line therapy should be under culture guidance to select the most effective regimens (such as levofloxacin-based, rifabutin-based, or furazolidone-based therapies). Antibiotics resistance, patient compliance, and CYP 2C19 genotypes could influence the outcome. Clinicians should use antibiotics according to local reports.     

Treating IPF—all or nothing? A PRO‐CON debate

The Idiopathic Pulmonary Fibrosis (IPF) is a progressive fibrotic lung disease with poor prognosis. It is distinct from other idiopathic interstitial pneumonias by its histopathological pattern of usual interstitial pneumonia which is characterized by accumulation of fibroblasts, extracellular matrix and honeycombing. Inflammation is only scarce in true IPF. The use of anti-inflammatory therapy is still part of guidelines for IPF management, although not specifically recommended, because convincing evidence showing beneficial effects of this approach is lacking. This review provides a summary of important arguments PRO and CON using anti-inflammatory and anti-oxidant therapy for patients with IPF in form of a debate with a concluding statement of both positions at the end.     

Endoscopic alcohol injection therapy of giant gastric leiomyomas: an alternative method to surgery

Leiomyomas are the most common benign mesenchymal tumours of the upper gastrointestinal tract. They rarely cause symptoms when they are smaller than 5 cm in diameter. Observation with repeated endoscopies is recommended in asymptomatic patients with small lesions. Surgical resection remains the main therapy option for symptomatic and complicated patients. The treatment of esophageal leiomyoma has been enhanced by improvements in diagnostic and therapeutic endoscopic techniques; however, the same cannot be said for gastric leiomyoma management. The present article describes the management of two cases involving giant gastric leiomyomas that were  successfully treated using endoscopic injection of alcohol. To the authors' knowledge, the present study is the first report of the treatment of such hemorrhagic gastric tumours using this alternative and low-cost technique. Endoscopic local ethanol injection may be the treatment of choice in carefully selected patients with hemorrhagic leiomyomas of the upper gastrointestinal tract.     

The Steroid-Sparing Effect of Long-Term Plasmapheresis in Pemphigus: An Update

Abstract: Glucocorticoids and immunosuppressive agents can induce remission in most pemphigus patients, but mortality remains at 5 to 15% as a result of side effects. We reviewed the adjunctive effect of long-term plasmapheresis in 8 pemphigus patients. Four cases had been resistant to conventional therapy. One or 2 large-volume plasmapheresis treatments were given monthly over 5 to 141 months. All patients, were in clinical remission within 2 months. Relapses seldom occurred: the patients stayed in remission 90% (40–94) (median, ranges) of the period. In all cases the daily dose of glucocorticoid was reduced. The prednisone level could be decreased from 38 (15–80) mg/day to 7.5 (2.5–35) mg/day (p = 0.002). The overall level of other immunosuppressive agents remained unchanged, except in 1 patient for whom cyclosporine was introduced. This indicates that long-term plasmapheresis could have a steroid-sparing effect and clinical efficacy in pemphigus.—     

胰腺癌治疗进展

胰腺癌是高度恶性的消化系统肿瘤，约90%起源于腺管上皮的导管腺癌，其发病率和死亡率近几年明显上升，5年生存率<6%，是预后最差的恶性肿瘤之一。该病早期确诊率较低，手术死亡率较高。男女发病率之比约为(1.5～2)∶1，其治疗方案由单一手术治疗转为多学科综合治疗。近几年内外科治疗方案并无太多新的突破，分子靶向治疗的热度逐年上升，其重要性也越来越引起专家的重视，部分治疗靶点已经应用于临床，并取得可喜的治疗效果。     

四联疗法与序贯疗法在幽门螺杆菌根除补救治疗中的疗效比较

[目的]比较四联疗法与序贯疗法在幽门螺杆菌(Hp)根除补救治疗中的疗效及安全性,旨在寻找一种有效、安全、经济的补救治疗方案。[方法]将首次根除Hp治疗失败的90例慢性胃炎患者,随机分为四联疗法组和序贯疗法组,每组45例。四联疗法组患者治疗方案为埃索美拉唑、枸橼酸铋钾、阿莫西林、莫西沙星,疗程14d。序贯疗法组患者治疗方案为前5d给予埃索美拉唑、阿莫西林;后5d给予埃索美拉唑、克拉霉素、奥硝唑。所有患者在疗程结束停药4周后行14 C尿素呼气试验检测Hp。比较2组患者治疗前后的不良反应。[结果]四联疗法组Hp根除率(91.1%)显著高于序贯疗法组(75.6%),差异有统计学意义(P<0.05)。2组不良反应均很轻微,组间不良反应发生率比较差异无统计学意义(P>0.05)。[结论]对于Hp补救治疗,四联疗法较序贯疗法疗效更好,且不良反应小,患者依从性好,值得在临床上推广。     

肥胖症的药物治疗现状与展望

肥胖是一个严重的公众健康问题，人们迫切希望能有安全、有效的减肥药物。目前用于减肥的药物主要有两类：即西布曲明和赛尼可，前者主要抑制食物的摄取，后者抑制脂肪的吸收。由于对复杂的体重调节机制的认识越来越深入，很多新的减肥药物正在研制过程之中。目前正在研究的具有较大潜力的减肥药物共有30余种，其中研究较多的有瘦素、黑皮质素受体激动剂、神经肽Y拮抗剂、β3肾上腺素能受体激动剂、胰高血糖素样肽－1激动剂以及激活或增加解偶联蛋白表达的药物。