中国居民银屑病发病危险因素的meta分析

目的:系统评价中国居民银屑病发病危险因素.方法:计算机检索中国知网、万方、维普、中国生物医学文献、PubMed、Embase、Cochrane Library及Web of Science 8个数据库,并由2名研究员独立筛选文献、提取资料和质量评价,采用Stata 15.0软件进行meta分析.结果:纳入17项研究,涉及危险因素18个.控制混杂因素后结果显示受潮[OR=3.97,95％ CI(2.94,5.37)]、感染[OR=2.80,95％ CI(2.14,3.68)]、外伤[OR=2.24,95％ CI(1.79,2.79)]、精神紧张[OR =3.16,95％ CI(2.69,3.71)]、服药[OR=2.27,95％ CI(1.41,3.65)]、吸烟OR=1.85,95％CI(1.26,2.72)]、饮酒[OR =2.39,95％ CI(1.77,3.21)]、家族史[OR=5.28,95％CI(3.57,7.80)]和食鱼虾[OR=1.91,95％CI(1.70,2.15)]是银屑病患者发病的危险因素(P＜0.01).结论:受潮、感染、外伤、精神紧张、服药、吸烟、饮酒、家族史和食鱼虾与中国居民银屑病的发病有关.     

上海市某社区居民血脂异常及影响因素分析

目的:分析上海市某社区居民血脂异常情况及影响因素,为社区健康教育提供依据.方法:以上海某社区35岁及以上且自愿参加体检的1199名常住居民为调查对象,其中男性360名(30.0％),女性839名(70.0％);年龄中位数60岁.分析血脂(总胆固醇、甘油三脂、低密度脂蛋白胆固醇和高密度脂蛋白胆固醇)异常情况及影响因素.结果:有713例被检出血脂异常,异常检出率占59.5％.以甘油三酯升高和总胆固醇升高为主,检出率分别为37.5％和35.7％.多因素Logistics回归分析显示,性别(OR=1.411,95％CI:1.091-1.825)、年龄(OR=1.468,95％CI:1.157-1.864)、空腹血糖(OR=1.522,95％CI:1.181-1.962)、体重指数(BMI)(OR=1.294,95％CI:1.084-1.546)、腰围(OR=1.301,95％CI:0.970-1.623)、腰臀比(OR=1.405,95％CI:1.012-1.985)是血脂异常的独立危险因素.结论:在上海某社区居民中有较高的血脂异常检出率,提示血脂异常的防治工作亟待加强,以降低动脉粥样硬化性心血管疾病发生风险.     

吸烟、饮酒与银屑病发病及治疗结局影响的研究进展

银屑病(psoriasis)是一种皮肤科常见的慢性、复发性、炎症性疾病,其确切病因尚未完全明确,遗传及环境因素是诱发或加重银屑病的重要因素,其中吸烟和饮酒是常见可控危险因素。研究显示,银屑病患者吸烟率高于一般人群,吸烟可能通过增强银屑病相关基因表达、激活银屑病发病相关信号通路等途径影响银屑病的发病和进展,从而增加银屑病的发生风险,导致银屑病患者病情加重。但吸烟是否会影响银屑病患者的治疗效果仍存争议,尚需更多研究来确认吸烟和戒烟对银屑病患者治疗效果的影响。流行病学调查显示,银屑病患者饮酒率高于一般人群。现有研究证据表明,饮酒可能通过影响银屑病相关易感基因、角质形成细胞增殖分化以及诱导免疫细胞异常活化对银屑病的发生、发展产生不利影响,同时饮酒会减弱银屑病的治疗反应,使治疗效果欠佳。但饮酒与银屑病发病和严重程度之间的关系尚无统一结论,仍需开展更多研究来探讨饮酒与银屑病之间的关联。     

2型糖尿病并发脑梗死的危险因素研究

目的 分析2型糖尿病并发脑梗死的相关危险因素,为脑梗死的临床防治提供指导.方法 选取本院2007年6月～2012年11月收治的516例2型糖尿病患者,根据是否并发脑梗死进行分组,其中研究组98患者并发脑梗死,而对照组418例未并发脑梗死.分析两组患者的临床资料,并通过单因素相关分析筛选出与脑梗死发生相关的因素,再进行多因素Logistic回归分析.结果 2型糖尿病患者发生脑梗死的独立危险因素为吸烟(OR=2.13,95％CI:1.36～5.85)、暴饮暴食(OR=1.93,95％CI:1.19～3.20)、高血压病史(OR =2.65,95％CI:1.02～4.36)、冠心病史(OR=2.07,95％CI:1.48～5.57)、用药不规则(OR=1.27,95％CI:1.13～4.48)、血糖控制欠佳(OR=3.21,95％CI:1.65～3.91)、TG≥2.6 mmol/L(OR=2.88,95％CI:1.13～4.63)、LDL-C≥3.36 mmol/L(OR=1.81,95％CI:1.13～3.15)、HDL-C≤0.91 mmol/L (OR =2.32,95％ CI:1.65～4.75).结论 对于2型糖尿病患者,平时节制饮食,戒除烟酒,按时服用降血压、降血脂药物,并控制血糖,可降低并发脑梗死的危险度.     

难治性高血压病合并阻塞性睡眠呼吸暂停低通气综合征患者危险因素分析

目的 研究住院患者难治性高血压病(RH)合并阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的独立危险因素.方法 选择我院RH患者100例,按多导睡眠监测结果分为:RH+ OSAHS组(n=54),RH组(n=46),收集患者的性别、身高、体重、BMI、吸烟史、服用降压药种类、高血压病程、血脂、血糖、血清尿酸、估算的肾小球滤过率(eGFR)、晨起卧位肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮和24h动态BP监测相关数据:24h平均SBP(24 h SBP)、24h平均DBP(24 h DBP)、24 h平均动脉压(24 h MAP).通过单因素和多因素Logistic回归分析RH合并OSAHS的独立危险因素.结果 ①RH+ OSAHS组患者24h DBP、24hMAP、LDL-C、血清尿酸、PRA、服用降压药种类均高于RH组[(86±10)mm Hg(1 mm Hg=0.133 kPa)比(81±10)mm Hg,(101 ±9)mm Hg比(97±8)mm Hg,(3.0±0.6)mmol/L比(2.7±0.5)mmol/L,(437 ±81).μmol/L比(385 ±72) μmol/L,1.44(0.56,3.09)ng/(ml·h)比0.78(0.19,1.96)ng/(ml·h),(4.0±0.7)种比(3.6±0.5)种,P＜0.05];而年龄、病程低于RH组,差异有统计学意义[(48±12)岁比(54±12)岁,9(3,16)年比10(6,20)年,P＜0.05].②年龄(P=0.031,OR =0.964,95％ CI:0.932 -0.997)、高血压病程(P =0.015,OR=0.943,95％ CI:0.90 ～0.989)、24 h DBP(P=0.016,OR=1.054,95％ CI:1.010 ～1.101)、24 h MAP(P=0.014,OR=1.065,95％CI:1.013～1.121)、血清尿酸(P=0.002,OR=1.009,95％CI:1.003～1.014)、LDL-C(P =0.035,OR=2.193,95％ CI:1.003 ～1.014)与OSAHS独立相关;24 h MAP(P=0.02,0R=1.065,95％ CI:1.008～1.124),UA(P =0.002,OR=1.009,95％ CI:1.003 ～ 1.015),LDL-C(P=0.117,OR=1.877,95％ CI:0.854～4.128)为RH合并OSAHS的独立危险因素.结论 在RH患者中合并代谢异常是OSAHS的重要预测因子.     

过敏性紫癜临床特征及其肾损害危险因素分析

目的 分析过敏性紫癜(Henoch schonlein purpura,HSP)患者临床特征及其肾损害的致病危险因素.方法 选择2005年1月至2013年12月在我院治疗并定期随访的187例HSP患者作为观察对象,根据病理资料分为肾损害(Renal impairment group,RIG)组和尿检正常(None renal impairment group,NRIG)组,对其病理资料进行回顾性分析.结果 IgA(OR=1.945,95％CI:1.015～3.764)、IgG(OR=1.182,95％ CI:1.023～1.354)、PDF(OR=1.068,95％ CI:1.004～10.63)、PLT(OR=1.005,95％CI:1.001～1.012)、WBC(OR=1.135,95％CI:1.035～1.246)和年龄(OR=1.025,95％CI:1.025～1.436)是HSP患者肾损害发生的危险因素.结论 血清IgA和IgG升高,PDF、PLT和WBC值超标,年龄偏大均为HSP患者肾损害的危险因素,对于有上述症状的HSP患者应及时进行干预和治疗,避免肾损害的发生.     

伊立替康联合铂类治疗复发性卵巢癌临床疗效的Meta分析

目的 评价伊立替康联合铂类与伊立替康单药治疗复发性卵巢癌的有效性和安全性.方法 计算机检索Cochrane Database of Systematic Reviews,Cochrane Central Register of Controlled Trials,Medline,EMBASE,National Research Register,Conference Papers Index,Open Grey,中国知网(CNKI),万方数据知识服务平台等数据库,对符合纳入标准的随机对照试验进行质量评价和Meta分析.结果 纳入6个随机对照试验,共计438例患者,联合用药在完全缓解率(OR =0.53,95％ CI;0.25 ～ 1.09,P =0.08)方面与单药相当,在部分缓解率(OR =0.40,95％CI:0.27 ～0.60,P＜0.000 01)、临床有效率(OR =0.34,95％CI:0.23 ～0.51,P＜0.000 01)上却表现出明显优于单药伊立替康的疗效,安全性方面联合用药有较高的白细胞(OR=0.25,95％CI:0.10 ～0.65,P=0.005)、血小板(0R=0.34,95％CI:0.16 ～0.71,P=0.004)骨髓抑制发生风险,但在贫血(OR =0.71,95％ CI:0.37 ～ 1.33,P=0.28)、恶心呕吐(OR =0.25,95％ CI:0.05～1.25,P=0.09)、腹泻(OR =0.79,95％CI:0.44～1.43,P =0.44)、神经毒性(OR =0.86,95％ CI:0.44 ～ 1.06,P=0.65)及肝功能损害(OR =0.60,95％ CI:0.27～1.33,P=0.21)等毒副作用发生率上与单药伊立替康比较差异无统计学意义.结论 对于复发性卵巢癌患者,在排除化疗禁忌后,采取伊立替康联合铂类化疗方案能够取得较单药伊立替康更好的疗效;但对于白细胞、血小板明显降低,伴有出血倾向或不能应用升白细胞或升血小板药物的患者,可考虑使用单药伊立替康治疗.     

98例肝吸虫病危险因素分析

目的:探索肝吸虫感染的影响因素,为采取相应干预措施提供科学依据.方法:采用以医院为基础的病例对照研究方法,对确诊病例及选取的对照进行问卷调查.结果:肝吸虫病相关危险因素包括年龄40～50岁(OR=4.034,95％ CI 1.334～12.203);文化程度:文盲及小学(OR=10.294,95％ CI 2.866～ 36.973)、初中(OR=3.219,95％ CI 1.228～8.820);经常及偶尔生食或半生食淡水鱼(OR=20.774,95％ CI 5.992～ 72.025),(OR=14.714,95％ CI 5.564～38.908);经常食用生或半生淡水虾(OR=3.151,95％ CI 1.533～5.865);经常有过抓生鱼后不洗手就抓食物吃(OR=2.759,95％ CI 1.262～6.033).结论:影响肝吸虫感染的主要因素为不同年龄、不同文化程度、是否生食或半生食淡水鱼、是否生食或半生淡水虾、是否有过抓生鱼后不洗手就抓食物吃.     

颈动脉内中膜厚度及斑块稳定性与代谢综合征的相关性

目的 研究颈动脉内中膜厚度(IMT)及斑块稳定性与代谢综合征的相关性.方法 收集2011年3月至2012年12月于北京安贞医院健康体检中心进行颈动脉超声检查患者2 292例,根据斑块检出情况分为无斑块组(1 582例)和斑块组(710例),依据颈动脉超声检查斑块回声特征,斑块组分为稳定斑块亚组(301例)和不稳定斑块亚组(425例).结果 超重和/或肥胖(662例)、糖尿病(713例)、高血压(742例)、血脂紊乱(624例)的患者IMT分别为(1.36±0.35)、(1.49±0.41)、(1.43±0.38)、(1.51±0.48) mm,明显高于无超重和/或肥胖(737例)、糖尿病(686例)、高血压(657例)、血脂紊乱(775例)患者的(1.16 ±0.24)、(1.18±0.22)、(1.09 ±0.19)、(1.05 ±0.13) mm(P ＜0.05).超重和/或肥胖、糖尿病、高血压、血脂紊乱的患者颈动脉斑块检出率分别为55.1％(365/662)、58.6％ (418/713)、60.5％ (449/742)、68.1％(425/624),明显高于无超重和/或肥胖、糖尿病、高血压、血脂紊乱患者的46.8％(345/737)、42.6％(292/686)、39.7％ (261/657)、36.8％(285/775)(P＜0.05).具备1、2、3个代谢综合征组分患者的IMT分别为(1.31±0.24)、(1.46±0.35)、(1.66 ±0.39) mm,颈动脉斑块检出率分别为38.2％(233/610)、54.7％(223/408)、66.7％(254/381),IMT厚度及颈动脉斑块检出率均随着代谢综合征组分数目增加而增加(P＜0.05).收缩压[比值比(OR) =3.212,95％置信区间(CI):1.542～ 5.295]、空腹血糖(OR =3.082,95％ CI:1.416 ～4.985)、低密度脂蛋白胆固醇(OR=3.087,95％CI:1.654 ～7.395)、代谢综合征(OR =4.624,95％CI:1.654 ～ 7.295)是颈动脉斑块形成的独立危险因素(P＜0.05),高密度脂蛋白胆固醇(OR =0.735,95％CI:0.449 ～0.952)是颈动脉斑块形成保护因素(P＜0.05).空腹血糖(OR=2.156,95％ CI:1.424 ～5.249)、总胆固醇(OR=1.895,95％ CI:1.169 ～3.195)、代谢综合征(OR =3.652,95％ CI:1.752 ～8.985)是颈动脉不稳定斑块的独立危险因素(P＜0.05),高密度脂蛋白胆固醇(OR =0.758,95％CI:0.424～0.946)是颈动脉斑块稳定保护因素(P＜0.05).结论 代谢综合征及代谢综合征组分可增加颈动脉粥样硬化发生风险,并且与IMT增厚、斑块形成及斑块不稳定型密切相关,颈动脉超声检查有助于早期预防心血管事件发生.     

龙岗区社区居民急性脑梗死出院后复发情况及危险因素分析

目的研究龙岗区社区居民急性脑梗死出院后脑梗死复发的危险因素以及如何控制这些因素。方法通过对龙岗区社区居民2016年7月～2018年7月期间的125例急性脑梗死出院后两年内的复发情况进行单因素回顾性分析和多因素Logistic回归分析来探讨脑梗死复发的危险因素。结果复发组患者患有高血压、糖尿病和高血脂病的比例较高,差异具有统计学意义(P 0.05),说明高血压病史、糖尿病病史和高血脂病病史与脑梗死复发有关。脑梗死出院后复发与吸烟,饮酒,肾功,凝血功能和入院血压,血糖,血脂等各成分上的差异无统计学意义(P 0.05),与总胆固醇(TC)水平有一定关联,有待进一步研究。通过多因素Logistic分析发现高血压(OR=1.923)、高血脂(OR=1.291)、糖尿病(OR=1.464)为脑梗死复发的危险因素,差异具有统计学意义(P 0.05),吸烟与饮酒史与脑梗死复发无明显联系,差异无统计学意义(P 0.05)。结论高血压、高血糖和高血脂是急性脑梗死复发的危险因素之一,患者体内总胆固醇(TC)水平与急性脑梗死复发有一定关联。     

Tattoo sites and psoriasis

The Koebner phenomenon refers to the development of lesions in response to injury of previously uninvolved skin. It occurs in psoriasis and a number of other inflammatory diseases. We present a patient who developed a Koebner reaction at the site of a tattoo. Treatment with ustekinumab resulted in striking clearance of the psoriasis changes at the tattoo site.     

CC趋化因子与银屑病

银屑病是一种由免疫介导的自身免疫性皮肤病。其主要特征为表皮过度增厚和异常分化,伴有全身性炎症反应。银屑病发病机制伴随着大量免疫细胞浸润,这些炎症细胞及其释放的细胞因子在银屑病发生发展中起到重要的作用。目前大量研究提示,在银屑病皮损部位皮肤中存在多种CC趋化因子,通过参与银屑病炎症部位T淋巴细胞、巨噬细胞和中性粒细胞的募集和激活,积极参与到银屑病炎症循环中。因此,了解CC趋化因子及其受体在银屑病中作用,将有助于银屑病发病机制的探索,并为银屑病治疗靶点的开发提供新的思路。本文综述了目前已报道与银屑病相关的CC趋化因子,并探讨它们在银屑病发病机制中可能发挥的作用。     

Immunopathogenesis of psoriasis

Psoriasis is characterized by sustained T cell activation by antigen-presenting cells (APCs) in the lesions, and by a deviation of T cell differentiation to type 1 helper T and type 1 cytotoxic T cells, although no specific antigens have yet been determined. These characteristics are at least promoted by decreased IL-10 expression and the increased IL-12 expression observed in both the skin and stimulated peripheral blood mononuclear cells of psoriatic patients. Some of the cytokines produced by activated T cells are suspected to stimulate the proliferation of psoriatic keratinocytes. Among them, interferon-gamma is the most likely candidate, although interferon-gamma does not promote the growth of normal keratinocytes. In addition to the abnormal proliferation, psoriatic keratinocytes show abnormal differentiation and resistance to apoptosis. So far, however, it is still unknown whether these phenotypic and functional characteristics of psoriatic keratinocytes are only the consequences of the stimulation by activated T cells or are at least based on an inherent susceptibility. Recently, it has become clear that chemokines derived from activated keratinocytes or endothelial cells play a crucial role in recruiting T cells in the skin and inducing the neutrophilic infiltration that leads to the formation of subcorneal pustules (Munro's microabscess). Finally, recent developments in the detection and analysis of gene expression have revealed the molecules responsible for these steps. Some of them have become target molecules for the treatment of psoriasis. And indeed, it has become possible now to treat patients with new, innovative drugs.     

Pharmacogenetics of psoriasis

Psoriasis is an inflammatory hyperproliferative skin disorder with a strong genetic predisposition. While many effective modalities are currently available for treating psoriasis, response to therapy is quite variable among patients. The genetic component underlying the response to pharmacotherapy in psoriasis is slowly beginning to emerge and represents a specialized field of genetics referred to as pharmacogenetics. The identification of genetic variants has the potential to improve the management of patient care by identifying which patients should avoid a specific drug and which patients should be administered a modified dose. A suitable approach in implementing such a strategy could potentially reduce medical costs and improve success of drug therapy. This article summarizes the clinical aspects of psoriasis, its genetic susceptibility and highlights the current landscape of genetic targets for psoriasis pharmacotherapy.     

Epidemiology of psoriasis

The prevalence of psoriasis is relatively high in the general population, ranging between 0.6% and 4.8%, mainly as a result of chronicity and the absence of a cure. Although genetic-environmental interaction has been proposed as a model for the causation of psoriasis, the evidence for environmental factors is rather scarce. Risk factors, which have been documented in epidemiological studies include smoking, alcohol consumption, diet, infection, drugs, and stressful life events. Psoriasis affects the quality of life to substantial degree. Apart from a few cross-sectional surveys of large series of psoriatic patients, there have been no formal studies of the natural history and prognosis of established psoriasis. By imposing methodologic control and a numerate approach, epidemiology can offer a major contribution to understand psoriasis.     

Established treatments of psoriasis

Psoriasis is a complex disease with a spectrum of clinical manifestations. Psoriasis may express as a few coin-sized erythemato-squamous plaques up to widespread disease covering the entire body surface (erythrodermic psoriasis). Psoriasis may present as a few stable plaques or unstable disease, rapidly relapsing after treatment. Some patients may respond excellently to topical treatments whereas other patients may be difficult to manage, showing treatment resistance even to the systemic treatments. Therefore, a spectrum of treatments is available to individualize care of psoriasis. In this chapter the available treatments are presented. The vast majority of patients is treated with topical treatments, with vitamin D(3)analogs and topical corticosteroids as the first line treatments. Tazarotene is an alternative for vitamin D(3) treatment if this treatment fails. In some special cases, dithranol and tar treatment may be used. Phototherapy with UVB and photochemotherapy (PUVA) are indicated in patients not responding sufficiently to topical treatment. However, chronic exposure, in particular to photochemotherapy implies an increased risk for photo- carcinogenicity. Systemic treatments including methotrexate, cyclosporin, acitretin and fumarates are indicated in patients who cannot be managed with topical treatments or phototherapy, either for treatment resistance or cumulative toxicity. In this article the opportunities and limitations of the available treatments are presented.