文拉法新治疗上消化道癌伴发抑郁状态的疗效观察-2003
文拉法辛缓释剂治疗抑郁症的疗效观察
抑 郁 症 是 目前 社 会 危 害 人 类 健 康 的 常 见 主 要 慢 性 致 残 性 精神障碍 , 可严重 影 响患者生 活质 量 , 降 低 生 活 质 量 。文 拉 法辛 是 一 种 5 一 羟色 胺 ( 5 一 HT) 和去 甲肾上腺 素 ( N E) 神 经
递 质 双 重 h再 摄 取 抑 制 剂 ( S N RI s ) _ ] ] , 经 全 球 多 中 心 对 照 研 究证 实文拉法辛治疗抑郁症疗效显著 , 本 文 评 价 文 法 拉 辛 缓 释剂治疗抑郁症临床效果 , 现总结如下。
治 疗 脑 出血 的方 法 较 多 , 本 文 运 用 颅 内 血 肿 微 创 清 除 加 腰 穿 脑 脊 液 置 换 联 合 醒脑 静 治 疗 , 因颅 内血 肿 微 创 清 除 术 可 在 几 分 钟 内迅 速 进 入 血 肿 腔 , 尽 快 迅 速 降颅 内高压 , 减 轻 了对 正 常 脑 组 织 及 血 管 的损 伤 。本 文 所 有 患 者 行 侧 脑 室 引 流 术 后 早 期 进 行 了腰 穿 , 按照“ 等量 置换” 的原则 , 用 生 理 盐 水 置 换 出 血 性脑脊液 , 注入激素 防止蛛 网膜 粘连 , 以保 障 脑 室 系 统 循 环 通 畅 J 。醒 脑 静 注 射 液 可 通 过 血 脑 屏 障 直 接 作 用 于 中 枢 神 经系统 , 有效 减轻 脑水肿 , 降 低 颅 内压 , 改 善脑缺 氧 , 减 轻 神 经细胞损害 , 且 具有抗氧化作用 , 有 助 于 清 除 氧 自 由基 , 减 轻 钙超载 , 增 强脑细胞耐缺氧能力 。 总之 , 侧脑室引流加 腰穿 脑脊 液置换 术损 害小 , 对 患 者 影响不大 , 患者常能耐 受 , 亦 适 用 重 症 脑 出 血 伴 有 循 环 系 统 或其他器官并发症 不 能耐受 大手术 者 , 操作 简单 安全 , 不 需 特殊设备 , 在病 房即可操作 , 是 抢 救 脑 室 出血 一 种 迅 速 有 效 、 简单实用的应急措施 , 并 配 合 中药 醒 脑 静 进 行 治 疗 , 降低 了
文拉法辛对抑郁伴发焦虑症状患者的治疗效果观察
文拉法辛对抑郁伴发焦虑症状患者的治疗效果观察发表时间:2017-04-24T16:56:18.170Z 来源:《中国蒙医药》2017年4月第4期作者:周志强[导读] 文拉法辛对抑郁伴发焦虑症状患者具有较高的疗效,明显改善患者焦虑、抑郁症状,值得推广。
湖南省第二人民医院湖南省脑科医院 410007【摘要】目的:观察文拉法辛对抑郁伴发焦虑症状患者的治疗效果。
方法:选择本院收治的42例抑郁伴发焦虑症状患者作为研究对象,均为本院于2014年9月至2016年9月期间接收,采用随机数字抽取表法将患者分为对照组(21例)与观察组(21例),对照组采用氟西汀治疗,观察组采用文拉法辛治疗,比较治疗效果。
结果:治疗后3周和治疗后6周,两组患者焦虑、抑郁症状评分均明显降低,但观察组患者降低程度更加明显,与同时段对照组比较差异具有统计学意义(P<0.05);观察组患者治疗总有效率为95.24%,对照组治疗总有效率为71.43%,数据比较差异具有统计学意义(P<0.05)。
结论:文拉法辛对抑郁伴发焦虑症状患者具有较高的疗效,明显改善患者焦虑、抑郁症状,值得推广。
【关键词】文拉法辛;抑郁;焦虑抑郁症作为社会上较为常见的精神障碍疾病,具有慢性、致残性特征,严重影响患者的生活能力和生活质量,甚至伴随较高的病死率[1]。
焦虑症状属于抑郁症患者常见症状,也是影响治疗效果的重要因素,传统采用5-HT治疗方式难以起到有效的效果,且需要在治疗过程经常换药[2]。
而文拉法辛作为去甲肾上腺素再摄取抑制剂的主要药物,对治疗抑郁症具有起效快和作用范围广等优势。
本次研究对文拉法辛对抑郁伴发焦虑症状患者的治疗效果进行了探讨,并选择本院收治的42例抑郁伴发焦虑症状患者作为研究对象,详细内容报道如下。
1 资料与方法1.1 一般资料本次研究共选择42例患者进行研究分析,均为本院于2014年9月至2016年9月期间接收的抑郁伴发焦虑症状患者,均满足我国精神障碍分类与诊断标准第三版中相关诊断要求,并排除自杀倾向严重患者、相关药物过敏患者等[3]。
文拉法辛治疗抑郁症伴发焦虑的临床疗效及分析
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6 周 为1 疗程。在此期间不准使用其它抗精神病药物 。
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文拉法辛缓释剂治疗抑郁症的疗效及安全性
文拉法辛缓释剂治疗抑郁症的疗效及安全性【摘要】目的:探讨文拉法辛缓释剂治疗抑郁症的疗效及安全性.方法:采取随机平行对照研究方法,将我院收治的86例抑郁症患者随机分为两组,观察组与对照组各43例,观察组患者给予文拉法辛缓释剂治疗,对照组患者给予帕罗西汀药物治疗,观察并比较两组患者的治疗效果和药物不良反应发生情况,使用汉密尔顿抑郁量表17项对患者的抑郁状况进行评定。
结果:观察组与对照组治疗后HRSD评分比较差异有统计学意义,P0.05。
结论:文拉法辛缓释剂治疗抑郁症起效快,安全有效,且药物不良反应少,具有临床推广价值。
【关键词】文拉法辛缓释剂抑郁症疗效安全性本次研究选取了我院收治的86例抑郁症患者,将应用文拉法辛缓释剂与应用帕罗西汀药物的两组患者进行了对比分析,旨在探讨文拉法辛缓释剂治疗抑郁症患者的疗效及安全性,获得了满意结果,现报告如下。
1 资料与方法1.1 一般资料选取于2014年12月-2015年12月在我院住院治疗的抑郁症患者共86例为研究对象,将所有患者随机分为两组,观察组与对照组各43例,观察组中男性患者26例,女性患者17例,年龄18~60岁,平均年龄(42.38±7.95)岁,病程1~42个月,平均病程(19.58±2.61)个月;对照组中男性患者26例,女性患者17例,年龄18~60岁,平均年龄(42.38±7.95)岁,病程1~42个月,平均病程(19.58±2.61)个月。
两组患者一般资料方面比较均不均显著性差异,P>0.05,可做对照比较。
1.2 治疗方法观察组给予文拉法辛缓释剂进行治疗,每次剂量为75mg,1次/d,用药3d后将剂量增加至150mg/d,日后可根据患者病情增加剂量,最高剂量不可超过300mg/d。
对照组患者给予帕罗西汀进行治疗,10mg/d,于用药3d后将剂量增加至20mg/d,日后可根据患者病情增加剂量,最高剂量不可超过40mg/d。
文拉法辛缓释片治疗抑郁症疗效观察
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文拉法辛治疗抑郁症的疗效分析
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Depression in Cancer文拉法辛治疗肿瘤、癌症伴抑郁焦虑的国外文献
Depression in Cancer:New Developments Regarding Diagnosis and TreatmentCharles L.Raison and Andrew lerConsiderable data demonstrate the high prevalence of symptoms of depression in patients with a wide variety of neoplastic disorders.Moreover,the dire consequences of these depressive symptoms in cancer patients have been well documented.Recent conceptual developments in the potential contributing mechanisms include increasing ap-preciation of the possibility that behavioral alterations in cancer patients may represent a“sickness syndrome”that results from activation of the inflammatory cytokine net-work.This sickness syndrome,which has been well doc-umented in patients and laboratory animals exposed to inflammatory cytokines,includes symptoms that overlap with those seen in major depression.Conceptualizing these symptoms as components of cytokine-mediated sick-ness behavior has several important,and potentially novel,implications,including1)an expansion of the neurobehavioral symptoms that are relevant to diagnosis and treatment;and2)an increased appreciation of the potential diagnostic utility of peripheral markers of in-flammation,as well as cytokine-related neurocircuitry alterations as defined by brain imaging.Treatment impli-cations focus on the pathways by which inflammatory cytokines influence behavior,including therapeutic targets such as the inflammatory cytokines themselves,cortico-tropin-releasing hormone,and monoaminergic neuro-transmitters and their precursors.Finally,recent data suggest that aggressive treatment strategies initiated be-fore inflammation-inducing cancer treatments might pre-vent behavioral alterations,including depression,before they occur.Biol Psychiatry2003;54:283–294©2003 Society of Biological PsychiatryKey Words:Cancer,depression,sickness behavior,cyto-kines,antidepressants,inflammationIntroductionA diagnosis of cancer is one of life’s most disturbingand dispiriting events,bringing in its wake the possibility of psychological distress,physical suffering,and a foreshortened future.Our fear of cancer promotes the frequently unexamined assumption,even in health professionals,that depression is an understandable,and normal,reaction to the disease.Remarkably,however, despite prevalence rates far in excess of those seen in medically healthy individuals,most patients with cancer do not develop major depression,suggesting that cancer is a risk factor,rather than a mandate,for depression(Mc-Daniel et al1995).Cancer has long been recognized as a significant psy-chosocial stressor,and an extensive body of literature demonstrates that psychosocial stress predisposes toward the development of mood disorders(Holsboer2000). Newer data also highlight the importance of cancer-related physiologic changes in contributing to depression.Indeed, many studies are consistent with the notion that inflam-matory activation,whether resulting from cancer or its treatment,poses a significant risk for the development of depression and related symptoms,such as fatigue and anorexia(Dantzer2001).This article will review the current state of our knowl-edge regarding the diagnosis,prevalence,and treatment of depression in patients with cancer.Following this,we will revisit a long-standing debate concerning how to distin-guish the neurovegetative symptoms of depression,such as insomnia,anorexia,and fatigue,from symptoms that occur as a direct outcome of medical illness,discussing the possibility that depression and symptoms of illness are difficult to distinguish precisely because they represent a broader pathophysiologic syndrome in medically ill pa-tients that arises within the context of chronic immune activation.This syndrome,frequently referred to as sick-ness behavior,or sickness syndrome(Kent et al1992), may be a more appropriate target for intervention than is major depression as currently conceptualized.Moreover, expanding the range of neurobehavioral symptoms that are relevant in patients with cancer to include sickness symp-toms,such as pain and fatigue,may enhance the efficacy of treatments aimed at reducing these symptoms,high-lighting the potential benefits of an inclusive approach to the diagnosis of depression in patients with cancer and other medical illnesses.From the Mind-Body Program,Department of Psychiatry and Behavioral Sciences,Emory University School of Medicine,Atlanta,Georgia.Address reprint requests to Andrew ler,M.D.,Emory University School ofMedicine,Department of Psychiatry and Behavioral Sciences,1639PierceDrive,Suite4000,Atlanta,GA30322.Received November22,2002;revised February18,2003;accepted April1,2003.©2003Society of Biological Psychiatry0006-3223/03/$30.00doi:10.1016/S0006-3223(03)00413-XDiagnosing Depression in the Context of CancerDiagnosing depression in the context of cancer is compli-cated by the overlap of depressive and sickness symptoms, as well as by the question of whether depression should be viewed as a categoric disorder or a spectrum condition. Each of these issues will be considered in turn.Many symptoms common to major depression in the medically healthy are also frequently observed in patients with cancer who do not endorse full syndromic depression (McDaniel et al1995).Indeed,as can be seen in Table1, a striking overlap exists between symptoms required to meet DSM-IV criteria for major depression and symptoms commonly observed in the context of illness.Especially relevant in this regard are neurovegetative symptoms ofdepression that are often directly caused by pathophysio-logic processes inherent to neoplasia itself,or by concur-rent treatment modalities,such as chemotherapy and radiation.These symptoms include sleep alterations,an-orexia,weight loss,fatigue,cognitive impairment,and psychomotor slowing.Much discussion has occurred over the years as to whether symptoms shared by illness and depression should be excluded,or counted toward a diagnosis of depression in patients with cancer.An oft-quoted compromise in this debate was proposed by Co-hen-Cole and colleagues in1993,who recommended that two systems of diagnosis be employed in cancer patients (Cohen-Cole et al1993).They suggested that an exclusive approach is most appropriate for obtaining the specificity required by research,whereas an inclusive approach is more appropriate for managing cancer-related depression in the clinical arena.The exclusive approach removes fatigue and anorexia and requires only four of the remain-ing DSM-IV depressive symptoms(instead of five)to meet a diagnosis of major depression.A recent revision of the exclusive approach toward diagnosing major depres-sion in patients with medical illness has been elaborated in a study by von Ammon Cavanaugh and colleagues.These researchers attempted to increase the specificity of depres-sive symptoms seen in the context of illness by only counting symptoms if they coincide or intensify with the onset of depressed mood,anhedonia,or hopelessness(von Ammon Cavanaugh et al2001).In contradistinction to these approaches,an inclusive approach counts all symp-toms that qualify toward a diagnosis of depression,with-out making a determination of whether the symptoms result from illness or a mood disorder.Although research paradigms may benefit from the enhanced sensitivity of exclusive diagnostic approaches,it is increasingly clear that clinical purposes are better served by taking an inclusive approach toward depression in patients with cancer and other medical illnesses.Given the negative impact that depression has on outcome in medical illness(Wells et al1989),and given the excellent risk/ benefit ratio of the newer antidepressants,it is clinically prudent to recognize that patients with symptoms consis-tent with depression are likely to benefit from therapeutic interventions,whether or not these symptoms arise from “depression”or from very similar sickness syndromes that are common in the context of illness.Indeed,preclinical and clinical data indicate that sickness/depressive symp-toms respond to antidepressant therapy irrespective of putative etiology(Yirmiya et al1999).Moreover,antide-pressants are known to be of use in treating a number of sickness symptoms associated with depression,even when these symptoms occur outside the context of a diagnosable mood disorder.For example,many patients with depres-sion experience increased pain,and antidepressants(espe-cially tricyclics,venlafaxine,and bupropion)have been shown to decrease several types of pain in patients without depression(Max et al1992;Semenchuk et al2001; Sumpton and Moulin2001).Similarly,antidepressants can aid in the treatment of insomnia(i.e.,mirtazapine)(Kast 2001)and have been reported to decrease hot flashes in patients with cancer(fluoxetine,paroxetine,and venlafax-ine)(Loprinzi et al2000,2002;Stearns et al2000). Finally,several sickness-related symptoms,especially in-somnia and pain,have been shown to be significant risk factors for the development of depression,suggesting that their treatment in medically ill patients may forestall the development of a fully syndromal mood disorder(Breslau et al1996).Nonetheless,far less data are available on the use of antidepressants for the treatment of sickness symp-toms outside the context of major depression than are available for the treatment of major depression,and this must be taken into account when initiating antidepressant treatment in patients with cancer,who are frequently on multiple other medications and who may be especially sensitive to antidepressant-related adverse events.parison of Cytokine-Induced Sickness Syndrome and Major DepressionSickness Behavior Major Depression Anhedonia AnhedoniaSocial Isolation Social isolation Fatigue FatigueAnorexia AnorexiaWeight Loss Weight lossSleep Disturbance Sleep disturbance Cognitive Disturbance Cognitive disturbance Decreased Libido Decreased libido Psychomotor Retardation Psychomotor retardation Hyperalgesia Depressed mood aGuilt/worthlessness aSuicidal ideation aa More common in major depression than sickness.284 C.L.Raison and ler BIOL PSYCHIATRY2003;54:283–294The question of whether mood disorders are best con-ceived as discrete categories or as spectrum disorders has been an ongoing debate within the field of psychiatry (Kendler and Gardner1998).This issue has clear impli-cations for the diagnosis of depression in patients with cancer,given that many cancer patients will suffer from dysphoric stress reactions currently subsumed under the rubric of“adjustment disorders”in the DSM-IV. Other patients will manifest depressive reactions currently diagnosed as minor depression in the DSM-IV.An even larger group of patients may experience depressive symp-toms too few or mild to qualify for any syndromal diagnosis.As with the exclusive/inclusive debate,increasing evi-dence argues for viewing depression in broader terms as a symptomatic,as well as a categoric,condition in patients with cancer and other medical illnesses.Much data dem-onstrates that subsyndromal depression is associated with significant morbidity,in patients both with and without concurrent medical conditions(Wells et al1989).Like-wise,depressive symptoms,even when not qualifying for major depression,can increase mortality and morbidityacross a range of medical conditions(Evans et al1999). Finally,depressive symptoms,even when not qualifying for major depression,have been shown to respond to antidepressant treatment in patients with cancer(Evans et al1988).The widespread tendency to excuse depression as a natural reaction to cancer and the overlap between sick-ness and depressive symptoms both highlight the impor-tance of accurately assessing depression in the context of neoplastic illness.Standardized instruments are especially valuable in this regard,whether they be highly valid and reliable self-report questionnaires,such as the Beck De-pression Inventory(Beck1988)or Zung Self-Rating Depression Scale(Zung1965),or interview-based assess-ments,such as the Hamilton Depression Rating Scale (Hamilton1960)or the Montgomery Asberg Depression Rating Scale(Davidson et al1986).Self-report question-naires have the advantage of not requiring the presence of a trained psychiatric interviewer and can thus be com-pleted by patients while they are waiting to see the physician.Interviewer-based assessments benefit from the insight of a trained clinical interviewer and may avoid self-reporting biases.And whereas assessment interviews tend to define overlapping populations,specific instru-ments are more useful for identifying depression either exclusively or inclusively in patients with cancer.For example,the Beck Depression Inventory emphasizes mood and cognitive symptoms that are more specific to depression than are neurovegetative symptoms shared by major depression and physical illness.Similarly,the Montgomery Asberg Depression Rating Scale was de-signed to reduce the impact of neurovegetative symptoms on the identification of depression in the context of medical illness.At the other end of the inclusive/exclusive spectrum,we have found the Neurotoxicity Rating Scale (a39-item self-report instrument)to be extremely useful for assessing the full range of neurobehavioral symptoms that frequently afflict patients with cancer(Valentine et al 1998).Nevertheless,further validation of the Neurotoxic-ity Rating Scale in medically ill patients is required. Prevalence of Depression in Cancer Patients How depression is diagnosed is germane to the question of how prevalent the condition is in patients with cancer. Clearly,prevalence rates will increase if depression is defined inclusively and symptomatically,rather than ex-clusively and categorically.A significant source of vari-ance in reported depression rates arises from the fact that studies have used each of these approaches(McDaniel et al1997).Even when assessed symptomatically,different assessment instruments have been shown to identify par-tially nonoverlapping populations.Prevalence rates for depression in patients with cancer have been reported to range from1.5%to50%(McDaniel et al1995).Reviews of the literature place median point prevalence rates between22%and29%(Hotopf et al 2002),which is significantly higher than prevalence rates for the general U.S.population(Kessler et al1994).In addition to diagnostic issues,a number of other factors contribute to the widely divergent depression rates re-ported across studies(see Table2).Prevalence of depres-Table2.Factors that Affect the Prevalence of Depression in Patients with CancerType of CancerPancreasϾoropharynxϾbreastϾcolonϾgynecologicϾlymphomaϾgastricϾleukemiaSeverity of DiseaseChemotherapeutic RegimenInterferon-␣Interleukin-2Amphotericin-BCycloserineGlucocorticoidsL-asparaginaseLeuprolideProcarbazineTamoxifenVinblastineVincristineSurgery TypeMastectomyϾbreast conservationDepression Diagnostic CriteriaInclusiveϾexclusiveSymptomaticϾcategoricDepression in Cancer285BIOL PSYCHIATRY2003;54:283–294sion varies based on the type of cancer involved,with depression rates generally reported to be highest for pancreatic,oropharyngeal,and breast carcinomas and lowest for lymphoma,leukemia,and gastric cancers(Mc-Daniel et al1995).As with medical illnesses in general (Evans et al1999),rates of depression in cancer patients increase as disease severity intensifies(Ciaramella and Poli2001;Moffic and Paykel1975).The type of treatment patients undergo can also signif-icantly affect the likelihood of developing depression.As discussed below,cytokines such as interleukin(IL)-2or interferon-␣-2-(IFN-␣),which are used in the treatment of several malignancies,are notorious for inducing depres-sive symptoms(Capuron et al2001).For example,rates of developing major depression approach50%in patients receiving chronic,high-dose,IFN-␣therapy(Musselman et al2001a).Other cancer-related medications frequently associated with depression include amphotericin-B,cy-closerine,glucocorticoids,L-asparaginase,leuprolide, procarbazine,tamoxifen,vinblastine,and vincristine(Rai-son and Nemeroff2000).Recent data suggest that in some instances chemotherapeutic regimens may have long-term effects on mood.In a large study of adults who had survived childhood leukemia,Hodgkin’s disease,or non-Hodgkin’s lymphoma,depressive symptoms were signif-icantly more common in cancer survivors than in nonaf-fected siblings(Zebrack et al2002).Intensity of chemotherapeutic exposure in childhood predicted the prevalence of depressive symptoms in adulthood(Zebrack et al2002).Finally,oncologic surgery may increase the risk of developing depression.A prospective study re-ported that depression is more common in women who undergo mastectomies compared with women who have breast-conserving treatment(Omne-Ponten et al1992). Although this observation has been traditionally ascribed to psychological stress resulting from an altered body image after mastectomy,more invasive surgical proce-dures also induce higher levels of IL-6and C-reactive protein(Jakeways et al1994;Kristiansson et al1999). Hence,it is possible that surgery may promote depression in cancer patients at least in part via activation of the proinflammatory cytokine network(Yirmiya et al1999). Consistent with this notion,increased serum concentra-tions of IL-6have been reported to correlate with increas-ing depressive symptom scores in patients undergoing abdominal surgery(Kudoh et al2001).It should be noted, however,that several studies have failed to replicate an association between mastectomy and increased depression (Fallowfield et al1990;Levy et al1992).Moreover,the effects of surgery on immune function appear to be complex,and not all studies report increased proinflam-matory activity after surgery(Di Padova et al1991; Kruimel et al1999).Consequences of DepressionWhether depression represents a significant risk factor for the development of cancer remains unclear(McDaniel et al1995;McGee et al1994;McKenna et al1999). Nevertheless,several studies have suggested that depres-sion predisposes toward a worsened clinical outcome once cancer has developed.A recent study reports that patients with a history of depressive symptoms are at a2.6times increased risk of dying from their cancer within the first19 months after diagnosis(Stommel et al2002).In another study of103cancer patients,a depressive coping style correlated with decreased survival time,even when other biomedical risk factors,such as tumor stage and histologic classification,were taken into account(Faller et al1999). In addition to potential direct effects on survival,depres-sion is known to decrease compliance with therapy, increase length of hospital stay,and diminish both quality of life and the ability to care for oneself(Koenig et al 1989,1992;Pelletier et al2002;Stoudemire and Thomp-son1983).Depression that develops in response to med-ication treatment may also impact therapeutic efficacy, and by extension,both quality of life and survival.For example,patients who develop major depression while receiving IFN-␣for malignant melanoma were signifi-cantly more likely to discontinue treatment than were patients without depression(35%vs.5%)(Musselman et al2001a).Similarly,patients who become depressed after stem cell transplant have been found to have a threefold increased risk of dying between6and12months after the procedure,even after adjusting for other prognostic factors (Loberiza et al2002).Treatment of Depression in Patients with CancerThe paucity of well-controlled trials of antidepressants in patients with cancer and comorbid depression underscores the tremendous need for data on how to best treat this patient population.Fortunately,however,the bulk of available data suggests that,as is the case with major depression in general,depression that arises in the context of cancer is responsive to antidepressant treatment(Raison and Nemeroff2000).Initial evidence that antidepressants were useful in depressed cancer patients came from an open trial of the tricyclic antidepressant imipramine by Evans and colleagues in the late1980s(Evans et al1988). Since that time,five controlled,randomized trials have been published(see Table3).Three of these trials were placebo controlled(Costa et al1985;Razavi et al1996; van Heeringen and Zivkov1996);two of the trials used an active comparator without placebo(Holland et al1998; Pezzella et al2001).With various measures of depression286 C.L.Raison and ler BIOL PSYCHIATRY2003;54:283–294and outcome,these studies indicate that paroxetine (one study)(Pezzella et al 2001),mianserin (two studies)(Costa et al 1985;van Heeringen and Zivkov 1996),fluoxetine (one study)(Razavi et al 1996),amitriptyline (one study)(Pezzella et al 2001),and desipramine (one study)(Holland et al 1998)are useful in treating depres-sion in patients with cancer.A recent open-label,cross-over trial suggests that mirtazapine decreased depressive symptoms,improved functional capacity,and reduced cachexia (Theobald et al 2002).In addition to effects on core depressive symptoms,antidepressants hold promise as adjunctive treatments for other symptoms related to cancer or its treatment.In double-blind trials,fluoxetine,paroxetine,and venlafaxine have been shown to reduce hot flashes in cancer patients (Loprinzi et al 2000,2002;Stearns et al 2000).Venlafax-ine,bupropion,and the tricyclic antidepressants have been shown to relieve neuropathic pain,which frequently ac-companies cancer and its treatment (Max et al 1992;Semenchuk et al 2001;Sumpton and Moulin 2001).In addition to antidepressants,several studies suggest that psychosocial interventions might benefit patients with cancer.Significant data suggest that psychotherapy can alleviate depressive symptoms and improve coping skills (Ross et al 2002).Moreover,two landmark studies have shown that group therapy has the potential to extend survival in patients with breast cancer (Spiegel et al 1989)and malignant melanoma (Fawzy et al 1993).In the studies in malignant melanoma,group therapy enhanced active coping,decreased affective disturbance,and in-creased the number and activity of natural killer cells (Fawzy et al 1990a,1990b).These findings of increased longevity have been replicated in one study of individual psychotherapy and in another that used recurrent home visits from a specialty nurse (Kuchler et al 1999;Mc-Corkle et al 2000);however,these results need to be tempered by the fact that several studies have failed to confirm that psychotherapeutic intervention promotes sur-vival in patients with cancer (Ross et al 2002).A final treatment issue relates to the need for character-ization of individual vulnerability factors that predispose to behavioral alterations during cancer and its treatment.Indi-viduals loaded with vulnerability factors may be the most likely to respond to treatment and pretreatment interventions,thus improving the ability to identify effective treatment strategies and obviate negative results in individuals who are unlikely to experience behavioral alterations regardless of the clinical conditions.Relevant in this regard,our group re-cently observed that patients who developed major depres-sion during IFN-␣treatment exhibited an increased produc-tion of adrenocorticotropic hormone (ACTH)and cortisol in response to the initial dose of IFN-␣(Capuron et al,in press a).Interestingly,elevations in IFN-induced ACTH and cortisol production also correlated with the presence of mild depressive symptoms before IFN-␣therapy (Capuron et al 2002).These results suggest that patients with evidence of preexisting stress system hyperactivity may be at increased risk of developing depressive symptoms during IFN-␣therapy.Thus,patients who demonstrate even mild depression or anxiety before inflammatory challenge (such as happens during chronic illness)may represent a vulnerable population that would benefit from early identification and aggressive (and perhaps prophy-lactic)antidepressant treatment.New Conceptual DevelopmentsSickness BehaviorAlthough there has been substantial focus on the psycho-social factors that may contribute to the high rate ofTable 3.Controlled Trials of Antidepressants in Patients with CancerInvestigators Population/Cancer Type N DesignResultsPezzella et al 2001Female/breast179Multicenter 8weeks PAROX vs.AMIEqually significant decrease in depressive symptoms and improvement in quality of life with both antidepressants.Holland et al 1998Female/mixed 401week PBO washout,then 6weeks FLUOX vs.DESIPSignificant decrease in depression and anxiety symptoms with both antidepressantsRazavi et al 1996Male/female/mixed 96Multicenter 6-weeks trial,1week PBO wash-out,then FLUOX vs.PBONo difference between FLUOX and PBO for most measures of depressive symptomsvan Heeringen and Zivkov 1996Female/breast 551week PBO washout,then 6weeks MIAN vs.PBO;LOCFSignificant decrease in depressive symptom severity and increased number of responders in MIAN groupCosta et al 1985Female/mixed 734-week trial of MIAN vs.PBO.No PBO washout;LOCFSignificant decrease in depressive symptoms on multiple scales in patients on MIAN compared with placeboPAROX,paroxetine;AMI,amitriptyline;PBO,placebo;FLUOX,fluoxetine;DESIP,desipramine;MIAN,mianserin;LOCF,last observation carried forward.Depression in Cancer287BIOL PSYCHIATRY 2003;54:283–294depression in patients with cancer,new developments in the biology of mood disorders have raised novel consid-erations regarding the pathophysiology and treatment of depression in neoplastic disorders and other medical ill-nesses(Maier and Watkins1998).Specifically,data have demonstrated that proinflammatory cytokines released during tissue damage and destruction(and the resultant inflammation)can have a substantial impact on neuro-transmitter function,neuroendocrine function,and behav-ior(Dunn et al1999).Behavioral changes include the induction of a syndrome,called sickness behavior,that hasmany overlapping features with major depression(see Table1)(Kent et al1992).Therefore,it has been proposed that proinflammatory cytokines released in the context of immune activation and inflammation may in turn contrib-ute to the high rate of depression in cancer patients (Dantzer2001).Further understanding of the pathways by which proinflammatory cytokines influence behavior,in-cluding,most importantly,the neural substrates involved, may provide a foundation for developing new strategies for identifying and treating depression in patients with cancer and other medical conditions.Relevant in this regard are data demonstrating that aggressive treatment strategies can prevent depressive symptoms in cancer patients at high risk for mood disorders(see below) (Musselman et al2001a).Cytokines and BehaviorA rich database has been developed that substantiates the capacity of proinflammatory cytokines,including tumor necrosis factor(TNF)-␣,IL-1,and IL-6,to induce the syndrome of sickness behavior(Yirmiya et al1999). Sickness behavior is typically associated with the behav-ioral changes seen in humans and laboratory animals suffering from microbial infections and includes anhedo-nia,cognitive dysfunction,anxiety and irritability,psy-chomotor slowing,anergia and fatigue,anorexia,sleep alterations,and increased sensitivity to pain(Kent et al 1992).Relevant to its mediation by proinflammatory cytokines,sickness behavior can be reliably reproduced by administration of each of the proinflammatory cytokines in isolation or by administering agents(e.g.,endotoxin or lipopolysaccharide)that induce the proinflammatory cyto-kine cascade(TNF-␣to IL-1to IL-6)(Yirmiya et al1999). Although proinflammatory cytokines are too large to freely pass through the blood–brain barrier,several path-ways by which cytokine signals can access the brain have been elucidated,including passage of cytokines through leaky regions in the blood–brain barrier,active transport, and transmission of cytokine signals via afferent nerve fibers(e.g.,vagus)(Plotkin et al1996;Rivest et al2000; Watkins et al1995).Within the brain,a cytokine network has been described that consists of cell types that can both produce cytokines(glia/neurons)and receive their signals via relevant receptors(Benveniste1998). Interestingly,recent work by our group and others has demonstrated that proinflammatory cytokines are elevated in medically ill patients with depression and correlate with symptoms of sickness behavior.For example,plasma concentrations of IL-6were found to be significantly increased in cancer patients with depression compared with nondepressed control subjects with cancer(Mussel-man et al2001b).In addition,in several studies,both IL-1 and IL-6have been found to significantly correlate with fatigue in cancer patients undergoing treatment with radi-ation or chemotherapy(Bower et al2002;Greenberg et al 1993).At present,the source(host vs.neoplastic cells)of these proinflammatory cytokines is unknown;however, studies in which advanced flow cytometric techniques as well as microarray analyses are used are under way to isolate the presence of specific cytokines as they appear in specific cell types.Nevertheless,based on the noted findings(albeit limited to date),one might speculate that cancers that are associated with more aggressive inflam-matory reactions or cancers in which neoplastic cells produce cytokines,might be most likely to be associated with behavioral disturbances.In terms of mood regulation,there are at least five pathways by which proinflammatory cytokines may cause depression or sickness behavior(see Table4).First, proinflammatory cytokines(especially IL-1,IL-6,and TNF-␣)have been shown to alter the metabolism of the monoamines,including norepinephrine,serotonin,and dopamine,all of which have been implicated in the pathophysiology of mood disorders(Dunn et al1999). Second,cytokines have been shown to have potent stim-ulatory effects on the hypothalamic–pituitary–adrenal (HPA)axis,in large part through activation of corticotrop-in-releasing hormone(CRH)(Besedovsky et al1986; Rivier1995).Corticotropin-releasing hormone has behav-ioral effects in animals that are similar to those seen in patients suffering from depression or sickness behavior, including alterations in activity,appetite,and sleep (Owens and Nemeroff1991).Moreover,patients with Table4.Potential Pathways to Sickness Behavior in Medically Ill PatientsCytokine disruption of monoamine metabolism in the central nervous systemCytokine induction of corticotropin-releasing factorCytokine disruption of glucocorticoid receptor–mediated feedback inhibition of inflammation and corticotropin–releasing factor Cytokine induction of enzymes that metabolize tryptophanCytokine inhibition of pathways involved in thyroid hormone metabolism(euthyroid sick syndrome)288 C.L.Raison and ler BIOL PSYCHIATRY2003;54:283–294。
文拉法辛缓释剂对抑郁伴发焦虑障碍患者的疗效
a o t d o v u t t e fi a . S f t w es m e b T S , l or o nd hy i a d p e t e al a e he f c cy a e y as ti at d y E S ab at ry a p s c 1
0 1 例;年龄 复杂。 文拉法辛不仅对 抑郁症治疗有 效, 而且对抑 门诊患者,共 2 例 ,其中男 1 例 ,女 9 郁伴发的焦虑症状 也有效 。国外文献报道文拉 1  ̄6 岁,平均 (4± 1) 8 0 3 3 岁;有阳性精神 病家族 例;首次抑郁发作伴发广泛性焦虑 1 例 , 3 复 法辛缓释剂治疗广 泛性焦虑症有 效f刚 5 ,对抑郁症 史者 8 . 发性抑郁症伴发广泛性焦虑 7 病 期 ( 1 ) 例; 2 ±9 个 共患焦虑障碍也有一定的疗效 。 ] 国内对新型抗抑 1项 A D 1) 郁药物治疗 两者共病 的报道较少 , 我们对抑郁症伴 月 ;汉密尔顿抑郁量表 (7 ,H N 一 7 评分均
4 周末评定汉密尔顿抑郁量表 ( 项,H M 和汉密尔顿焦虑量表 ( A A , 、6 1 7 A D) H M )并监测血压,记录 不 良反应 。结果 文拉 法辛缓释 剂对抑郁伴 发 焦虑障碍效 果 良好 ,H M A D评分 自第 1 周起 均有显著 改 善 ,且一 直持 续至 治疗第 6周末 。H M A A评 分 自第 1周起也有 显著 改善 。不 良反应轻微 。结论 文拉 法辛 缓释 剂抗抑 郁及 抗 焦虑作 用 尚可 ,可 用于抑 郁症 伴发 焦 虑障碍 的 治疗 。
文拉法辛缓释片治疗抑郁症的疗效和不良反应评价
文拉法辛缓释片治疗抑郁症的疗效和不良反应评价刘杰(大同市第六人民医院,山西大同037045)(46.28±2.67)岁;致伤原因:车祸20例,坠落12例,砸伤2例;Anderson-Custilo 分类:Ⅱ度22例,Ⅲ度12例。
2组患者基线资料无统计学差异(P >0.05),具有可比性。
1.2方法对照组行常规灌注冲洗联合外固定架治疗。
观察组行持续VSD 联合外固定架治疗:采用可调节固定架对骨折断端予以固定,后将创面失活皮肤组织、脓液清除,止血。
对伴骨外露处,于表面皮质钻孔,确保双侧皮质钻透,行创缘皮肤清洁。
伤口表面给予VSD 敷料覆盖,适当修剪并缝合,以半透生物膜将伤口封闭,确保VSD 敷料超过伤口边缘且与皮肤密合,形成闭合伤口。
行硅胶管、三通管、负压吸引器连接,持续负压引流(375~450mm Hg )。
1.3观察指标观察2组疗效及控制感染、创面闭合、骨折愈合、功能恢复时间。
疗效标准:显效:患肢功能基本恢复,症状、肿痛消失;有效:症状好转,肿痛、患肢功能改善;无效:上述无改变,或加重[3]。
总有效率=显效率+有效率。
1.4统计学方法采取SPSS22.0统计学软件分析数据,计量资料以x ±s 表示,采用t 检验,计数资料以n (%)表示,采用χ2检验,P <0.05为差异有统计学意义。
2结果2.1临床指标观察组控制感染、创面闭合、骨折愈合、功能恢复时间均短于对照组,差异有统计学意义(P <0.05)。
见表1。
2.2临床疗效观察组总有效率(97.06%)高于对照组(79.41%),差异有统计学意义(P <0.05)。
见表2。
3讨论胫腓骨开放性骨折是一种常见的骨折类型,多为高能量损伤所致,且容易引发创面感染,持续负压封闭引流加外固定架治疗是目前理想的治疗方式。
外固定架操作简单、对骨血供破坏少,有助于骨组织血液循环改善。
VSD 在难治性伤口治疗中应用广泛,其可有效覆盖、保护创面,起到抑菌作用,能够减少再污染风险[4]。
文拉法辛用于抑郁症治疗的临床效果探究
甘肃科技Gansu Science and Technology第36卷第3期2020年2月Vol.36 No.3Feb.2020文拉法辛用于抑郁症*疗的临床/果1究张光武(甘肃省酒泉市中医院,甘肃酒泉735000)摘要:探究文拉法辛用于抑郁症治疗的临床效果$将符合本次研究标准的84例抑郁症患者分为2组,对照组42 例服用舍曲林,研究组42例服用文拉法辛$比较汉密顿抑郁量表(HAMD )评分、血清单胺类神经递质水平、生活质量量表(SF-36)评分、不良反应情况。
治疗后2组HAMD 评分较治疗前明显变小(P<0.05),且治疗后研究组HAMD评分明显小于对照组(P<0.05);治疗后2组多巴胺、去甲肾上腺素、5-軽色胺水平均高于治疗前(!<0.05),且治疗后研究组上述血清单胺类神经递质水平明显高于对照组(!<0.05);治疗后2组SF-36各维度评定分值均大于治疗前(P<0.05),且治疗后研究组SF-36各维度评定分值明显大于对照组(P<0.05);2组不良反应发生率比较差异无统计学意义(P>0.05)$抑郁症治疗使用文拉法辛,抑郁程度明显减轻,血清单胺类神经递质水平趋于合理范围,生活质量大幅改善,且安全性高$关键词:文拉法辛;抑郁症;临床效果中图分类号:R749.4抑郁症是一种具有“高发病率、高自杀率”特点 的精神患,的情绪低落, 生后多 、法中等,对患者正常生活与工作产生明显不利叫临床治 疗治疗方案,文拉法辛为5-{色胺 去甲肾上腺素 抑 ,服用 后,可影响中枢神经元处5-{色胺、去甲肾上腺素,使 再摄取进程被阻断,中枢神经神经递质(主要包括5-{色胺、去甲肾上腺素)浓度发生改变,产生抗抑郁作用527$ 于此,本研究 抑郁症治疗程中使用文拉法辛,$1临床资料与方法1.1临床资料研究对象为84例抑郁症患者,到院诊治时间均 为2017年1月~2019年6月,治时间先后顺序分组,对照组42例,男23,女19例,年龄25-54岁,平均年龄*36.74±9.18)岁;研究组42例,男24例,女18例,年龄26-55岁,平均年龄(36.77±9.21)$ 2组上述 比较,(!>0.05)$1.2纳入与排除标准纳入标准:①符合《中国精神障碍分类与诊断标 准第3版》中关于抑郁症的诊断标准;②本次研究所用 未出现过敏情况,且治疗前并未使用其他抗抑郁药物进行治疗;③患者知情且同意参与本次研究,且本次研究得到医院伦理委员会批准$排除标准:①伴有严重的器官功能性障碍疾病;②患者病情危急;③ 或酒依赖者;④哺乳期或妊 娠期女性患者。
文拉法辛缓释剂治疗抑郁症的临床效果探析
2 . 1 治疗效果 不 良
本组患者第 4周治疗有效率 3 7 . 5 %、 第8 周
【 关键 词 】抑 郁症
反 应
文拉 法辛缓释 剂 治疗 效果
治疗有效率 9 3 . 3 %, 患者治疗效果不断提高。见表 1 。
表1 本 组 患者 不 同 时 间段 的 治 疗 效 果
抑郁 障碍简称为抑郁 症 , 是一种 以患者持 续性 、 显著性 的 心境低 落 、 情绪失落为相应 临床特征 的心理 障碍性疾病 , 病情 严 重者将会 出现幻觉 、 妄想 等精神病性 症状 , 更甚者 甚至表现 出明显 的 自杀倾 向或 者 自杀行 为 , 对 患者 的家庭 幸福 、 生活质 2 . 2 症 状变化 本组患者第 4周抑郁量 表得分 ( 1 4 - 3 ±
由于当前 临床针对 抑郁症患者 的发病原 因仍 然缺乏透彻
统一 的认识 , 因此也无法针对性实施对症治疗 、 根除病 因。 但可
以明确 的是 , 包括生物 因素 、 心理 因素 、 社会 因素等多种 因素参
与到了发病过程 中, 而每一种 因素又包括 多种 影响 内容 , 因此
展调整用药 剂量 , 最大用药剂量 42 2 5 mg / 次, 维持用药剂量在 1 4 0 - 1 8 0 mr , / 次左右 。 持续治疗 8周 , 治疗过程 中可以根据患者 实 际情况给予镇静 、 催 眠类药物合用。
不 断 改善 。 本 组 患者 治 疗 期 间 不 良反 应 发 生 率 1 6 . 7 %, 给 予 对 症
患者治疗后汉密尔顿抑郁量表得分相较治疗前下降幅度为 3 0 %~
4 9 %; 无效: 患者治疗后 汉密尔顿抑郁量 表得分相 较治疗 前下
降幅度 < 3 O %。 评定患者治疗期间不 良反应发生情况 , 依据不 良 反应量表 ( T E S S ) 测定本组患者血压 、 心率 、 呼吸等 多项 生命指
文拉法辛缓释片治疗抑郁症疗效观察
龙源期刊网
文拉法辛缓释片治疗抑郁症疗效观察
作者:罗彦
来源:《中国当代医药》2012年第23期
[摘要] 目的探讨文拉法辛缓释片治疗抑郁症的临床疗效。
方法选取2009年1月~2012
年1月本院收治入院的抑郁症患者60例,将其分为观察组和对照组各30例,观察组采用文拉法辛缓释片治疗,对照组采用西酞普兰治疗,两组均治疗8周,疗程结束后用汉密尔顿抑郁量表(HAMD)评定临床疗效。
结果治疗8周后,观察组治疗抑郁症的总有效率为83.33%,对照组为70.00%,两组差异有统计学意义(P < 0.05)。
治疗后两组HAMD评分均较治疗前降低,且观察组下降较对照组明显,两组差异有统计学意义(P < 0.05)。
结论文拉法辛缓释片治疗抑郁症疗效显著,起效快,安全可靠,值得临床推广应用。
[关键词] 文拉法辛缓释片;西酞普兰;抑郁症;疗效观察。
文拉法辛治疗抑郁症疗效观察(附20例临床分析)
文拉法辛治疗抑郁症疗效观察(附20例临床分析)
李秀娥
【期刊名称】《中国健康心理学杂志》
【年(卷),期】2005(13)4
【摘要】目的文拉法辛治疗抑郁性神经症、卒中后抑郁临床疗效观察及探讨口服剂量、用药时间、副反应等相关问题。
方法符合中国精神疾病分类方案及诊断标准第2版修订本的抑郁症诊断标准的患者20例,其中10例符合1995年全国第四届脑血管病学术会议制定的脑卒中诊断标准,均口服文拉法辛治疗8周,分别在用药前及用药1、2、6周进行汉密尔顿抑郁量表评分,观察疗效及临床出现副反应情况。
结果抑郁症患者口服文拉法辛1周起效,治疗有效剂量75~225mg;卒中后抑郁的患者2周后起效,治疗有效剂量为100~225mg;副反应主要为胃肠道反应,与口服剂量大小无关。
结论文拉法辛治疗抑郁症起效迅速,疗效可靠,安全性能好。
【总页数】2页(P263-264)
【作者】李秀娥
【作者单位】内蒙古包头市中心医院神经内科
【正文语种】中文
【中图分类】R749.4;R743.3
【相关文献】
1.文拉法辛缓释剂治疗39例抑郁症的临床疗效观察
2.文拉法辛与多塞平治疗抑郁症临床对照观察(附80例报告)
3.文拉法辛与氯丙咪嗪对比治疗焦虑性抑郁症患者
的临床疗效观察4.度洛西汀与文拉法辛在治疗抑郁症同时减轻躯体疼痛症状的临床疗效观察5.伏硫西汀与文拉法辛治疗抑郁症的临床疗效观察
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文拉法新治疗功能性消化不良合并抑郁疗效观察
文拉法新治疗功能性消化不良合并抑郁疗效观察
鲁建瑞;李代秀;张集慧;金兰花
【期刊名称】《精神医学杂志》
【年(卷),期】2005(018)001
【摘要】目的了解文拉法新治疗功能性消化不良(FD)合并抑郁的疗效.方法采用文拉法新对52例门诊及住院患者功能性消化不良用汉密尔顿抑郁量表(HAMD)进行评定,以探讨文拉法新的临床疗效及安全性.结果合用文拉法新疗效显著,两组间(HAMD)评分在疗程结束时有显著差异.结论合用小剂量文拉法新治疗功能性消化不良合并抑郁可显著提高疗效.
【总页数】1页(P50-50)
【作者】鲁建瑞;李代秀;张集慧;金兰花
【作者单位】014030,内蒙古包头,内蒙古科技大学第三附属医院;014030,内蒙古包头,内蒙古科技大学第三附属医院;014030,内蒙古包头,内蒙古科技大学第三附属医院;014030,内蒙古包头,内蒙古科技大学第三附属医院
【正文语种】中文
【中图分类】R749.7;R57
【相关文献】
1.文拉法新合并无抽搐电休克治疗抑郁症疗效分析 [J], 吴凡;谢宪平;刘汝震
2.抗抑郁药治疗缺血性脑血管病合并功能性消化不良患者情绪障碍的疗效观察 [J], 郭锐;王萌
3.文拉法新合并无抽搐电休克治疗抑郁症疗效分析 [J], 孙海华;刘汝震;吴凡
4.文拉法新治疗冠心病合并抑郁症疗效观察 [J], 陈波; 李代秀; 张集慧
5.文拉法新治疗冠心病合并抑郁症疗效观察 [J], 陈波; 李代秀; 张集慧
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文拉法辛治疗伴心区不适抑郁症的临床观察
文拉法辛治疗伴心区不适抑郁症的临床观察
范毅;路卫成;张艳;王文普
【期刊名称】《天津药学》
【年(卷),期】2003(15)3
【摘要】目的:观察文拉法辛对伴心区不适抑郁症患者的疗效和副作用.方法:对43例伴有心区不适的隐匿性抑郁症患者用文拉法辛治疗4周;采用汉密尔顿抑郁量表(HAMD) 评定疗效; 不良反应症状量表(TESS)评价副作用.结果:文拉法辛治疗有效率95.3%,起效时间1~2周 .不良反应轻且随治疗时间可逐步缓解.结论:文拉法辛对伴心区不适的抑郁症病人有非常好的疗效,值得推广.
【总页数】2页(P20-21)
【作者】范毅;路卫成;张艳;王文普
【作者单位】天津市公安局安康医院,天津,300240;天津市公安局安康医院,天津,300240;天津市公安局安康医院,天津,300240;天津市公安局安康医院,天
津,300240
【正文语种】中文
【中图分类】R971+.43
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2.米氮平联合文拉法辛治疗伴失眠的老年抑郁症患者效果观察及对睡眠质量、血清5-HT的影响 [J], 鲍莎莎;宋哲;张金峰;张世阳;张秋伏
3.抑郁症伴焦虑症患者采用文拉法辛治疗的效果观察 [J], 周中华; 郑又祥; 刘卫斌; 钟衔江; 曾艳
4.伏硫西汀与文拉法辛治疗伴认知功能损害抑郁症临床疗效对比 [J], 周小艳;冉江峰;范征莉;杨辉;黄雪萍
5.文拉法辛联合阿普唑仑治疗伴焦虑的抑郁症的效果 [J], 吴波
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文拉法辛治疗30例脑卒中后抑郁患者的疗效观察
文拉法辛治疗30例脑卒中后抑郁患者的疗效观察
周志壮;于永达;高毅
【期刊名称】《哈尔滨医药》
【年(卷),期】2005(025)006
【摘要】脑卒中后抑郁状态(PSD)是一种常见的脑血管病并发症,它的存在不仅使患者神经功能缺损恢复时间延长,生活质量下降,而且使死亡率增加。
文拉法辛做为一种新型的抗抑郁剂,临床报道可应用于多种类型的抑制症的治疗,且疗效肯定。
本文收集了我院2003年1月1日至2004年12月30日门诊及住院患者30例,采用中、低剂量文拉法辛治疗,观察其疗效和副反应,现报道如下。
【总页数】1页(P33)
【作者】周志壮;于永达;高毅
【作者单位】150066,哈尔滨242医院;150066,哈尔滨242医院;150066,哈尔滨242医院
【正文语种】中文
【中图分类】R749.4
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2.盐酸文拉法辛缓释片治疗脑卒中后抑郁的疗效观察 [J],
3.文拉法辛与黛力新治疗脑卒中后抑郁的疗效观察 [J], 戴萍;许忠强;李卫飞
4.脑心通联合文拉法辛治疗脑卒中后抑郁的疗效观察 [J], 韦奇;覃少东;黄东明
5.乌灵胶囊联合文拉法辛配合针灸治疗脑卒中后抑郁的疗效观察 [J], 陶珍;郭洪伟;高丽;赵磊;程明;宋景贵
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文拉法辛缓释片治疗抑郁症临床对照观察实践
文拉法辛缓释片治疗抑郁症临床对照观察实践发布时间:2022-06-30T05:39:53.668Z 来源:《中国医学人文》2022年10期作者:魏伟[导读] 分析抑郁症疾病特点,评价药物文拉法辛缓释片治疗的预后效果。
魏伟大庆油田总医院黑龙江大庆 163001【摘要】目的:分析抑郁症疾病特点,评价药物文拉法辛缓释片治疗的预后效果。
方法:选择我院2019年10月-2020年12月期间收治的抑郁症患者,选择符合研究纳入标准的110例患者作为研究对象,进行随机法分组。
对照组采取氟西汀治疗,观察组采取文拉法辛缓释片治疗。
比较抑郁症患者治疗情况,即抑郁情绪评分、不良反应情况。
结果:汉密尔顿抑郁量表HAMD评估后,观察组患者治疗后评分明显低于对照组,P<0.05;不良反应方面,观察组有口干、恶心以及视物模糊等反应,对照组有呕吐、食欲不振以及便秘等反应,观察组与对照组发生率接近(P>0.05)。
结论:文拉法辛缓释片治疗抑郁症兼具安全性、有效性优势,促进患者治疗预后。
【关键词】:文拉法辛缓释片;抑郁症;抑郁情绪评分;不良反应抑郁症属于精神障碍,近年来发病率一直较高,长期抑郁症甚至有自杀风险。
所以,主张尽早诊断与治疗。
治疗方面,以药物治疗为主。
关于治疗抑郁症的药物种类较多。
随着临床治疗工作的开展,文拉法辛缓释片治疗取得了显著的效果。
本文就此进行对照研究。
内容如下:1 资料与方法1.1基线资料研究对象均为抑郁症患者(n=110),符合中国精神障碍分类与诊断标准,时间选自2019年10月-2020年12月。
纳入对象均为成人,治疗药物患者知情同意。
此次研究排除了合并其他精神疾病、重大脏器疾病、药物过敏体质情况患者。
随机数字表法分组,申报伦理委员会。
对照组:其中,男性28例、女性27例;患者年龄20-60岁,平均年龄(30.50±4.50)岁;患者病程8-30周,平均(15.50±3.50)周。
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万拉法新治疗上消化道癌伴发抑郁状态的疗效观察
马现仓,高成阁
(西安交通大学第一医院,陕西西安710061)
【关键词】 上消化道癌 抑郁状态 万拉法新
【中图分类号】 R74914 【文献标识码】 B 【文章编号】 100420501(2003)0520473202
癌症可以导致患者出现明显的抑郁,而抑郁对癌症的发展、预后均产生明显的负面影响,包括治疗效果、住院时间、依从性、自我照料能力及生活质量等[1]。
上消化道癌是最常见的癌症。
万拉法新(Venlafaxine)作为一种新型抗抑郁药,在情感性精神障碍的抑郁症治疗中已取得较好的疗效[2],本文收集了107例上消化道癌伴发抑郁状态的患者,采用万拉法新治疗,对其疗效及副作用临床观察和分析如下。
1 临床资料
111 一般资料:收集2001年5月至2002年1月在我院肿瘤科住院的上消化道癌伴发抑郁状态患者107例,其中男57例,女50例,年龄53±8岁。
其中胃癌60例,食管癌47例。
患者入组标准为:①所有病例均通过病理切片确诊;②符合《中国精神疾病分类与诊断标准》(CC MD222R)躯体疾病所致精神障碍抑郁状态的诊断标准;③汉密尔顿抑郁量表(H AMD)评定总分≥8分[3];④入组前血尿常规及肝、肾功能均无明显异常;
⑤无精神疾病及癫痫病史,无药物过敏史。
112 治疗方法:107例每日早、晚2次服用万拉法新(成都大西南制药股份有限公司生产),日剂量50~150mg,平均78±23mg,治疗时程为42天。
治疗前后分别查血、尿常规及肝肾功能。
113 疗效评定:应用H AMD量表进行评定,分别在用药前、用药后2、4、6周末各测定1次,疗效按H AMD减分率标准:减分率≥90%为痊愈,60%~89%为显著好转,30%~59%为好转,<30%为无效。
为了更好地分析疗效,同时对H AMD量表的7个因子,针对性地选择4个因子进行分析。
副反应用TESS量表进行评定。
114 统计分析:结果用随机配对t检验进行统计分析。
115 结果:治疗前后H AMD总分及4因子评分结果见表1。
表中显示,应用万拉法新治疗2周后,患者的H AMD总分降低了4413%,治疗4周后降低了7114%,治疗6周后降低了7210%。
4因子的平均数在治疗后第2、4周及第6周较治疗前显著降低(P<0.05或P <0.01),其中焦虑/躯体化(包括精神性焦虑、躯体性焦虑、胃肠道症状、全身性症状及自知力)平均分数在服药后2周降低约50%,4周及6周后降低77%;睡眠障碍(包括入睡困难、睡眠不深及早醒)平均分数在用药后2周降低约60%,4周及6周后降低81%;迟滞(包括抑郁情绪或工作和兴趣及迟滞)平均分数在用药后2周降低45%,4周及6周后降低71%;绝望感(包括能力减退感、绝望感及自卑感)平均分数在用药后2周降低53%,4周及6周后降低约72%。
表1 治疗前后H AMD总分及4因子评分项 目治疗前治疗2周后治疗4周后治疗6周后HAM D总分21.05
±
4.2
11.73±
2.8①
6.01±
0.6①
5.9±
0.7①
焦虑/躯体化 1.72±
0.6
0.87±
0.3①
0.40±
0.2①
0.39±
0.1①
睡眠障碍 1.41±
0.5
0.56±
0.2①
0.27±
0.1①
0.24±
0.1①
迟滞 2.41±
0.6
1.31±
0.3①
0.71±
0.3①
0.66±
0.3①
绝望感 1.90±
0.4
0.89±
0.3②
0..53±
0.3②
0.52±
0.3②
①与治疗前比较P<0.05;②与治疗前比较P<0.01
本组107例患者无中断治疗,整个疗程未出现严重副反应。
仅11例出现恶心、厌食、口干,6例出现头昏、嗜睡,无须处理,数日后自行缓解。
治疗6周后,复查肝、肾功能及血、尿常规均无明显异常。
2 讨 论
本研究观察的107例上消化道癌伴发抑郁状态患者应用万拉法新治疗都取得了较好的疗效。
总体疗效方面,在治疗2周后,患者的自觉症状已有显著改善, H AMD平均总分亦明显降低,4周及6周后,H AMD平均减分率达7516%,按减分率标准为显著好转。
研究还显示,万拉法新治疗上消化道癌所致抑郁状态起效较快。
上消化道癌伴发抑郁状态与情感性精神障碍抑郁症的表现基本相似,但在H AMD量表的各项目中,更集中表现在焦虑/躯体化、睡眠障碍、迟滞和绝望感4个因子方面。
本组观察显示,万拉法新对这4方面均有明显的改善,从而达到对上消化道癌伴发抑郁状态患者有效的治疗作用。
本组应用万拉法新治疗上消化道癌所致抑郁状态,剂量为中等剂量,未发现对肝、肾、心等重要脏器有明显的毒副作用。
青年人大肠癌临床分析
冷 凯,主鹤亭
(贵州省遵义医院,贵州遵义563002)
【关键词】 青年人大肠癌 诊断 治疗
【中图分类号】 R73513+4 【文献标识码】 B 【文章编号】 100420501(2003)0520474201
大肠癌为最常见的恶性肿瘤之一。
好发于中老年,青年人较少见,而在近年的临床诊治过程中,青年人大肠癌呈增多趋势。
现对我院手术治疗的37例青年人大肠癌患者进行回顾性分析,现报告如下。
1 临床资料
111 一般资料:我院1995~2001年经手术治疗和病理证实的大肠癌患者共230例,其中青年人(≤35岁)大肠癌患者37例(占1611%),男20例,女17例,男女之比为1118∶1,年龄16~35岁,平均2817岁。
112 症状及体征:腹痛30例(8111%),疼痛性血便或粘液血便24例(6419%),大便次数增多20例(5411%),便形改变19例(5114%),梗阻症状18例(4816%),体重减轻、食欲下降、贫血25例(5618%),腹部包块12例(3214%)。
出现症状至确诊时间为015~21个月,平均519月。
113 病理类型及Dukes分期:病理类型,粘液腺癌10例,印戒细胞癌8例,高、中、低分化腺癌分别为3、4、8例,乳头状腺癌3例,未分化腺癌1例。
组织学分型以浸润型多见,为27例(7219%)。
好发部位为直肠,28例(7516%)。
Dukes临床分期,A期1例,B期12例,C 期20例,D期4例。
114 治疗方法:根治性切除术23例(6212%),姑息性切除术8例(2116%),探查或结肠造瘘术6例(1612%),无手术死亡。
术后放疗13例,化疗15例。
115 随访结果:随访32例(8619%),随访时间3~50个月,平均2113个月,2年生存率为3418%,无5年生存者。
2 讨 论
大肠癌是临床最常见的恶性肿瘤之一,国外主张
<40岁作为划分青年人大肠癌标准,我们采用≤35岁为青年组,符合国人青年期大肠癌特点。
据文献报道,我国青年人大肠癌发病率为919%~1513%[1],本组资料略高于文献资料。
本组资料显示高群病理类型(粘液腺癌,印戒细胞癌,低分化腺癌)多见,为26例(7013%);组织学分型以浸润型为主,为27例(7219%);直肠为好发部位,为28例(7516%);与国内文献报告相符[2,3]。
其肿瘤具生长速度快,恶性程度高,易早期穿透肠壁侵犯临近组织及发生淋巴道、血行转移的生物学特性[4]。
且因青年人大肠癌早期症状无特异性,青年人对疾病的耐受性强,加之防癌知识不足,忽视了不典型的临床表现,以致延误诊断。
而且容易误诊为痔、痢疾、肠炎,延误就诊。
表明预后差主要与病理类型多,易误诊,诊断时间长,确诊时肿瘤已到进展期有关。
所以临床医生对此类就诊患者应高度重视,充分考虑肿瘤的可能性,并认真进行直肠指检,乙状结肠镜、纤维结肠镜及钡灌肠检查,直到排除肿瘤为止。
所以应对青年人大肠癌发病特点增加了解,增强对本病的警惕性,必要时定期复查。
对原因不明的腹泻、便秘、腹痛、体重减轻的病人均应坚持“一指三检查”,以减少漏诊、误诊,以期早诊断早治疗。
参考文献
1 刘宝善,等1大肠肛门肿瘤学1成都:四川科学技术出版社, 19981163
2 谭立新1青年人大肠癌31例临床病理分析1北京医学,1998,20:314 3 张兆祥148例青少年大肠癌病理与临床分析1中国肛肠病杂志, 1996,16(2):27
4 王振义,等1青年大肠癌临床病理特征1中国肛肠病杂志,1996,16
(2):25
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