Guidelines for the Treatment of Chronic Constipation
慢病管理 慢性肾脏病 操作流程
慢病管理慢性肾脏病操作流程1.科学饮食是慢性肾脏病管理的重要环节。
Scientific diet is an important part of the management of chronic kidney disease.2.慢性肾脏病患者应遵循肾病饮食指导原则。
Patients with chronic kidney disease should follow the dietary guidelines for kidney disease.3.控制蛋白质摄入是慢性肾脏病管理的关键。
Controlling protein intake is crucial for the management of chronic kidney disease.4.减少高钾食物的摄入有助于减轻肾脏负担。
Reducing the intake of high-potassium foods helps to reduce the burden on the kidneys.5.限制高磷食物的摄入对于肾脏健康非常重要。
Limiting the intake of high-phosphorus foods is very important for kidney health.6.积极控制高血压有助于延缓慢性肾脏病的进展。
Actively controlling high blood pressure helps to delay the progression of chronic kidney disease.7.定期监测血压和血糖是慢性肾脏病管理的必要步骤。
Regular monitoring of blood pressure and blood sugar is a necessary step in the management of chronic kidney disease.8.减轻肥胖有助于改善肾脏功能。
2016年04月急性冠脉综合征治疗新药临床研究指导原则.(英文版)
30 Churchill Place ● Canary Wharf ● London E14 5EU ● United Kingdom1 April 2016 1 EMA/CHMP/207892/20152 Committee for medicinal products for human use (CHMP)3 Guideline on clinical investigation of new medicinal 4products for the treatment of acute coronary syndrome 5(CPMP/EWP/570/98) 6Draft7 Draft agreed by Cardiovascular Working PartyFebruary 2016 Adopted by CHMP for release for consultation1 April 2016 Start of public consultation 27 April 2016 End of consultation (deadline for comments)31 October 2016 8 This guideline replaces 'Points to consider on the clinical investigation of new medicinal products for the 9 treatment of acute coronary syndrome (ACS) without persistent ST segment elevation' 10 (CPMP/EWP/570/98). 1112 Comments should be provided using this template . The completed comments form should be sent to CVSWPSecretariat@ema.europa.eu .13Keywords Acute coronary syndrome, STE-ACS, NSTE-ACS, guideline, CHMP1415Table of contents16Executive summary (4)171. Introduction (background) (4)182. Scope (5)193. Legal basis and relevant guidelines (5)204. Choice of efficacy criteria (endpoints) (6)214.1. All-cause mortality and CV mortality (6)224.2. New myocardial infarction (6)234.3. Revascularisation (6)244.4. Unstable angina pectoris necessitating hospitalisation (6)254.5. Stent thrombosis (6)264.6. Stroke (7)274.7. Left ventricular function and heart failure (7)284.8. Composite endpoints (7)294.9. Endpoints in fibrinolysis studies (7)305. Methods to assess efficacy (how to measure the endpoints) (8)315.1. Mortality (8)325.2. New myocardial infarction (8)335.3. Revascularisation (8)345.4. Unstable angina pectoris necessitating hospitalisation (8)355.5. Stent thrombosis (8)365.6. Ventricular function and heart failure (9)375.7. Angiographic endpoints (9)386. Selection of patients (9)396.1. Study population (9)406.1.1. STE-ACS (ST elevation acute coronary syndrome) (9)416.1.2. NSTE-ACS (Non-ST elevation acute coronary syndrome) (9)426.1.3. Unstable angina (9)436.2. Inclusion criteria for the therapeutic studies (10)446.3. Exclusion criteria for the therapeutic studies (10)456.4. Risk Stratification (10)466.5. Special populations (11)476.5.1. Older patients (11)487. Strategy and design of clinical trials (11)497.1. Clinical pharmacology (11)507.2. Therapeutic exploratory studies (12)517.2.1. Objectives (12)527.2.2. Design (12)537.3. Confirmatory Therapeutic Studies (12)547.3.1. Objectives (12)557.3.2. Background therapy (12)567.3.3. Choice of comparator (13)577.3.4. Duration of clinical studies (13)587.3.5. Analyses and subgroup analysis (13)598. Safety aspects (14)608.1. Bleedings (14)618.2. All-cause mortality (15)628.3. Thrombocytopenia (15)638.4. Rebound effect (15)648.5. Effects on laboratory variables (15)658.6. Effects on concomitant diseases (15)66References (16)6768Executive summary6970Two CHMP Guidelines have been previously developed to address clinical investigations of new71medicinal products for the treatment of acute coronary syndrome (ACS): (I) the CHMP points toconsider (PtC) on the clinical investigation of new medicinal products for the treatment of acute7273coronary syndrome without persistent ST-segment elevation (CPMP/EWP/570/98), published in 2000 74[1], and (II) the CHMP PtC on the clinical development of fibrinolytic products in the treatment of75patients with ST segment elevation myocardial infarction (CPMP/EWP/967/01), published in 2003 [2].76Since their finalisation, major developments have taken place in the definitions, diagnosis,77interventions and management of ACS, as reflected in the relevant European Society of Cardiology78(ESC) clinical practice guidelines (3, 4). Currently, an update of the above mentioned CHMP Guidelines 79is considered necessary to take these new developments into consideration based on literature review 80and experience gained with medicinal products intended for treatment during the acute phase and81beyond. The present update includes the following changes: 1) guidance addressing both ST-segment 82elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction83(NSTEMI), as well as unstable angina (UA), 2) update in their definitions, 3) risk stratification using84different scoring systems, 4) investigated endpoints, and 5) clinical developments of new medicinal85products beyond the acute stage, including agents other than antiplatelets and anticoagulants.1. Introduction (background)8687Cardiovascular diseases are currently the leading cause of death in industrialized countries and also 88expected to become so in emerging countries by 2020 [3, 4]. Among these, coronary artery disease 89(CAD) is the most prevalent manifestation and is associated with high mortality and morbidity. ACS 90has evolved as a useful operational term to refer to any constellation of clinical symptoms that are91compatible with acute myocardial ischemia. It encompasses (STEMI), NSTEMI, and UA.92ACS represents a life-threatening manifestation of atherosclerosis. It is usually precipitated by acute 93thrombosis induced by a ruptured or eroded atherosclerotic coronary plaque, with or without94concomitant vasoconstriction, causing a sudden and critical reduction in blood flow. In the complex95process of plaque disruption, inflammation was revealed as a key pathophysiological element. Non-96atherosclerotic aetiologies are rare e.g. such as arteritis and dissection.97The leading symptom of ACS is typically chest pain. Patients with acute chest pain and persistent (>20 min) ST-segment elevation have ST-elevation ACS (STE-ACS) that generally reflect an acute total9899coronary occlusion. Patients with acute chest pain but without persistent ST-segment elevation have 100rather persistent or transient ST-segment depression or T-wave inversion, flat T waves, pseudo-101normalization of T waves, or no ECG changes. At presentation, based on the measurement of102troponins, it is possible to further discriminate between the working diagnosis of non-ST-elevation ACS 103(NSTE-ACS) and unstable angina.104NSTE-ACS is more frequent than STE-ACS [5] with an annual incidence around 3 per 1000 inhabitants, 105but varying between countries [6]. Hospital mortality is higher in patients with STEMI than among 106those with NSTEMI (7% vs. 3–5%, respectively), but at 6 months the mortality rates are very similar 107in both conditions (12% and 13%, respectively) [5,7,8]. Long term follow-up shows that death rates 108were higher among patients with NSTE-ACS than with STE-ACS, with a two-fold difference at 4 years[8]. This difference in mid- and long-term evolution may be due to different patient profiles, since 109110NSTE-ACS patients tend to be older with more co-morbidities, especially diabetes and renal failure.2. Scope111112The aim of this guideline is to provide guidance when performing trials to develop medicinal products 113in the management of ACS. The primary goals of therapy for patients with ACS are to:1. Treat acute, life-threatening complications of ACS, such as serious arrhythmias, pulmonary 114115oedema, cardiogenic shock and mechanical complications of acute myocardial infarction (AMI). [9] 1162. Reduce the amount of myocardial necrosis that occurs in patients with AMI, thus preserving 117left ventricular (LV) function, preventing heart failure (HF), and limiting other cardiovascular118complications.1193. Prevent major adverse cardiac events like death, non-fatal myocardial infarction (MI), andneed for urgent revascularization.120121The focus in this Guideline concerns mainly the medical treatment of ACS (treatment goals 2 and 3). 122The choice of interventional procedures [percutaneous coronary intervention (PCI) or coronary artery 123bypass graft CABG)] falls outside the scope of this guideline.3. Legal basis and relevant guidelines124125This guideline has to be read in conjunction with the introduction and general principles and parts I 126and II of the Annex I to Directive 2001/83 as amended.127Pertinent elements outlined in current and future EU and ICH guidelines, should also be taken into 128account, especially those listed below:129•Dose-Response Information to Support Drug Registration (ICH E4; CPMP/ICH/378/95).130•Statistical Principles for Clinical Trials (ICH E9; CPMP/ICH/363/96).131•Choice of Control Group and Related Issues in Clinical Trials (ICH E10; CPMP/ICH/364/96).132•Points to consider on an Application with 1) Meta-analyses 2) One pivotal study133(CPMP/EWP/2330/99).134•Points to consider on multiplicity issues in clinical trials (CPMP/EWP/908/99).135•Investigation of subgroups in confirmatory clinical trials (EMA/CHMP/539146/2013).136•The Extent of Population Exposure to Assess Clinical Safety for Drugs (ICH E1A;137CPMP/ICH/375/95).138•Pharmacokinetic Studies in Man (3CC3A).139•Studies in Support of Special Populations: Geriatrics (ICH E7 CHMP/ICH/379/95) and related Q&A 140document (EMA/CHMP/ICH/604661/2009).141•Note for Guidance on the Investigation of Drug Interactions (CPMP/EWP/560/95).142•Reporting the Results of Population Pharmacokinetic Analyses (CHMP/EWP/185990/06).143•Reflection paper on the extrapolation of results from clinical studies conducted outside the EU to 144the EU-population (EMEA/CHMP/EWP/692702/2008).145•Draft Guideline on clinical investigation of medicinal products for the treatment of chronic heart 146failure (EMA/392958/2015 )•Guideline on clinical investigation of medicinal products for the treatment of acute heart failure147148(CPMP/EWP/2986/03 Rev. 1)4. Choice of efficacy criteria (endpoints)149150Definitions of clinical endpoints in confirmatory trials should be in line with the relevant clinical151guidelines to facilitate interpretation of the results, to allow comparisons across clinical studies and to 152extrapolate to clinical practice. Endpoints should be centrally adjudicated by a blinded committee. The 153following endpoints are relevant to the investigation of efficacy in patients with ACS.4.1. All-cause mortality and CV mortality154155As one of the goals of treatment of ACS is reduction of mortality, this is an important endpoint to156measure. There is an ongoing debate around the use of all-cause versus cardiovascular mortality in 157cardiovascular (CV) trials. All cause mortality is the most important endpoint in clinical trials for the 158estimation of the benefit-risk balance of a drug, in particular when investigating newer medicinal159products with possible safety issues. On the other hand, CV mortality is more specifically linked to the 160mode of action of CV medicinal products/intervention and is especially relevant when the earliest part 161of the follow up is assessed. The choice is also dependent on the objective of the study i.e. in non-162inferiority trials, CVmortality may be preferred while in superiority trials all cause mortality is usually 163used. In fibrinolysis studies, all cause mortality is preferred (see section 4.9).164As such, one of the two mortality endpoints should be included as a component of the primary165endpoint, with the other investigated as a key secondary endpoint.4.2. New myocardial infarction166167New onset MIis a relevant endpoint in studies of ACS and should always be investigated. The definition 168of MI has evolved through the years; at the time of drafting of this Guideline, the third universal169definition of MI is applicable [10]. Criteria of MI are the same as those used to define the index event 170(see below).4.3. Revascularisation171172Some clinical trials have included revascularization endpoints (PCI or CABG) as part of the primary 173composite with conflicting results [11, 12]. Such endpoints are considered more relevant tointerventional studies, and in the scope of this Guideline, their inclusion as a primary endpoint should 174175be clearly justified and their assessment pre-defined and systematically assessed.4.4. Unstable angina pectoris necessitating hospitalisation176177Unstable angina has been investigated in ACS clinical trials. Due to the varying definitions used, the 178associated subjectivity and the influence of local clinical practice, this endpoint is not encouraged to be 179included in the composite primary endpoint.4.5. Stent thrombosis180181Stent thrombosis (ST) is a rare event that can have fatal consequences. ST has been captured in some 182registration studies, but not consistently in the primary endpoint (PEP). The investigation of ST as part 183of the primary endpoint is not encouraged due to the uncertainty of the clinical relevance of all184captured events, except for the "definite" subcategory. Another category identified by the timing isintra-procedural stent thrombosis (IPST), which is a rare event indicating the development of occlusive 185186or non-occlusive new thrombus in or adjacent to a recently implanted stent before the PCI procedure is187completed. Some recent studies [13,14] show that these events may be of prognostic value. As such they should also be collected and presented as secondary endpoint but not included in the analysis of 188189ST.4.6. Stroke190191Stroke should be defined by a generally accepted definition [15]. Clinical studies in ACS have used192non-fatal stroke in the primary endpoint , including any types of strokes. However it is preferred to193include only ischemic strokes in the primary endpoint, as this is the true measure of efficacy;194haemorrhagic stroke should be included as a safety endpoint. An ischaemic stroke with haemorrhagic195conversion should be considered as “primary ischaemic”. The subgroup of “undefined strokes” should196be as small as possible in order to be able to properly assess the effect of the study treatment. In case 197all types of strokes are included in the primary endpoint, a sensitivity analysis including only ischemic198stroke should be submitted.4.7. Left ventricular function and heart failure199Some medicinal products such as modulators of reperfusion injury or inflammation, or gene/cell200201therapy are developed to improve myocardial function and reduce the occurrence of HF. In these202cases, measurement of myocardial function could be a relevant endpoint to investigate the mechanismof action. In phase III studies, these endpoints can be investigated as secondary endpoints to support 203204the clinical endpoints. Occurrence of HF should be considered as a clinical endpoint in phase III studies205aimed at showing benefit in long-term cardiovascular outcome. All-cause mortality and long term206follow-up are mandatory in studies with novel interventions.4.8. Composite endpoints207Due to the rather low incidence of cardiovascular events during the follow-up period after the acute 208209phase of the ACS, composite endpoints consisting of relevant components are acceptable, both as210primary and secondary endpoints. The composite of CV death, non-fatal MI and non-fatal stroke (Major211Adverse Cardiovascular Events, [MACE]) has commonly been used in registration studies, with non-212fatal strokes showing limited contribution to the results. As such, it is preferred to investigate the213composite of death and non-fatal MI in confirmatory studies; non-fatal ischaemic stroke could beincluded in the composite if justified. Sometimes different definitions of MACE are being used with214215novel therapies [16], that should be justified when used in place of MACE. The inclusion of less216objective and clinically derived outcomes in the same composite is generally not encouraged, as they217may either drive the efficacy or dilute the results. In case these endpoints are included they have to be218stringently defined, and adjudicated. Each component of the primary composite endpoint should be219analysed as secondary endpoint.220The net clinical benefit that includes both benefit and safety issues of the studied drug may be used as221a secondary endpoint to be evaluated if it contributes to the discussion on the benefit-risk balance of222the studied drug.4.9. Endpoints in fibrinolysis studies223224In fibrinolysis studies, angiographic studies using the TIMI (Thrombolysisi in Myocardial Infarction)perfusion grades as evaluation criteria are often used. However, complete recanalization cannot be 225226considered as a surrogate for survival when assessing fibrinolytic drugs, as some medicinal productsproviding higher complete recanalization rates than alteplase, failed to demonstrate additional survival 227228benefit. For this reason, all cause mortality is the most relevant endpoint or a combined endpoint as 229previously discussed (see 4.1). Secondary endpoints such as heart failure hospitalisations, left230ventricular function, ventricular arrhythmias, the need for rescue recanalization (emergent and/or231planned) should also be considered and justified.5. Methods to assess efficacy (how to measure the232endpoints)2335.1. Mortality234235Definition of CV death should be clearly defined, in line with acceptable standards [17]. It is mandatory 236to report and centrally adjudicate all mortality data where survival is an endpoint of the study.237Assessment of cardiovascular mortality will require censoring of other “types” of mortality, which may 238complicate its interpretation, in particular when non-CV deaths are in high proportion.5.2. New myocardial infarction239240The diagnostic of MI is based on the detection of a rise and/or fall of cardiac biomarker values241[preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference 242limit (URL). All MIs should be collected and also classified by their different sub types (i.e,243spontaneous, secondary to an ischemic imbalance, related to PCI, related to ST or CABG) [10]. This is 244particularly important considering the different prognostic values of each type of MI. For the same 245reason and to support the clinical relevance of post procedural MIs, these events should be presented 246with higher cut-off values (≥ 5 and ≥10x upper level of normal ULN, in case of CK-MB or ≥70x ULN of 247cTn) [18]. These higher cut-off values can also help in diagnosing MIs in the setting of elevated248baseline biomarkers, which is a problematic situation. In such cases, serial measurements of the249biomarkers are necessary, in addition to new ECG changes or signs of worsening of cardiac function, 250e.g. HFor hypotension [18].5.3. Revascularisation251252The underlying cause of revascularization should be identified: restenosis, ST or disease progression. 253In the latter case target vessel revascularization (TVR) could be included. Early target lesion eventsafter revascularization (before 30 days) are more likely to be caused by an angiographic complication 254255and should preferably be included as safety endpoint (see ST).5.4. Unstable angina pectoris necessitating hospitalisation256257When investigated, robust definitions should be employed. In order to support the seriousness of the 258event it should also be shown that it has led to a revascularisation procedure. Since a medicinalproduct that prevents death and/or new MI might result in more patients suffering from UA, the259260analysis of this endpoint should take into account censoring issues as well.5.5. Stent thrombosis261262ST should be collected and classified as definite, probable and possible in line with acceptable263definitions [19]. In addition, the timing of ST should be documented (acute, sub-acute, late and very 264late), as risk factors and clinical sequels differ with timing.5.6. Ventricular function and heart failure265266Investigation of cardiac function should follow state of the art methods. This can include among others 267measurement of ventricular function by isotopic method and/or by cardiac magnetic resonance imaging 268and/or echocardiography. Investigation of HFshould follow the relevant CHMP guidelines.5.7. Angiographic endpoints269270Angiograms should undergo central blinded reading. In principle, the rate of TIMI 3 flow (complete 271revascularization) of the infarct related artery at 90 minutes is considered the most relevant272angiographic endpoint, as it has been shown to correlate with an improved outcome in terms of273mortality and left ventricular function. An earlier evaluation of the patency pattern (i.e. 30 and 60274minutes) may provide important information on the speed of recanalization. Whatever is the time-point 275selected as primary outcome, it must be properly justified and pre-specified in the clinical trial.6. Selection of patients2766.1. Study population277The definition of the different ACS subtypes should be based on current guidelines/universal definition 278279of MI including STEMI and NSTEMI as well as UA [3, 4, 10].6.1.1. STE-ACS (ST elevation acute coronary syndrome)280281In patients with acute chest pain and persistent (>20 min) ST-segment elevation on ECG the282diagnostic of STE-ACS is made [3]. This condition generally reflects an acute total coronary occlusion.Most patients will ultimately develop an ST-elevation myocardial infarction (STEMI) with the criteria of 283284acute myocardial infarction described before [see 5.2].6.1.2. NSTE-ACS (Non-ST elevation acute coronary syndrome)285286In patients with acute chest pain but no persistent ST-segment elevation the diagnostic of NSTE-ACS is 287made [4]. ECG changes may include transient ST-segment elevation, persistent or transient ST-288segment depression, T-wave inversion, flat T waves or pseudo-normalization of T waves or the ECG 289may be normal. The clinical spectrum of non-ST-elevation ACS (NSTE-ACS) may range from patients 290free of symptoms at presentation to individuals with ongoing ischaemia, electrical or haemodynamic 291instability or cardiac arrest. The pathological correlate at the myocardial level is cardiomyocyte292necrosis (NSTEMI) or, less frequently, myocardial ischaemia without cell loss (UA). Currently, cardiac 293troponins play a central role in establishing a diagnosis and stratifying risk, and make it possible to 294distinguish between NSTEMI and UA[4].6.1.3. Unstable angina295296Unstable angina (UA) is defined as myocardial ischemia at rest or minimal exertion in the absence of 297cardiomyocytes necrosis, i.e. without troponin elevation. Among NSTE-ACS population, the higher298sensitivity of troponin has resulted in an increase in the detection of MI [4]; the diagnosis of UAis less 299frequently made.6.2. Inclusion criteria for the therapeutic studies300301Inclusion of both STEMI and NSTEMI and/or NSTE-ACS patients in the same clinical trial (or not)302should be justified based on the mechanism of action of the investigated product and the proposed 303time of intervention. If both subgroups are investigated in the same trial, both subgroups should be 304well represented. For interventions aimed at post-acute and longer term phases (secondary305prevention or plaque stabilisation) it may be justified to address both conditions in the same clinical 306trial. Time of inclusion of the patients in relation to the index event should be set and adequately307discussed a priori.308Patients with unstable angina represent a different risk category and prognosis that necessitates309different interventions than NSTEMI patients. However, during the acute presentation of NSTE-ACS it may be difficult to discriminate NSTEMI from UA so both groups have been included in some clinical 310311studies. In general, the investigation of interventions in these patients is encouraged, but preferably in 312separate clinical trials.If fibrinolysis is considered, inclusion criteria should be in line with the current treatment guidelines 313314concerning the inclusion for fibrinolysis [3].6.3. Exclusion criteria for the therapeutic studies315316If the patients do not fulfil the above criteria for ACS they should be excluded from the ACS studies. 317Other life-threatening conditions presenting with chest pain, such as dissecting aneurysm,318myopericarditis or pulmonary embolism may also result in elevated troponins and should always be 319considered as differential diagnoses [4].320If drugs interfering with the haemostatic system are tested, patients with a significant risk of bleeding 321(e.g. recent stroke, recent bleeding, major trauma or surgical intervention) and/or a propensity to 322bleed (e.g. thrombocytopenia, clotting disturbances, intracranial vascular diseases, peptic ulcers,323haemophilia) should be excluded from participation in the clinical studies.324Attention should be paid to the time elapsed between a previous application of antiplatelet or325anticoagulant acting agent beforehand and the administration of study drug (e.g. the pharmacokinetic 326[PK] and even more importantly, the pharmacodynamic [PD] half-life of these previously administered 327drugs).328For reasons of generalisability of the study results to the future target population it is strongly advised 329not to define the exclusion criteria too narrow, i.e. polymorbid patients (e.g. renal and/or hepatic330impairment, heart failure), should not automatically be excluded from the main therapeutic clinical 331trials.332When fibrinolysis is considered, exclusion criteria for fibrinolysis should be strictly respected [3].6.4. Risk Stratification333334In clinical trials, the ability of the therapy to demonstrate a treatment effect may depend on the335underlying risk and expected event rates. Enrichment strategies are sometimes used in trials to obtain 336the required number of events with a reasonable time in specific subgroups who are likely to exhibit a 337higher event rate than the overall target population and potentially larger treatment effect. In thatcase, it has to be shown that the results of this enriched study population can be extrapolated to the 338339general population.。
《慢性乙型肝炎防治指南(2022年版》解读
!()-.!DOI:10.3969/j.issn.1001-5256.2023.07.007《慢性乙型肝炎防治指南(2022年版)》解读谢艳迪,封 波,饶慧瑛北京大学人民医院,北京大学肝病研究所,北京100044通信作者:饶慧瑛,rao.huiying@163.com(ORCID:0000-0003-2431-3872)摘要:《慢性乙型肝炎防治指南(2022年版)》是以国内外慢性HBV感染的研究进展为依据,在既往多版指南基础上进行更新和修订而成。
本文介绍了新版指南在自然史、无创纤维化诊断、治疗等多方面的更新内容。
尤其是进一步扩大了慢性HBV感染者的治疗适应证,对干扰素的优势人群选择限定更清晰,对口服核苷(酸)类似物标准进行了更严格限制,对低病毒血症患者的处理更加积极,对免疫耐受期儿童的治疗也更积极。
新版指南将为我国扩大筛查HBV感染者、提高诊断率、优化治疗方案、规范临床管理提供重要依据。
关键词:乙型肝炎,慢性;乙型肝炎病毒;诊疗准则InterpretationofguidelinesforthepreventionandtreatmentofchronichepatitisB(2022edition)XIEYandi,FENGBo,RAOHuiying.(PekingUniversityPeople’sHospital,PekingUniversityHepatologyInstitute,Beijing100044,China)Correspondingauthor:RAOHuiying,rao.huiying@163.com(ORCID:0000-0003-2431-3872)Abstract:GuidelinesforthepreventionandtreatmentofchronichepatitisB(2022edition)areupdatedandrevisedbasedontheresearchadvancesinchronichepatitisBvirusinfectioninChinaandgloballyandthepreviouseditionsoftheguidelines.Thisarticleintroducestheupdatesinnaturalhistoryandthenoninvasivediagnosisandtreatmentoffibrosis.Inparticular,theguidelinesfurtherexpandtheindicationsforpatientswithchronichepatitisBvirusinfection,clearlydefinestheselectionofthepopulationbenefitingfrominterferontherapy,andstrictlylimitsthestandardoforalnucleos(t)ideanalogues.Meanwhile,theguidelinesalsorecommendmoreactivetreatmentofpatientswithlow-levelviremiaandchildrenintheimmune-tolerantphase.TheneweditionoftheguidelineswillprovideanimportantbasisforexpandingthescreeningforhepatitisBvirusinfec tion,improvingdiagnosticrate,optimizingtreatmentregimens,andstandardizingclinicalmanagementinChina.Keywords:HepatitisB,Chronic;HepatitisBvirus;PracticeGuidelines 自2005年起,至今历时18年,中华医学会感染病学分会和肝病学分会发布并更新《慢性乙型肝炎防治指南》(下称《指南》)共5版,在最新版的2022年《指南》[1]中,再次强调世界卫生组织提出的“2030年消除病毒性肝炎作为公共卫生危害”的目标,相较于2015年,2030年慢性乙型肝炎(CHB)新发感染率要减少90%,死亡率减少65%,诊断率达到90%和治疗率达到80%[2]。
山东门诊慢特病办理流程
山东门诊慢特病办理流程1.患者需要到医院门诊慢特病办理窗口取号。
Patients need to get a number at the outpatient clinic for the treatment of chronic diseases.2.填写相关表格并提交必要的证件。
Fill out the relevant forms and submit the necessary documents.3.等待叫号到指定的窗口办理手续。
Wait to be called to the designated window to go through the procedures.4.跟工作人员核对个人信息和病情资料。
Verify personal information and medical records with the staff.5.缴纳相关的诊疗费用。
Pay the relevant medical fees.6.安排医生面诊。
Arrange for a doctor's consultation.7.按时前往医生的诊室接受诊治。
Go to the doctor's office for treatment on time.8.遵循医生的嘱咐进行治疗。
Follow the doctor's instructions for treatment.9.持续进行后续的复诊和治疗。
Continue with follow-up consultations and treatment.10.根据医生建议定期检查病情。
Regularly check the condition according to the doctor's advice.11.患者家属也可以陪同办理相关手续。
Family members of the patient can also accompany them to complete the relevant procedures.12.如果有特殊情况需要申请住院治疗,须先接受医生的评估。
谵妄的治疗指南
Guideline Watch Array Practice Guideline for the Treatment of Patients WithDeliriumIan A. Cook, M.D.The American Psychiatric Association’s (APA’s) practice guidelines aredeveloped by expert work groups using an explicit methodology that includesrigorous review of available evidence, broad peer review of iterative drafts,and formal approval by the APA Assembly and Board of Trustees. APApractice guidelines are intended to assist psychiatrists in clinical decision-making. They are not intended to be a standard of care. The ultimatejudgment regarding a particular clinical procedure or treatment plan must bemade by the psychiatrist in light of the clinical data presented by the patientand the diagnostic and treatment options available. Guideline watchessummarize significant developments in practice since publication of an APApractice guideline. Watches may be authored and reviewed by expertsassociated with the original guideline development effort and are approvedfor publication by APA’s Executive Committee on Practice Guidelines. Thus,watches represent opinion of the authors and approval of the ExecutiveCommittee but not policy of the APA.This guideline watch was published in August 2004. © APA. All rightsreserved.Since the 1999 publication of APA’s Practice Guideline for the Treatment of Patients With Delirium (1), advances in the clinical neurosciences and other areas have contributed to the understanding of delirium and have expanded options for its management. This guideline watch summarizes important elements of the incremental progress in this area. DetectionThe 1999 guideline notes that the presence of delirium is frequently undetected by clinicians until psychiatric consultation is obtained, often triggered by dangerous behaviors. In the years since 1999, many papers providing easily remembered strategies for clinical detectionand management of delirium have been published, not only in the psychiatric literature butalso in journals that focus on critical care, pain management, oncology, medical-surgicalSuggested citaton: Cook, I.A. (2004). Guideline watch: Practice guideline for the treatment ofnursing, substance abuse, and geriatric medicine. Despite this broadening literature base, it has been noted that many cases of delirium continue to be missed (2). Reasons for this under-recognition are varied but may include the absence of routine, systematic screening (3). Improved attention to and recognition of delirium should be motivated by its clinical importance (e.g., association with elevated mortality (4)).One step toward improved detection may be the use of instruments that have demonstrated sensitivity to the presence of delirium. Examples include the Delirium Rating Scale–98–Revised (5;6), including a version for use with children (7); the Delirium Observation Screening Scale (8); and the Confusion Assessment Method for the Intensive Care Unit (9-11). Instruments have variable concordance with the diagnostic criteria detailed in DSM-IV, and each instrument may be better suited to particular clinical contexts.Neuropathophysiologic ModelsThe etiologic heterogeneity of delirium is a persistent theme in the more recent literature (10;12-15). The role of anticholinergic properties of a variety of medications continues to be noted (16;17). In a patient population with a mixture of putative causes of delirium, regional cerebral perfusion was consistently reported to show significant reductions during periods of delirium in comparison with blood flow patterns after recovery (18). The possibility of a final common pathway, involving acetylcholine and dopamine, has been advanced (15;19;20). The feature of sleep-wake cycle disruption in delirium has led others to speculate about the possible role of melatonin (21;22). While more research could prove illuminating, there are practical challenges to performing controlled clinical investigations with delirious persons, thoughtfully summarized by Meager (23). Despite these challenges, there is pressing need for more research in this area.ManagementManagement of patients with delirium continues to focus on ensuring safety from behavioral disturbances while simultaneously assessing for a probable etiology and definitive treatment. Safety can best be addressed by combining environmental, behavioral, and pharmacological means. In addition to the alterations in the hospital environment noted in the 1999 guideline, low-tech but potentially labor-intensive changes in nurse-patient interactions as well asflexibility within hospital systems to individualize processes of care may be able to reduce the impact of delirium (24). Behavioral programs can be highly effective but appear to be critically dependent on adherence to the details of the program (25).Current pharmacologic interventions expand the options reported in the 1999 guideline. Data supporting the use of first-generation antipsychotic medications (12) have been joined by case reports, case series, and a limited number of open-label trials supporting the use of second-generation antipsychotic medications (26) such as olanzapine (27-30), risperidone (27;31;32), ziprasidone (33), and quetiapine (34-38). The prophylactic use of haloperidol has been examined in hip-surgery patients in a prospective double-blind placebo-controlled trial (39), and although the incidence of delirium was not significantly altered by the intervention, there were significant differences in important secondary measures (duration of delirium, length of stay, Delirium Rating Scale scores) in this prevention trial. Given the dearth of research data, there is a clear need for prospective randomized controlled efficacy trials of second-generation antipsychotic medications for the management of delirium. Cholinesterase inhibitors also have shown success in managing delirium in some case reports, but usually for reversing drug-induced delirium, both for donepezil (40-43) and rivastigmine (44). The avoidance of benzodiazepines except for particular indications (e.g., alcohol or gamma-hydroxybutyric acid [GHA] withdrawal delirium, delirium related to seizures) continues to be a recommendation (12). In addition, if patients in critical care settings are already receiving high doses of parenteral lorazepam, the clinician will want to be alert for toxicity (e.g., renal dysfunction, hyperosmolar metabolic acidosis) associated with lorazepam's propylene glycol vehicle (45-47).References1. American Psychiatric Association: Practice guideline for the treatment of patients with delirium. Am J Psychiatry 1999; 156:1-202. Laurila JV, Pitkala KH, Strandberg TE, Tilvis RS: Detection and documentation of dementia and delirium in acute geriatric wards. Gen Hosp Psychiatry 2004; 26:31-353. Ely EW, Stephens RK, Jackson JC, Thomason JW, Truman B, Gordon S, Dittus RS, Bernard GR: Current opinions regarding the importance, diagnosis, andmanagement of delirium in the intensive care unit: a survey of 912 healthcare professionals. Crit Care Med 2004; 32:106-1124. McCusker J, Cole M, Abrahamowicz M, Primeau F, Belzile E: Delirium predicts 12-month mortality. Arch Intern.Med 2002; 162:457-4635. Trzepacz PT: The Delirium Rating Scale. Its use in consultation-liaison research. Psychosomatics 1999; 40:193-2046. Trzepacz PT, Mittal D, Torres R, Kanary K, Norton J, Jimerson N: Validation of the Delirium Rating Scale-revised-98: comparison with the delirium rating scale and the cognitive test for delirium. J Neuropsychiatry Clin Neurosci 2001; 13:229-2427. Turkel SB, Braslow K, Tavare CJ, Trzepacz PT: The delirium rating scale in children and adolescents. Psychosomatics 2003; 44:126-1298. Schuurmans MJ, Shortridge-Baggett LM, Duursma SA: The Delirium Observation Screening Scale: a screening instrument for delirium. Res Theory Nurs Pract 2003; 17:31-509. Inouye SK, van Dyck CH, Alessi CA, Balkin S, Siegal AP, Horwitz RI: Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Ann Intern.Med 1990; 113:941-94810. Ely EW, Margolin R, Francis J, May L, Truman B, Dittus R, Speroff T, Gautam S, Bernard GR, Inouye SK: Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit Care Med 2001; 29:1370-137911. Laurila JV, Pitkala KH, Strandberg TE, Tilvis RS: Confusion assessment method in the diagnostics of delirium among aged hospital patients: would it serve better in screening than as a diagnostic instrument? Int J Geriatr Psychiatry 2002; 17:1112-111912. Meagher DJ: Delirium: optimising management. BMJ 2001; 322:144-14913. Packard RC: Delirium. Neurologist 2001; 7:327-34014. Cole MG: Delirium in elderly patients. Am J Geriatr Psychiatry 2004; 12:7-2115. Trzepacz PT, Meager DJ: Delirium in Textbook of Psychosomatic Medicine Edited by Levenson JL. Arlington, VA, American Psychiatric Publishing, Inc., In press16. Tune LE: Anticholinergic effects of medication in elderly patients. J Clin Psychiatry 2001; 62 Suppl 21:11-1417. Mulsant BH, Pollock BG, Kirshner M, Shen C, Dodge H, Ganguli M: Serum anticholinergic activity in a community-based sample of older adults: relationship with cognitive performance. Arch Gen Psychiatry 2003; 60:198-20318. Yokota H, Ogawa S, Kurokawa A, Yamamoto Y: Regional cerebral blood flow in delirium patients. Psychiatry Clin Neurosci 2003; 57:337-33919. Trzepacz PT: Update on the neuropathogenesis of delirium. Dement.Geriatr Cogn Disord 1999; 10:330-33420. Trzepacz PT: Is there a final common neural pathway in delirium? Focus on acetylcholine and dopamine. Semin.Clin Neuropsychiatry 2000; 5:132-14821. Hanania M, Kitain E: Melatonin for treatment and prevention of postoperative delirium. Anesth.Analg. 2002; 94:338-9, table22. Balan S, Leibovitz A, Zila SO, Ruth M, Chana W, Yassica B, Rahel B, Richard G, Neumann E, Blagman B, Habot B: The relation between the clinical subtypes of delirium and the urinary level of 6-SMT. J Neuropsychiatry Clin Neurosci 2003; 15:363-36623. Meagher DJ: Optimising management of delirium [letter]. BMJ 2001; 322:160324. Flaherty JH, Tariq SH, Raghavan S, Bakshi S, Moinuddin A, Morley JE: A model for managing delirious older inpatients. J Am Geriatr Soc 2003; 51:1031-103525. Inouye SK, Bogardus ST, Jr., Williams CS, Leo-Summers L, Agostini JV: The role of adherence on the effectiveness of nonpharmacologic interventions: evidence from the delirium prevention trial. Arch Intern.Med 2003; 163:958-96426. Schwartz TL, Masand PS: The role of atypical antipsychotics in the treatment of delirium. Psychosomatics 2002; 43:171-17427. Sipahimalani A, Sime RM, Masand PS: Treatment of delirium with risperidone. Int J Geriatr Psychopharmacol 1997; 1:24-2628. Passik SD, Cooper M: Complicated delirium in a cancer patient successfully treated with olanzapine. J Pain Symptom.Manage. 1999; 17:219-22329. Kim KS, Pae CU, Chae JH, Bahk WM, Jun T: An open pilot trial of olanzapine for delirium in the Korean population. Psychiatry Clin Neurosci 2001; 55:515-51930. Breitbart W, Tremblay A, Gibson C: An open trial of olanzapine for the treatment of delirium in hospitalized cancer patients. Psychosomatics 2002; 43:175-18231. Furmaga KM, DeLeon OA, Sinha SB, Jobe TH, Gaviria M: Psychosis in medical conditions: response to risperidone. Gen Hosp Psychiatry 1997; 19:223-22832. Horikawa N, Yamazaki T, Miyamoto K, Kurosawa A, Oiso H, Matsumoto F, Nishimura K, Karasawa K, Takamatsu K: Treatment for delirium with risperidone: results ofa prospective open trial with 10 patients. Gen Hosp Psychiatry 2003; 25:289-29233. Leso L, Schwartz TL: Ziprasidone treatment of delirium. Psychosomatics 2002; 43:61-6234. Schwartz TL, Masand PS: Treatment of Delirium With Quetiapine. Prim.Care Companion.J Clin Psychiatry 2000; 2:10-1235. Torres R, Mittal D, Kennedy R: Use of quetiapine in delirium: case reports. Psychosomatics 2001; 42:347-34936. Sasaki Y, Matsuyama T, Inoue S, Sunami T, Inoue T, Denda K, Koyama T: A prospective, open-label, flexible-dose study of quetiapine in the treatment of delirium. J Clin Psychiatry 2003; 64:1316-132137. Al Samarrai S, Dunn J, Newmark T, Gupta S: Quetiapine for treatment-resistant delirium. Psychosomatics 2003; 44:350-35138. Kim KY, Bader GM, Kotlyar V, Gropper D: Treatment of delirium in older adults with quetiapine. J Geriatr Psychiatry Neurol 2003; 16:29-3139. Kalisvaart KJ, de Jonghe J, Bogaards MJ, Burger BJ, van Gool PA, Egberts TC, Eikelenboom P: A placebo-controlled study of haloperidol prophylaxis for post-operative delirium in elderly hip-surgery patients. J Am Geriatr Soc 2003; 51(s4):239-25540. Wengel SP, Roccaforte WH, Burke WJ: Donepezil improves symptoms of delirium in dementia: implications for future research. J Geriatr Psychiatry Neurol 1998; 11:159-16141. Wengel SP, Burke WJ, Roccaforte WH: Donepezil for postoperative delirium associated with Alzheimer's disease. J Am Geriatr Soc 1999; 47:379-38042. Burt T: Donepezil and related cholinesterase inhibitors as mood and behavioral controlling agents. Curr Psychiatry Rep 2000; 2:473-47843. Gleason OC: Donepezil for postoperative delirium. Psychosomatics 2003; 44:437-43844. Dautzenberg PL, Wouters CJ, Oudejans I, Samson MM: Rivastigmine in prevention of delirium in a 65 years old man with Parkinson's disease. Int J Geriatr Psychiatry 2003; 18:555-55645. Yaucher NE, Fish JT, Smith HW, Wells JA: Propylene glycol-associated renal toxicity from lorazepam infusion. Pharmacotherapy 2003; 23:1094-109946. Mullins ME, Barnes BJ: Hyperosmolar metabolic acidosis and intravenous Lorazepam. N Engl J Med 2002; 347:857-85847. Reynolds HN, Teiken P, Regan ME, Habashi NM, Cottingham C, McCunn M, Scalea TM: Hyperlactatemia, increased osmolar gap, and renal dysfunction during continuous lorazepam infusion. Crit Care Med 2000; 28:1631-1634。
2023版《慢性非酒精性肝病治疗指南》正式推出英文版
2023版《慢性非酒精性肝病治疗指南》正式推出英文版Title: Official Launch of the 2023 Edition of the "Treatment Guidelines for Chronic Non-Alcoholic Liver Disease"We are pleased to announce the official release of the 2023 edition of the "Treatment Guidelines for Chronic Non-Alcoholic Liver Disease." These guidelines aim to provide healthcare professionals with updated and evidence-based recommendations for the management of patients with chronic non-alcoholic liver disease.The 2023 edition incorporates the latest research findings and clinical evidence to offer comprehensive guidance on the diagnosis, treatment, and prevention of chronic non-alcoholic liver disease. Healthcare providers can use these guidelines to enhance their clinical practice and improve patient outcomes.With a focus on simplicity and effectiveness, the 2023 edition emphasizes practical strategies that can be easily implemented in varioushealthcare settings. By following these guidelines, healthcare professionals can optimize the care they provide to patients with chronic non-alcoholic liver disease.We encourage all healthcare professionals involved in the management of chronic non-alcoholic liver disease to familiarize themselves with the recommendations outlined in the 2023 edition of the guidelines. Together, we can work towards improving the quality of care for patients with this challenging condition.Stay tuned for more updates and resources related to the 2023 edition of the "Treatment Guidelines for Chronic Non-Alcoholic Liver Disease." Thank you for your dedication to advancing patient care in the field of liver disease.。
低频脉冲电治疗诊疗规范与流程
低频脉冲电治疗诊疗规范与流程英文回答:Low-frequency pulse electrical therapy is a commonly used treatment modality in physiotherapy. It involves the application of electrical pulses with a frequency below 1000 Hz to the body for therapeutic purposes. In this response, we will discuss the guidelines and procedures for low-frequency pulse electrical therapy.1. Indications for Low-Frequency Pulse Electrical Therapy:Low-frequency pulse electrical therapy can be used for various conditions, including musculoskeletal pain, muscle spasms, edema, and wound healing. It is particularly effective in managing chronic pain and promoting tissue repair.2. Pre-treatment Assessment:Before initiating low-frequency pulse electrical therapy, a thorough assessment of the patient's condition is necessary. This includes evaluating the patient's medical history, conducting a physical examination, and identifying any contraindications or precautions.3. Contraindications and Precautions:Low-frequency pulse electrical therapy should not be used in patients with implanted electronic devices, such as pacemakers or defibrillators. It should also be avoided in individuals with open wounds, skin infections, or malignancies in the treatment area. Precautions should be taken in patients with sensory impairments or decreased skin sensation to prevent potential burns or injuries.4. Treatment Parameters:The selection of treatment parameters, including pulse frequency, pulse duration, and intensity, should be based on the patient's condition and treatment goals. Generally,a frequency range of 2-100 Hz is used for low-frequency pulse electrical therapy. The pulse duration and intensity should be set at levels that are comfortable for thepatient while still producing therapeutic effects.5. Electrode Placement:Proper electrode placement is crucial for the effectiveness of low-frequency pulse electrical therapy. Electrodes should be placed over the target area, ensuring good skin contact. The size and shape of the electrodes may vary depending on the treatment area and the desired treatment effect.6. Treatment Duration and Frequency:The duration of each treatment session can range from 10 to 30 minutes, depending on the patient's tolerance and the treatment goals. The frequency of treatment sessions may vary, but typically, multiple sessions per week are recommended for optimal results.7. Monitoring and Evaluation:During the treatment session, the patient's response to low-frequency pulse electrical therapy should be monitored. This includes assessing the patient's comfort level, any adverse reactions, and the therapeutic effects. Regular evaluation of the treatment progress is important to determine the need for any adjustments or modifications in the treatment plan.中文回答:低频脉冲电治疗是物理治疗中常用的治疗方法。
慢性稳定性心绞痛的治疗(英文)共65页文档
• GP IIb-IIIa inhibitors displace fibrinogen in existing thrombi to disaggregate thrombus and prevent further platelet crosslinking and thrombosis
• GP IIb-IIIa inhibitors prevent platelet activation by blocking GP IIb-IIa (outsidein signaling)
PHYSICIANS' HEALTH STUDY
Primary Endpoints
• Total cancer • Prostate cancer • Cardiovascular disease • Eye disease
Cataract Macular degeneration
PHYSICIANS' HEALTH STUDY
III (not indicated)
– 1. Dipyridamole B – 2. Chelation therapy B
CURE
Approach to the treatment of chest pain
OXYGEN DEMAND
Double product = (Heart Rate) (systolic blood pressure)
3. ACE inhibitor in all patients with CAD who also have diabetes and/or LV systolic dysfunction A
4. LDL-lowering therapy in patients with documented or suspected CAD and LDL cholesterol >130 mg/dl, with a target LDL of <100 mg/dl A
卒中单元在脑出血急性期治疗研究进展
❖ 2023年版美国ICH治疗指南意见修改后的建议认 为,对于大局部ICH患者,外科手术治疗的效果仍不 明确(IIb级,C类证据)。
ICH治疗现有的争论结果仍旧无法找到确实有 效的循证医学证据,做为循证医学唯一证明有效的 两种治疗手段,卒中单元在ICH的急性期治疗中更 日益凸显出其重要意义。
卒中单元
卒中单元
❖Nikolaus 等[1]对20个试验中的卒中患者3864例 的争论结果进展Meta分析,结果显示经卒中单元 治疗的患者比一般病房治疗的患者的病死率降低( OR 0.83 , 95 % CI0.71~0.97)。
❖ Rudd等[2]调查英国2023至2023年240家医院共 8 200例患者觉察,在卒中单元内患者能得到更好 的治疗,病死率较非卒中单元下降25%.
1. Lindsay P, Bayley M, McDonald A,et al. Toward a more effective approach to stroke:canadian bestpractice recommendations for stroke care[J]. CMAJ, 2023, 178(11): 1418-1425
2021gold指南慢阻肺诊断标准
2021gold指南慢阻肺诊断标准Chronic obstructive pulmonary disease (COPD) is a common and serious lung disease that makes it hard to breathe. It is characterized by chronic inflammation of the airways and lungs. Most cases of COPD are caused by long-term exposure to irritants such as cigarette smoke, air pollution, and dust. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) was established to raise awareness about COPD and provide guidelines for its diagnosis and management. GOLD guidelines are widely used by healthcare professionals around the world to standardize the diagnosis and treatment of COPD.慢性阻塞性肺病(COPD)是一种常见且严重的肺部疾病,使呼吸困难。
它的特点是气道和肺部的慢性炎症。
大多数COPD病例是由长期暴露于刺激物引起的,如香烟烟雾、空气污染和尘埃。
全球慢性阻塞性肺病倡议(GOLD)成立的目的是提高人们对COPD的认识,并为其诊断和治疗提供指导方针。
GOLD指南被世界各地的医疗专业人员广泛使用,以规范COPD 的诊断和治疗。
To diagnose COPD, healthcare providers use a combination of medical history, physical examination, lung function tests, and imaging studies. GOLD guidelines recommend spirometry as the primary diagnostic tool for COPD. Spirometry measures lung function by assessing the amount of air a person can exhale in one second (FEV1) and the total amount of air a person can exhale (FVC). Based on spirometry results, COPD is classified into four stages: mild, moderate, severe, and very severe. Each stage has different treatment options and management strategies.为了诊断COPD,医疗提供者会结合病史、体格检查、肺功能测试和影像学研究。
《2024年世界卫生组织慢性乙型肝炎患者的预防、诊断、关怀和治疗指南》推荐意见要点
《2024年世界卫生组织慢性乙型肝炎患者的预防、诊断、关怀和治疗指南》推荐意见要点艾小委,张梦阳,孙亚朦,尤红首都医科大学附属北京友谊医院肝病中心,北京 100050通信作者:尤红,******************(ORCID:0000-0001-9409-1158)摘要:2024年3月世界卫生组织(WHO)发布了最新版《慢性乙型肝炎患者的预防、诊断、关怀和治疗指南》。
该指南在以下方面进行了更新:扩大并简化慢性乙型肝炎治疗适应证,增加可选的抗病毒治疗方案,扩大抗病毒治疗预防母婴传播的适应证,提高乙型肝炎病毒诊断,增加合并丁型肝炎病毒的检测等。
本文对指南中的推荐意见进行归纳及摘译。
关键词:乙型肝炎,慢性;预防;诊断;治疗学;世界卫生组织;诊疗准则Key recommendations in guidelines for the prevention,diagnosis,care and treatment for people with chronic hepatitis B infection released by the World Health Organization in 2024AI Xiaowei, ZHANG Mengyang, SUN Yameng, YOU Hong.(Liver Research Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China)Corresponding author: YOU Hong,******************(ORCID: 0000-0001-9409-1158)Abstract:In March 2024, the World Health Organization released the latest version of guidelines for the prevention, diagnosis,care and treatment for people with chronic hepatitis B infection. The guidelines were updated in several aspects,including expanding and simplifying the indications for chronic hepatitis B treatment,adding alternative antiviral treatment regimens,broadening the indications for antiviral therapy to prevent mother-to-child transmission,improving the diagnosis of hepatitis B virus,and adding hepatitis D virus (HDV)testing. This article summarizes and gives an excerpt of the recommendations in the guidelines.Key words:Hepatitis B, Chronic; Prevention; Diagnosis; Therapeutics; World Health Organization; Practice Guideline近年来,慢性乙型肝炎(CHB)在预防、诊断、治疗等方面取得重要进展。
世界卫生组织1999年糖尿病诊断标准英文版
世界卫生组织1999年糖尿病诊断标准英文版全文共3篇示例,供读者参考篇1World Health Organization 1999 Diabetes Diagnosis CriteriaIn 1999, the World Health Organization (WHO) released updated guidelines for the diagnosis of diabetes mellitus. These guidelines aim to provide a standardized approach to diagnosing diabetes, which is essential for proper management and treatment of the condition. The criteria set forth by the WHO in 1999 have since been widely adopted by healthcare professionals around the world.The WHO 1999 criteria for the diagnosis of diabetes mellitus are based on measurements of fasting plasma glucose (FPG) and oral glucose tolerance test (OGTT) results. According to these criteria, a diagnosis of diabetes can be made if any one of the following conditions is met:1. Fasting Plasma Glucose (FPG) ≥126 mg/dl (7.0 mmol/L): A fasting plasma glucose level of 126 mg/dl or higher indicates diabetes. Fasting means that the individual has not consumedany food or beverages other than water for at least 8 hours prior to the test.2. 2-Hour Plasma Glucose ≥ 200mg/dl (11.1 mmol/L) during an Oral Glucose Tolerance Test (OGTT): An OGTT involves drinking a glucose solution after fasting overnight, then testing blood glucose levels 2 hours later. A result of 200 mg/dl or higher indicates diabetes.3. Casual Plasma Glucose ≥ 200mg/dl (11.1 mmol/L): If an individual has symptoms of hyperglycemia (e.g., increased thirst, frequent urination) and a random plasma glucose level of 200 mg/dl or higher, a diagnosis of diabetes can be made.It is important to note that these diagnostic criteria are meant to be used in non-pregnant individuals. For pregnant women, the WHO recommends using different criteria to diagnose gestational diabetes.The WHO 1999 criteria also include guidelines for the diagnosis of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), which are conditions that precede diabetes and increase the risk of developing the disease. According to these guidelines, IFG is defined as a fasting plasma glucose level of 110-125 mg/dl (6.1-6.9 mmol/L), while IGT is diagnosed if the2-hour plasma glucose level during an OGTT is between 140-199 mg/dl (7.8-11.0 mmol/L).Diabetes is a chronic condition that affects millions of people worldwide and can lead to serious complications if not properly managed. By using standardized diagnostic criteria such as those set forth by the WHO in 1999, healthcare professionals can accurately identify individuals with diabetes and initiate appropriate treatment and monitoring to prevent complications and improve outcomes.In conclusion, the World Health Organization 1999 diabetes diagnosis criteria have become the gold standard for diagnosing diabetes mellitus worldwide. These criteria provide clear guidelines for healthcare professionals to identify individuals with diabetes and ensure they receive the necessary care and treatment. By following these criteria, healthcare providers can effectively manage diabetes and improve the quality of life for those affected by this chronic condition.篇2World Health Organization 1999 Diabetes Diagnosis CriteriaIn 1999, the World Health Organization (WHO) revised the diagnostic criteria for diabetes in order to better reflect thecurrent understanding of the disease. These criteria are important in accurately identifying individuals who have diabetes and ensuring they receive appropriate treatment and care. The 1999 WHO criteria for diabetes diagnosis are as follows:1. Fasting Plasma Glucose (FPG) Level:- Normal: FPG < 6.1 mmol/L (110 mg/dL)- Impaired Fasting Glucose (IFG): FPG 6.1-6.9 mmol/L (110-125 mg/dL)- Diabetes: FPG ≥ 7.0 mmol/L (126 mg/dL)2. 2-hour Plasma Glucose Level after Oral Glucose Tolerance Test (OGTT):- Normal: < 7.8 mmol/L (140 mg/dL)- Impaired Glucose Tolerance (IGT): 7.8-11.0 mmol/L (140-199 mg/dL)- Diabetes: ≥ 11.1 mmol/L (200 mg/dL)3. Symptoms of hyperglycemia and casual plasma glucose concentration ≥ 11.1 mmol/L (200 mg/dL) indicate the presence of diabetes.It is important to note that these criteria were established based on evidence that individuals with glucose levels above the specified thresholds have an increased risk of developing diabetes-related complications. Additionally, the WHO recommends that the diagnosis of diabetes should be confirmed by repeating the test on a different day if the results are borderline or inconsistent.These diagnostic criteria have been widely adopted by healthcare professionals around the world and are used to identify individuals with diabetes, prediabetes, and normal glucose metabolism. Early detection and management of diabetes are crucial in preventing complications such as cardiovascular disease, kidney failure, blindness, and lower limb amputations.In addition to the diagnostic criteria, the WHO also emphasizes the importance of lifestyle modifications, including a healthy diet, regular physical activity, and weight management, in the prevention and management of diabetes. Individuals with diabetes are also advised to monitor their blood glucose levels regularly, take prescribed medications as directed, and seek medical advice if they experience any symptoms of hyperglycemia or hypoglycemia.Overall, the 1999 WHO diabetes diagnosis criteria provide a standardized approach to identifying individuals with diabetes and ensuring they receive appropriate care and management. By following these criteria, healthcare professionals can accurately diagnose diabetes, initiate timely interventions, and help individuals lead healthier lives.篇3World Health Organization 1999 Diabetes Diagnostic CriteriaIntroductionDiabetes is a chronic disease that affects millions of people worldwide. In 1999, the World Health Organization (WHO) released updated diagnostic criteria for diabetes in an effort to provide more accurate and consistent guidelines for diagnosing the disease. This document outlines the key criteria outlined by the WHO for diagnosing diabetes.Criteria for Diagnosis1. Fasting Plasma Glucose (FPG) Test: One of the most common tests used to diagnose diabetes is the fasting plasma glucose test. In this test, a person is required to fast for at least 8 hours before having their blood glucose levels measured. Ablood glucose level of 126 mg/dL (7.0 mmol/L) or higher on two separate occasions is indicative of diabetes.2. Oral Glucose Tolerance Test (OGTT): Another test that can be used to diagnose diabetes is the oral glucose tolerance test. In this test, a person is required to fast for at least 8 hours before consuming a glucose solution. Blood glucose levels are then measured 2 hours after consuming the solution. A blood glucose level of 200 mg/dL (11.1 mmol/L) or higher is indicative of diabetes.3. HbA1c Test: The HbA1c test, also known as the glycated hemoglobin test, measures the average blood glucose levels over the past 2-3 months. A HbA1c level of 6.5% or higher is indicative of diabetes.4. Symptoms of Diabetes: In some cases, a person may present with classic symptoms of diabetes such as frequent urination, increased thirst, unexplained weight loss, and fatigue. If these symptoms are present along with a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher, diabetes can be diagnosed.5. Gestational Diabetes: In pregnant women, gestational diabetes can develop. The diagnostic criteria for gestational diabetes are a bit different, with a 75g oral glucose tolerance testand the following cutoff va lues: Fasting glucose ≥92 mg/dL (5.1 mmol/L), 1-hour ≥180 mg/dL (10.0 mmol/L), and 2-hour ≥153 mg/dL (8.5 mmol/L).ConclusionThe 1999 WHO diabetes diagnostic criteria provide healthcare professionals with clear guidelines for diagnosing diabetes. By using these criteria, healthcare providers can accurately identify individuals with diabetes and provide appropriate treatment and management strategies. It is important to note that diagnosing diabetes early can help prevent complications and improve outcomes for patients with the disease.。
CIN中国专家共识
相关国际学会和临床指南中均已涉及 对比剂的合理应用与对比剂肾病的预防策略
ACC/SCA&I ACC/AHA/SCA&I ACC/AHA
ACR
ESUR French Society of Radiology German Cardiac Society NKF
2001 Clinical Expert Consensus Document on Cardiac Catheterization Laboratory Standards
苯环数
粘度 37°C时 (cP)
单体 3.4-9.0
低 (577)
离子型
碘克酸
双体 9.5
低 (610- 915)
非离子型
碘海醇
碘帕醇 碘佛醇
单体
8.1 – 12
Stacul F. Eur Radiol. 2001;11:690-697. American College of Radiology. Manual on Contrast Media, version 5.0; 2004.
Normal GFR
SCr
126-190 umol/l
(SCr Normal range 60120 umol/l)
ACS行PCI患者肾功能状态 多中心注册研究
牵头单位:中国介入心脏病学杂志 赞助单位:辉瑞制药有限公司
• 背景 肾功能不全是影响ACS病人预后的独立危险 因素,但目前我国对ACS病人合并肾功能不全缺乏足 够重视,同时也缺乏相关方面的大规模 临床研究
等滲 (290)
非离子型 碘克沙醇
双体 11.1
Viscosity粘滞度
mPa•s
°C
对比剂的渗透压
WHO的标准疼痛管理指南(2007)
4. Methodology .......................................................................................................................... 5
5. Results .................................................................................................................................... 6
6. Discussion ............................................................................................................................. 20
7. Conclusions ............................................................................................................................ 22
The best option chosen was to have a total of three guidelines for adults, with specific issues for children and older adults mentioned as a chapter, paragraph or appendix. However, this option was not acceptable to many paediatricians. It remained an issue whether there should be separate guidelines for children since there are only a few types of pain, especially chronic pain, that are common in both adults and children (e.g. sickle cell pain, burns, cancer, HIV). In addition, the assessment of pain, types and doses of medicines, route of administration and adverse effects are different in very small children. The WHO Guideline Steering Group of the Access to Controlled Medications Programme should consider both options. Although widest acceptability by the medical community is the most important consideration for widespread use of guidelines, the final decision by WHO will also depend upon the cost involved in terms of money, time frame and expertise.
GCP指南中英文对照
compliant clinical study. It is almost impossible to achieve the ideal proclaimed in the existing guidelines and regulations. However, this does not mean we should not strive for the best standard possible. You must think beyond the 'minimum standard' if you really want to do a good job and ensure the best quality possible. Slavish adherence to guidelines and regulations will not work: you must be convinced of the basic logic, ethics and science behind GCP requirements. Going for the most expedient and cheapest route will not only result in a poorer standard but it may also cost lives.首先,我们应该清楚,在我们看来,没有完全依从GCP的临床研究,完美遵从目前指导原则和法规几乎是不可能的。
但是,这并不意味着我们就不应该尽可能达到最好的标准。
如果你确实想要做好工作并尽可能确保高质量,就必须考虑超过最低标准。
机械的遵从指导原则和法规是没有用的,但必须遵循GCP要求的基本的逻辑、伦理和科学原则。
一味的寻求最方便、最便宜的途径将不仅仅导致一个更低的标准,也可能增加成本。
How much non-compliance should we tolerate? In 1996, we published a book on GCP compliance based on the findings of our audit experience at 226 investigator study sites, involving studies conducted in 20 different countries, and audited by an independent external audit team between 1991 and 1995. GCP compliance was compared for various factors and the data patterns suggested some interesting trends. First, the overall level of GCP compliance was generally poor across all investigator study sites and far below the expectations of guidelines and regulations. (In many areas, the studies were possibly dangerous for study subjects, in our opinion.) Second, there were no important differences in studies with regard to the year in which the study was conducted. Basically, all the new regulatory efforts, particularly in Europe, did not show a positive effect onstandards. (However, a survey over a five- to six-year time period is possibly too limited to draw conclusions on this point.) Third, there were no important differences in studies which used a CRO (contract research organization) compared to those which did not. This appears to be because CROs simply follow the standards of the sponsor responsible for the conduct of the study rather than setting consistent and better standards themselves. Fourth, some slight differences between phases of studies were observed, with better compliance in early phase studies. However, this should not be surprising since a Phase I single-centre study with 20 subjects is much easier to control than a Phase III multicentre multinational study involving several hundred study subjects. Fifth, there were some slight differences between therapeutic areas, but this was probably linked to the standards of the sponsor or CRO managing the studies. Sixth, overall, there were no basic overall differences between levels of GCPcompliance in different countries. (However, a later analysis of selected items showed some individual differences between countries: for example, direct access to source documents was achieved 100% of the time at US sites, but not as frequently in other countries.)The only apparent important differences in levels of GCP compliance were between the different sponsors (mostly pharmaceutical companies) managing the studies. The main conclusions reached from analysis of this audit database were that overall standards of GCP compliance greatly needed improvement, and that standards were only as good as the sponsor managing the study regardless of where in the world the study was being conducted. In theory, good research could be conducted anywhere provided it was managed properly.我们可容许多大的非依从性呢?1996年我们出版了一本关于GCP依从性的书,此书根据我们在226个研究基地的稽查发现编写,涉及了1991年到1995年间20个不同国家并由独立的外部稽查小组稽查的研究。
慢性阻塞性肺疾病基层诊疗指南(实践版·2018)
·基层常见疾病诊疗指南·慢性阻塞性肺疾病基层诊疗指南(实践版·2018)中华医学会中华医学会杂志社中华医学会全科医学分会中华医学会呼吸病学分会慢阻肺学组中华医学会《中华全科医师杂志》编辑委员会呼吸系统疾病基层诊疗指南编写专家组通信作者:陈荣昌,510120广州呼吸疾病健康研究院,Email:chenrc@;孙永昌,100191北京大学第三医院呼吸与危重症医学科,Email:suny@DOI:10.3760/cma.j.issn.1671⁃7368.2018.11.003Guideline for primary care of chronic obstructive pulmonary disease:practice version(2018)Chinese Medical Association,Chinese Medical Journal Publishing House,Chinese Society of General Practice,Chronic Obstructive Pulmonary Disease Group of Chinese Thoracic Society,Editorial Board of Chinese Journalof General Practitioners of Chinese Medical Association,Expert Group of Guidelines for Respiratory SystemDiseaseCorresponding author:Chen Rongchang,Guangzhou Health Acadamy of Respiratory Disease,Guangzhou510120,China,Email:chenrc@;Sun Yongchang,Department of Pulmonary and Critical CareMedicine,Peking University Third Hospital,Beijing100191,China,Email:suny@【关键词】指南;肺疾病,慢性阻塞性一、概述(一)定义慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)简称慢阻肺,是一种常见的以气流受限为特征的可以预防和治疗的疾病,气流受限多呈进行性发展,与气道和肺对有毒颗粒或气体的慢性炎症反应增强有关。
2024年糖尿病标准
2024年糖尿病标准In 2024, the standards for diabetes management are expected to evolve to address the growing prevalence and impact of this chronic condition. These standards encompass various aspects, including prevention, diagnosis, treatment, and patient education. This response will explore the potential changes in diabetes management guidelines for 2024, considering advancements in technology, personalized medicine, lifestyle interventions, and healthcare policies.Firstly, with the rapid development of technology, the 2024 diabetes standards will likely emphasize theintegration of digital health solutions. Continuous glucose monitoring (CGM) devices, insulin pumps, and mobile applications will play a pivotal role in diabetes management. These technologies enable real-time monitoringof blood glucose levels, provide personalized insulin delivery, and offer comprehensive data analysis for better treatment decisions. Additionally, telemedicine and remote patient monitoring will likely become more prevalent,allowing healthcare professionals to remotely support and monitor patients with diabetes, enhancing accessibility and improving overall care.Secondly, the 2024 diabetes standards may emphasize the importance of personalized medicine. With advancements in genetics and molecular biology, precision medicine approaches will gain prominence. Genetic testing and analysis can identify individuals at higher risk of developing diabetes or experiencing complications. This information can guide tailored treatment plans and preventive strategies. Moreover, advancements in pharmacogenomics may enable the selection of medications based on an individual's genetic profile, optimizing treatment outcomes and minimizing adverse effects.Thirdly, lifestyle interventions will continue to be a cornerstone of diabetes management in 2024. The standards will likely emphasize the importance of healthy eating, regular physical activity, and weight management. Nutritional guidelines may evolve to reflect the latest research on macronutrient composition, glycemic index/load,and individualized meal planning. Physical activity recommendations may be further refined, considering individual preferences, capabilities, and the incorporation of technology-based exercise interventions. Additionally, behavioral interventions and psychosocial support will be integrated into diabetes care to address the emotional and mental well-being of individuals living with diabetes.Fourthly, the 2024 diabetes standards may reflect changes in healthcare policies and reimbursement models. There may be an increased focus on value-based care, with reimbursement tied to patient outcomes rather than the volume of services provided. This shift can incentivize healthcare providers to deliver more comprehensive and patient-centered care, promoting better diabetes management. Additionally, policies may prioritize preventive measures, such as screening programs and community-based interventions, to identify individuals at risk andintervene early, reducing the burden of diabetes-related complications.Fifthly, patient education and empowerment will remaincrucial in the 2024 diabetes standards. The guidelines will likely emphasize the need for healthcare professionals to provide comprehensive education on self-management skills, including blood glucose monitoring, medication administration, healthy lifestyle habits, and problem-solving strategies. Additionally, the integration ofdigital platforms and mobile applications can facilitate patient education and engagement, enabling individuals to access personalized information, track their progress, and connect with support networks.Finally, the 2024 diabetes standards may address health disparities and inequalities in diabetes care. Efforts will be made to ensure equitable access to healthcare services, particularly for underserved populations who may face barriers to diabetes management. Culturally sensitive and linguistically appropriate care will be promoted to caterto diverse communities. Furthermore, the standards may emphasize the importance of interdisciplinary collaboration, involving healthcare providers, educators, policymakers,and community organizations to develop comprehensive strategies for diabetes prevention and management.In conclusion, the 2024 diabetes standards are expected to encompass advancements in technology, personalized medicine, lifestyle interventions, healthcare policies, and patient education. These standards will likely promote the integration of digital health solutions, emphasize personalized medicine approaches, prioritize lifestyle interventions, reflect changes in healthcare policies, prioritize patient education and empowerment, and address health disparities. By adopting these evolving standards, healthcare systems can strive towards improved diabetes management and better outcomes for individuals living with this chronic condition.。
cold and heat therapy英文短篇
cold and heat therapy英文短篇Cold and heat therapy are two of the most common and effective forms of treatment for a variety of physical conditions and injuries. Both methods work by altering the temperature of the affected area, which can have a range of beneficial effects on the body. Understanding the differences between cold and heat therapy, as well as when to use each one, is important for maximizing the effectiveness of these treatments.Cold therapy, also known as cryotherapy, involves the application of cold to an affected area. This can be done through the use of ice packs, cold water immersion, or specialized cryotherapy equipment. The purpose of cold therapy is to reduce inflammation, numb pain, and promote healing. When an injury or condition occurs, the body's natural response is to increase blood flow to the area, which can lead to swelling and pain. Cold therapy works by constricting blood vessels and reducing this inflammatory response.The cooling effect of cold therapy also has a numbing effect on the nerve endings in the affected area, providing pain relief. Additionally,the cold temperature can slow down the metabolic processes in the injured tissue, which can help to prevent further damage and promote the healing process. Cold therapy is commonly used to treat conditions such as sprains, strains, and other acute injuries, as well as chronic conditions like arthritis and bursitis.In contrast, heat therapy involves the application of warmth to an affected area. This can be done through the use of heating pads, warm water immersion, or specialized heat therapy equipment. The purpose of heat therapy is to increase blood flow, reduce muscle tension, and promote healing.When heat is applied to an area, the blood vessels dilate, allowing more blood to flow to the affected tissue. This increased blood flow brings more oxygen and nutrients to the area, which can aid in the healing process. Heat therapy also has a relaxing effect on the muscles, helping to reduce tension and spasms. This can be particularly beneficial for conditions like muscle strains, joint stiffness, and chronic pain.It is important to note that both cold and heat therapy should be used with caution and under the guidance of a healthcare professional. Overuse or improper application of these treatments can lead to further injury or discomfort. Additionally, certain medical conditions may contraindicate the use of either cold or heat therapy.When deciding whether to use cold or heat therapy, it is important to consider the specific condition or injury being treated. Generally, cold therapy is more effective for acute injuries and conditions characterized by inflammation, such as sprains, strains, and overuse injuries. Heat therapy, on the other hand, is more effective for chronic conditions and those characterized by muscle tension or stiffness, such as arthritis and chronic pain.In some cases, a combination of cold and heat therapy may be the most effective approach. For example, after an acute injury, cold therapy can be used initially to reduce inflammation and pain, followed by heat therapy to promote healing and reduce muscle tension. This combined approach can be particularly effective in helping the body to recover from injury or manage chronic conditions.Regardless of whether cold or heat therapy is used, it is important to follow the proper protocols and guidelines for each treatment. This includes using the appropriate temperature and duration, as well as ensuring that the affected area is properly protected and monitored during the treatment. Failure to follow these guidelines can lead to further injury or discomfort.In conclusion, cold and heat therapy are two powerful tools in thetreatment of a variety of physical conditions and injuries. By understanding the differences between these two therapies and when to use them, healthcare professionals and individuals can maximize the effectiveness of these treatments and promote faster healing and recovery. Whether used individually or in combination, cold and heat therapy can be an important part of a comprehensive treatment plan for managing a wide range of physical ailments.。
Alcohol Withdrawl Syndromes:酒精戒断综合征_OK
By: David Bridgers, M.D.
1
Case Presentation:
43 y/o AAM with a hx, HTN, and long term ETOH abuse, who presented to the Urology service after being seen in the ED for Hematuria, and being diagnosed with a renal mass. He was 1 day s/p nephrectomy. He was on epidural pain medications per pain control. He was reported to be agitated when the nursing staff evaluated him.The
rhabdomyolysis.
15
Non-Pharmacological Management Principals
• PT should be closely monitored -Ideally a quiet and protective setting, unless pt. Is at higher risk for complications, then they should be in a ICU.
• Frequent evaluation by nursing AND medical staff • Other conditions may mimic DT: infection, OD, trauma, hepatic failure, GIB
16
Non-Pharmacological Management Principals cont.
2024年中医执业医师考试中医医学英语历年题目
2024年中医执业医师考试中医医学英语历年题目一、中医药学相关题目1. What does the term "Qi" refer to in traditional Chinese medicine?2. List the main categories of herbal medicine in traditional Chinese medicine.3. Explain the concept of "yin" and "yang" in traditional Chinese medicine.4. What is the role of acupuncture in traditional Chinese medicine? How does it work?5. Describe the basic principles of pulse diagnosis in traditional Chinese medicine.二、中医诊断相关题目1. How is the diagnosis in traditional Chinese medicine different from Western medicine?2. What are the major methods used in traditional Chinese medicine for diagnosing diseases?3. How does tongue diagnosis work in traditional Chinese medicine?4. Explain the concept of "pattern differentiation" in traditional Chinese medicine.5. List the different types of pulses and their corresponding meanings in traditional Chinese medicine.三、中医治疗相关题目1. What are the common treatment methods used in traditional Chinese medicine?2. How does acupuncture promote the flow of Qi and blood in the body?3. Explain the concept of "meridians" in acupuncture and its role in healing.4. What are the main therapeutic techniques used in traditional Chinese medicine, such as cupping and moxibustion?5. How does traditional Chinese medicine approach the treatment of chronic diseases?四、中医药研究相关题目1. What are the key principles of traditional Chinese medicine research?2. Describe the different types of clinical trials used in traditional Chinese medicine research.3. What are the challenges faced by researchers in studying traditional Chinese medicine?4. Explain the concept of "herb-drug interactions" in traditional Chinese medicine research.5. Discuss the potential benefits and limitations of integrating traditional Chinese medicine with Western medicine.总结:2024年中医执业医师考试中医医学英语历年题目主要涵盖了中医药学、中医诊断、中医治疗和中医药研究等方面的知识。
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Guidelines for the Treatment of Chronic Constipation: What Is the Evidence?Philip S. Schoenfeld, MD, MSEd, MScPosted: 07/12/2005Please note: The following announcement supersedes any information contained in this article. On March 30, 2007, Novartis, in compliance with an FDA request, suspended marketing and sales of its irritable bowel/constipation drug tegaserod maleate (Zelnorm) after an analysis of its clinical database pointed to a higher incidence of myocardial infarction, stroke, and unstable angina among patients taking the drug. For updated information on this issue, see the Medscape Alert Center on tegaserod.In July 2005, the American College of Gastroenterology Functional Gastrointestinal Disorders Task Force produced an evidence-based monograph on the management of chronic constipation in North America.[1] This monograph follows the evidence-based format used in a previous review on the treatment of irritable bowel syndrome (IBS),[2] and provides graded recommendations regarding the appropriate diagnosis and treatment of chronic constipation. This brief report outlines the recommendations of the Task Force and discusses the evidence that supports these recommendations.The prevalence of chronic constipation in North America is approximately 15%, although only a minority of sufferers seek medical care.[3] On the basis of data from population-based studies, chronic constipation is more common in women, the elderly, nonwhites, and individuals from lower socioeconomicgroups.[3] When these individuals complain about chronic constipation, they are referring to symptoms related to difficult stool passage: straining, hard/lumpy stools, prolonged time to stool, sense of incomplete evacuation, or need for manual maneuvers to pass stool. Only one third of chronic constipation sufferers complain of passing fewer than 3 bowel movements/week. Therefore, the Task Force defined chronic constipation as "unsatisfactory defecation characterized by infrequent stools, difficult stool passage, or both." Quality-of-life studies indicate that patients who self-report constipation suffer from a decreased quality of life.[3] Therefore, Task Force members recommended that physicians should institute treatment for chronic constipation after discussion with the patient and determination that the symptoms are diminishing the patient's quality of life.If the pre-test probability of an organic disorder (eg, hypothyroidism) is increased in patients with chronic constipation symptoms compared with healthy control patients, then appropriate diagnostic tests (eg, thyroid function tests) should be ordered routinely in patients with (chronic constipation) symptoms. However, if the pre-test probability of an organic disorder (eg, hypercalcemia) is similar in patients with chronic constipations symptoms as compared with healthy control patients, then the routine use of diagnostic tests (eg, serum calcium) should not be performed. Unfortunately, there are no well-designed studies that assess the pre-test probability of different organic disorders (eg, hypercalcemia, hypothyroidism, colon cancer) among patients who present with chronic constipation symptoms.Therefore, Task Force members concluded that there were inadequate data to make a recommendation about the routine use of flexible sigmoidoscopy, colonoscopy, barium enema, thyroid function tests, serum calcium, and other diagnostic tests in patients who present with chronic constipation symptoms. However, if a patient presents with alarm symptoms or signs (eg, hematochezia, weight loss of 10 or more pounds, family history of colon cancer or inflammatory bowel disease, positive fecal occult blood tests, iron-deficiency anemia, or acute onset of chronic constipation symptoms in patients 50 years of age and older), then diagnostic studies are indicated because these alarm signs or symptoms may increase a patient's pretest probability of chronic constipation symptoms secondary to an organic disorder. Furthermore, if history or physical exam identifies signs/symptoms of an organic disorder (eg, symptoms or physical exam signs of hypothyroidism), then additional diagnostic testing should be performed for these specific disorders.On the basis of the available evidence, colonoscopy does not identify organic disorders more frequentlyin patients with chronic constipation symptoms compared with healthy controls. Therefore, the Task Force recommends that colonoscopy should be used routinely as part of colon cancer screening in all patients 50 years of age and older. However, Task Force members suggest that the routine performance of colonoscopy in patients with symptoms of chronic constipation is not supported by available evidence. Task Force members suggest that the approach to patients with chronic constipation symptoms should involve empiric treatment without performance of diagnostic tests.Therapy of Chronic ConstipationBulking AgentsFindings from 3 placebo-controlled randomized controlled trials (RCTs) showed that psyllium improves stool frequency and stool consistency compared with placebo.[4-6] These trials were suboptimally designed, which led to a grade B recommendation (ie, recommendations based on evidence from RCTs with inadequate sample sizes, inappropriate methodology, or nonsignificant results). There are insufficientdata to make a recommendation about the efficacy of calcium polycarbophil, methylcellulose, and wheat bran in patients with chronic constipation. Specifically, there are 3 RCTs of wheat bran in patients with chronic constipation,[7-9] but only 1 is placebo-controlled.[7] This trial did not demonstrate a significant improvement in stool frequency or consistency when compared with placebo -- neither did 2 trials[8,9] that compared wheat bran with corn biscuit or corn bran. There are no placebo-controlled RCTs of methylcellulose or calcium polycarbophil, although poorly designed RCTs involving fewer than 100 patients do not demonstrate differences between calcium polycarbophil or methylcellulose compared with psyllium.Data on adverse events are quite limited, although taking 10-20 g/day of psyllium has been associated with bloating, which may be a bothersome event in these patients. Psyllium has also been associatedwith mechanical obstruction of the esophagus and colon and anaphylactic reactions in case reports.On the basis of the available RCT evidence, there are insufficient data to make a recommendation regarding the efficacy of stool softeners in patients with chronic constipation (Grade B recommendation). Stool softeners may be inferior to psyllium for improvement of stool frequency (Grade B recommendation). Four RCTs[10-13] compared stool softeners with active comparators or placebo in patients with chronic constipation. Overall, these studies were poorly designed with small sample sizes and a diverse patient population. Docusate sodium was inferior to psyllium for increase in stool frequency. Placebo-controlledtrials showed no difference in stool frequency or stool consistency between stool softeners and placebo. Overall, these data suggest that stool softeners are little more than a placebo for the treatment of chronic constipation. However, because the quality of the studies was so poor, Task Force members believed that there were insufficient data to state that stool softeners were similar to placebo. No data on adverse events with stool softeners were presented in these trials.Multiple well-designed RCTs,[14-17] demonstrate that polyethylene glycol appears superior to placebo for improving stool frequency and stool consistency in patients with chronic constipation (Grade A recommendation; Grade A recommendations are supported by 2 or more well-designed RCTs with adequate sample sizes and statistically significant results). Lactulose is also more effective than placebo in improving stool frequency and stool consistency in chronic constipation patients (Grade A recommendation).[18-20] However, only 1 RCT[21] assessed the efficacy of magnesium hydroxide in patients with chronic constipation, and this trial was not placebo-controlled. Therefore, Task Force members stated that there are insufficient data to make a recommendation about the effectiveness of magnesium hydroxide in patients with chronic constipation.Data on adverse events were not adequately reported for most of these trials. However, lactulose-treated patients demonstrated a significant increase in bloating/abdominal discomfort compared with placebo-treated patients. Polyethylene glycol was associated with diarrhea. Review of available adverse event data indicates that the prevalence of diarrhea in polyethylene glycol-treated patients ranged from 2% to 40% in clinical trials.There are no placebo-controlled RCTs assessing stimulant laxatives in the management of chronic constipation symptoms. There are 4 RCTs[22-25] comparing stimulant laxatives with other therapies in the management of chronic constipation symptoms. Stimulant laxatives did not demonstrate superiority to other treatments in treating constipation. In fact, stimulant laxatives appeared to be less effective than lactulose in 1 RCT.[25] Conversely, stimulant laxatives appear to be similar to bulking agents in their efficacy for improving stool frequency and stool consistency. Most of these studies were poorly designed. Because of the lack of placebo-controlled studies and the suboptimal design of the available trials, Task Force members concluded that there are insufficient data to make a recommendation regarding the effectiveness of stimulant laxatives in patients with chronic constipation.Senna-containing stimulant laxatives have been associated with melanosis coli. However, available evidence does not indicate that melanosis coli is associated with defects in colon physiology. Although cathartic colon (a syndrome characterized by colonic dilatation and loss of haustration) has been reported in patients using stimulant laxatives, this entity has not been reported in long-term users of currently available stimulant laxatives. Thus, it is unlikely that the long-term use of stimulant laxatives induces a permanent injury to colonic mucosa or to the enteric nervous system.On the basis of data from 2 large, well-designed RCTs,[26,27] the 5-HT4 receptor agonist tegaserod is superior to placebo in improving stool frequency, stool consistency, and global chronic constipation symptoms (Grade A recommendation). Tegaserod is the only US FDA-approved treatment for chronic constipation. (ie, most laxatives are only approved for short-term use in the treatment of occasionalconstipation). For chronic constipation, tegaserod is approved for chronic use (longer than 12 weeks) with periodic reassessment by the physician to confirm the need for ongoing therapy. Unlike the IBS indication which is only for women, tegaserod is approved for the treatment of chronic constipation in men as well, because subgroup analysis in male patients demonstrated superiority of effect for tegaserod-treated patients vs placebo-treated patients. However, efficacy has not been demonstrated in patients 65 years of age and older, and therefore tegaserod is only FDA-approved for the management of chronic constipation in men and women younger than 65 years. RCT data also demonstrated improvements in total spontaneous bowel movements, complete spontaneous bowel movements, straining, and other individual symptoms of chronic constipation.Adverse event data noted that diarrhea occurred more frequently in tegaserod-treated patients compared with placebo-treated patients (6.6% vs 3%), although it was usually mild and transient with fewer than 1% of patients discontinuing tegaserod due to diarrhea.Herbal Supplements, Alternative Treatments, Lubricants, and Combination LaxativesThere are no published RCTs examining the efficacy of herbal supplements available in the United States. There are no published RCTs of combination laxatives (eg, psyllium plus senna) available in the United States. Therefore, Task Force members concluded that there are insufficient data to make a recommendation regarding the effectiveness of these agents in the treatment of chronic constipation. There are no placebo-controlled RCTs of biofeedback therapy in the management of patients with chronic constipation, although there are multiple nonrandomized trials demonstrating an increase in stool frequency from baseline, with biofeedback. Much of these data come from chronic constipation patients with pelvic floor disorders in whom biofeedback may be particularly helpful. Because it is difficult to do a "sham" biofeedback trial, it is unlikely that an appropriately designed RCT of biofeedback therapy in patients with chronic constipation will be performed. There are no RCTs examining the efficacy of mineral oil in adult patients with chronic constipation, although RCTs performed in pediatric patients[28,29] with chronic constipation demonstrate that mineral oil is more effective than stimulant laxatives but less effective than osmotic laxatives in improving stool frequency and stool consistency. (However, mineral oil may pass through the rectum and stain underwear in some patients, which may be disconcerting.)On the basis of available data, the following conclusions may be drawn:1. Among those patients who seek medical care for chronic constipation, the symptoms induce aclinically important decrement in their quality of life.2. Traditional approaches to treating chronic constipation, including dietary changes, increasedwater intake, or increased exercise, have not demonstrated improvement in symptoms inappropriately designed trials. Although as a physician I may discuss these interventions withpatients, I do not emphasize these interventions.3. Pharmacologic intervention, including the use of psyllium, is appropriate for the initialmanagement of patients with chronic constipation.4. The majority of patients with chronic constipation do not have an organic disorder causing theirsymptoms. Therefore, the routine performance of multiple diagnostic tests is not indicated inthese individuals. If patients have alarm signs or symptoms or if patients fail to respond toappropriate therapy, then further diagnostic testing should be considered.5. On the basis of the available data, this physician recommends psyllium (10-20 g/day) as initialtherapy for patients with chronic constipation symptoms. [Author Note: if patients have abdominal discomfort associated with their chronic constipation, then the appropriate diagnosis is IBS. In the management of IBS, psyllium is similar to placebo. In fact, the bloating associated with psyllium use will likely worsen symptoms in an IBS patient.]6. If a patient does not respond adequately to psyllium, then he/she should be treated with either anosmotic laxative (eg, polyethylene glycol 3350) or a promotility agent (eg, tegaserod). Both of these treatments have demonstrated efficacy in improving stool frequency and stool consistency in multiple well-designed RCTs.7. In cases of severe chronic constipation, multiple therapies may be combined. This physician'spreference is to combine an osmotic laxative (eg, polyethylene glycol) with a promotility agent (eg, tegaserod). If necessary, a lubricant may be added (eg, mineral oil) to facilitate stool passage.1. Brandt L, Schoenfeld P, Prather C, Quigley E, Schiller L, Talley N. American College ofGastroenterology Functional Gastrointestinal Disorders Task Force. An Evidence BasedApproach to the Management of Chronic Constipation in North America. Am J Gastroenterol.2005;100:S1-S21.2. Brandt LJ, Locke GR, Olden K, et al. American College of Gastroenterology FunctionalGastrointestinal Disorders Task Force. An evidence-based approach to the management ofirritable bowel syndrome in North America. Am J Gastroenterol. 2002;97:S1-S26.3. Higgins PD, Johnson JF. Epidemiology of chronic constipation in North America: A systematicreview. Am J Gastroenterol. 2004;99:750-759. Abstract4. Cheskin LJ, Kamal N, Crowell MD, et al. Mechanisms of constipation in older persons and effectsof fiber compared with placebo. Am J Geriatr Soc. 1995;43:666-669.5. Fenn GC, Wilkinson PD, Lee CE, Akbar FA. A general practice study of the efficacy of Regulan infunctional constipation. Br J Clin Pract. 1986;40:192-197. Abstract6. Ashraf W, Park F, Lof J, Quigley EM. Effects of psyllium therapy on stool characteristics, colontransit and anorectal function in chronic idiopathic constipation. Aliment Pharmacol Ther.1995;9:639-647. Abstract7. Badiali D, Corazziari E, Habib FI, et al. Effect of wheat bran in treatment of chronic nonorganicconstipation. A double-blind controlled trial. Dig Dis Sci. 1995;40:349-356. Abstract8. Anderson AS, Whichelow MJ. Constipation during pregnancy: dietary fibre intake and the effect offibre supplementation.Hum Nutr Appl Nutr. 1985;39:202-207. Abstract9. Graham DY, Moser SE, Estes MK. The effect of bran on bowel function in constipation. Am JGastroenterol. 1982;77:599-603. Abstract10. Castle SC, Cantrell M, Israel DS, Samuelson MJ. Constipation prevention: empiric use of stoolsofteners questioned. Geriatrics. 1991;46:84-86. Abstract11. Hyland CM, Foran JD. Dioctyl sodium sulphosuccinate as a laxative in the elderly. Practitioner.1968;200:698-699. Abstract12. Fain AM, Susat R, Herring M, Dorton K. Treatment of constipation in geriatric and chronically illpatients: a comparison. South Med J. 1978;71:677-680. Abstract13. McRorie JW, Daggy BP, Morel JG, Diersing PS, Miner PB, Robinson M. Psyllium is superior todocusate sodium for treatment of chronic constipation. Aliment Pharmacol Ther. 1998;12:491-497. Abstract14. Corazziari E, Badiali D, Habib FI, et al. Small volume isosmotic polyethylene glycol electrolytebalanced solution (PMF-100) in treatment of chronic nonorganic constipation. Dig Dis Sci.1996;41:1636-1642. Abstract15. Corazziari E, Badiali D, Bassocchi G, et al. Long term efficacy, safety, and tolerabilitity of lowdaily doses of isosmotic polyethylene glycol electrolyte balanced solution (PMF-100) in thetreatment of functional chronic constipation. Gut. 2000;46:522-526. Abstract16. DiPalma JA, DeRidder JH, Orlando RC, Kolts BE, Cleveland MB. A randomized, placebo-controlled, multicenter study of the safety and efficacy of a new polyethylene glycol laxative. Am J Gastroenterol. 2000;95:446-450.Abstract17. Attar A, Lemann M, Ferguson A, et al. Comparison of a low dose polyethylene glycol electrolytesolution with lactulose for treatment of chronic constipation. Gut. 1999;44:226-230. Abstract18. Bass P, Dennis S. The laxative effects of lactulose in normal and constipated subjects. J ClinGastroenterol. 1981;3(suppl 1):23-28. Abstract19. Sanders JF. Lactulose syrup assessed in a double-blind study of elderly constipated patients. JAm Geriatr Soc. 1978;26:236-239. Abstract20. Wesselius-De Casparis A, Braadbaart S, Bergh-Bohlken GE, Mimica M. Treatment of chronicconstipation with lactulose syrup: results of a double-blind study. Gut. 1968;9:84-86. Abstract21. Kinnunen O, Salokannel J. Constipation in elderly long-stay patients: its treatment by magnesiumhydroxide and bulk-laxative. Ann Clin Res. 1987;19:321-323. Abstract22. MacLennan WJ, Pooler AFWM. A comparison of sodium picosulphate ("Laxoberal") withstandardised senna ("Senokot") in geriatric patients. Curr Med Res Opin. 1974-75;2:641-647.23. MacCallum G, Ballinger BR, Presly AS. A trial of bran and bran biscuits for constipation inmentally handicapped and psychogeriatric patients. J Hum Nutr. 1978;32:369-372. Abstract24. Rider JA. Treatment of acute and chronic constipation with bisoxatin acetate and bisacodyl.Double-blind crossover study. Curr Ther Res Clin Exp. 1971;13:386-392. Abstract25. Connolly P, Hughes IW, Ryan G. Comparison of "Duphalac" and "irritant" laxatives during andafter treatment of chronic constipation: a preliminary study. Curr Med Res Opin. 1974-75;2:620-625.26. Johanson J, Wald A, Tougas G, et al. Effect of tegaserod in chronic constipation: a randomized,double-blind, controlled trial. Clin Gastroenterol Hepatol. 2004;2:796-805. Abstract27. Kamm M, Muller-Lissner S, Talley NJ, et al. Tegaserod for the treatment of chronic constipation:a randomized, double-blind, placebo-controlled multinational study. Am J Gastroenterol.2005;100:362-372. Abstract28. Tolia V, Lin CH, Elitsur Y. A prospective randomized study with mineral oil and oral lavagesolution for treatment of faecal impaction in children. Aliment Pharmacol Ther. 1993;7:523-529. Abstract29. Sondheimer JM, Gervaise EP. Lubricant versus laxative in the treatment of chronic functionalconstipation of children: a comparative study. J Pediatr Gastroenterol Nutr. 1982;1:223-226. AbstractFunding InformationSupported by an independent educational grant from Novartis.Medscape Gastroenterology. 2005;7(2) © 2005 Medscape。