溃疡性结肠炎和克罗恩病临床特征分析

背景:溃疡性结肠炎(UC)和克罗恩病(CD)的发病率逐年升高,且极易误诊。目的:分析UC和CD的临床特征。方法:收集2003年1月～2012年6月湖南省人民医院83例UC和28例CD病例,回顾性分析患者的病变范围、实验室检查、并发症、治疗和误诊特点。结果:UC患者明显多于CD患者,UC病变部位以左半结肠为主,CD以回肠、末端回肠为主。UC病变范围和病情程度与CD相比差异均有统计学意义(P<0.05)。UC、CD患者血红蛋白(Hb)、白蛋白(ALB)降低,红细胞沉降率(ESR)、C反应蛋白(CRP)升高,但两者相比无明显差异(P>0.05)。CD常见并发症为肠梗阻、肛瘘,其并发症发生率显著高于UC(P<0.05)。UC治疗以氨基水杨酸为主,CD以手术治疗更多见。UC的复发率、误诊率与CD相比均无明显差异(P>0.05)。结论:UC患者以轻中度为主,并发症较少,治疗以内科治疗为主;重度CD患者多见,并发症多,手术率相对较高。UC和CD的复发率和误诊率均高,应早诊断、早治疗。     

炎症性肠病发病机制与治疗研究的最新进展

炎症性肠病(IBD)的传统治疗着眼于控制活动性炎症和调节免疫紊乱，常用的三类药物(水杨酸类、类固醇激素和免疫抑制剂)对克罗恩病(CD)与溃疡性结肠炎(UC)的缓解率分别仅70％与80％左右，最佳的维持缓解方案也仅能使复发率降低50％左右，分别约有2／3与1／3的病例最终需手术治     

溃疡性结肠炎合并巨细胞病毒感染的临床特点及转归

[目的]分析溃疡性结肠炎(UC)合并巨细胞病毒(CMV)感染的临床特点及治疗转归,探讨UC合并CMV感染的风险因素及预后。[方法]收集2013-01-01-2016-12-31期间于本院确诊为UC并进行CMV感染相关检测的全部住院患者,采用回顾性病例调查方法,记录CMV检测阳性(CMV阳性组)患者的人口学资料、临床特点、内镜表现、治疗及转归,并与同期住院的CMV检测阴性(CMV阴性组)的UC患者进行比较,通过单因素和多因素统计分析,评价UC合并CMV感染的危险因素。[结果]110例UC患者中UC合并CMV感染23例(23/110;20.9%);CMV阳性组病情明显重于CMV阴性组:发热、腹痛、体质量下降多见,血红蛋白、血白蛋白、血钠水平较低,而红细胞沉降率、C反应蛋白水平较高;CMV感染在中重度病例多见(91.3%)。CMV阳性组糖皮质激素依赖及抵抗者多于CMV阴性组,入院前3个月内糖皮质激素的使用率也显著高于CMV阴性组。在内镜表现方面,CMV阳性组深大溃疡多见。CMV阳性组住院时间明显长于CMV阴性组。多因素Logistic回归分析显示,入院前3个月内应用糖皮质激素是CMV感染的危险因素,血白蛋白水平较高是CMV感染的保护因素(P0.05)。CMV阳性组中,21例接受了抗病毒药物更昔洛韦治疗,治疗后20例好转;1例UC患者药物治疗效果欠佳,行手术治疗后好转。[结论]UC患者特别是中重度UC患者合并CMV感染比较常见,近期应用糖皮质激素治疗是合并CMV感染的危险因素。UC合并CMV感染者糖皮质激素依赖及抵抗的概率明显升高。UC合并CMV感染可使UC病情加重、复杂化,给治疗带来困难。对于合并CMV感染的UC患者进行抗病毒治疗对改善病情可能有一定意义。     

昆明市379例溃疡性结肠炎患者治疗分析

目的 回顾性调查昆明市近10年来溃疡性结肠炎(UC)住院病例的资料,以进一步了解昆明市UC患者的治疗状况.方法 选取昆明市1998年1月～2007年3月期间7家大型综合医院379例住院的炎症性肠病患者作为调查对象.诊断均符合2007年中华医学会消化病学分会的UC诊治标准,分析UC患者的治疗状况.结果 379例UC患者有...     

溃疡性结肠炎患者手术治疗预测因素分析

手术是溃疡性结肠炎（UC）内科治疗无效或发生严重并发症者的治疗选择.目的：分析UC患者行手术治疗的可能预测因素.方法：纳入1998年8月～2009年9月北京协和医院住院UC患者312例,其中34例接受手术治疗,278例接受非手术治疗,回顾性分析、比较两组患者的各类临床资料.结果：住院UC患者手术率为10.9%,手术死亡率为5.9%,重度UC患者手术率为23.9%.手术组13例患者为激素抵抗,8例为激素依赖,9例发生严重并发症,4例激素治疗有效者主动要求手术治疗.手术组平均住院次数显著多于非手术组（P〈0.05）,术前Hb、白蛋白显著低于非手术组（P〈0.05）,CRP显著高于非手术组（P〈0.05）,重度结肠炎、全结肠炎患者比例显著高于非手术组（P〈0.05）.结论：疾病严重程度高、病变范围广、对激素抵抗的UC患者,手术需求增加.     

中国溃疡性结肠炎诊治规范的解析

溃疡性结肠炎(UC)在我国的发病率呈上升趋势,严重危害人民健康。迄今我国已发布4版UC诊断治疗规范,这些版本在涉及UC诊断治疗的各个方面均出现了较大的变化,体现了我国消化内科在UC诊治过程中对该病的理解不断深入、诊疗手段逐渐丰富方面,取得了长足的进步和发展,但我国UC的外科治疗与发达国家相比存在较大差距,包括手术指征、手术时机和术式规范等多个方面。本文从诊断标准、诊断内容、疗效标准和治疗建议等方面对我国UC诊治规范的演变进行解读分析,并针对我国UC的临床现状进行总结,对未来的发展趋势和工作方向进行展望。     

重视炎症性肠病的临床研究

炎症性肠病(Inflammatory bowel disease,IBD)包括溃疡性结肠炎(UC)和克罗恩病(CD),在西方国家相当常见,最新统计资料显示二者患病率最高者均在200人/105左右.国内近年报道逐渐增多,据不完全统计二者病例总数已超过2万,其中尤以UC为多,是主要的胃肠道疾病和慢性腹泻的主要原因,其临床诊断与治疗变得复杂而棘手,因此,受到同行普遍重视.有研究指出,初诊时的UC大约有50%最终证实为感染性结肠炎(IC),而CD与肠结核相互误诊率有的高达70%,对此不可掉以轻心.传统的治疗对UC和CD的缓解率分别为80%和70%左右.在维持缓解方面,有报道指出即使最佳的维持治疗方案也仅能使复发率降低50%左右.国人维持治疗意识差、药物种类有限,短期治疗后停药更易导致疾病复发.UC与CD最终分别有1/3与2/3的病例需要手术,使疾病致残率高,生活质量受到相当大的影响.因此,应对IBD的诊断与治疗问题引起足够重视.     

中药治疗大鼠湿热型溃疡性结肠炎的疗效观察

[目的]研究中药对大鼠湿热型溃疡性结肠炎(UC)的治疗效果。[方法]将80只SPF级雄性wistar大鼠随机分为对照组(A组)、模型组(B组)、西药组(C组)、中药组(D组),每组20只。A组正常饲养,B、C、D组建立大鼠湿热证UC模型,建模成功第2天,B组大鼠以生理盐水灌胃,C组以美沙拉嗪灌胃治疗,D组以化湿疏郁方灌胃治疗,给药疗程7 d。观察指标包括症状学、结肠黏膜及病理组织学。[结果]造模后,与A组相比,B、C、D组大鼠均出现摄食量、摄水量、活动性减低及血便,B组疾病活动指数(DAI)评分明显升高(P<0.05),大体形态损伤指数(CMDI)评分明显升高(P<0.05);治疗7 d后,与B组相比,C组、D组大鼠摄食量、摄水量、活动性明显增加,DAI评分明显降低(P<0.05);且治疗7 d后,与B组相比,C组、D组大鼠结肠黏膜出血、溃疡,充血、水肿现象明显减轻,CMDI评分显著降低(P<0.05);C组、D组大鼠结肠黏膜病理观察细胞排列结构比较整齐、少量杯状细胞消失及淋巴细胞和中性粒细胞浸润。[结论]大鼠湿热证UC模型制备成功,化湿疏郁方可改善UC大鼠一般情况,增高湿热型UC模型大鼠黏膜愈合率(肉眼+病理学),治疗湿热型UC疗效肯定。     

Ⅰ型干扰素治疗溃疡性结肠炎有效性的荟萃分析

目的:采用荟萃分析的方法对Ⅰ型干扰素治疗溃疡性结肠炎(ulcerative colitis,UC)的有效性进行系统评价.方法:检索Pub Med、EMBASE、CNKI中国期刊全文数据库、CBM中国生物医学文献数据库、万方数据库中所有关于Ⅰ型干扰素治疗UC的随机对照研究.应用比值比(odds ratio,OR)及其95%CI为疗效分析统计量,采用Rev Man5.1进行荟萃分析,比较干扰素与安慰剂治疗UC的有效缓解率及严重不良反应发生率.结果:共4篇文献纳入荟萃分析.结果显示,Ⅰ型干扰素治疗UC与安慰剂相比,有效缓解率无明显差异(OR=1.23,95%CI:0.76-2.01,P=0.40),严重不良反应发生率无明显差异(OR=1.44,95%CI:0.21-9.82,P=0.71).结论:应用Ⅰ型干扰素治疗UC患者,其疗效不优于安慰剂.     

生物制剂治疗中重度溃疡性结肠炎的研究进展

溃疡性结肠炎(UC)是一种病因尚不明确、反复发作、迁延进展的肠道非特异性炎症性疾病.近年来生物制剂已用于治疗UC,其疗效优于传统的治疗药物,但也带来诸多不可避免的问题.本文就生物制剂在中重度UC中的应用、药物浓度监测以及用药过程中的特殊情况和处理作一综述.     

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。