逆转录病毒在类风湿性关节炎发病中的作用

类风湿性关节炎是一种常见的以关节组织慢性炎症病变为主的全身系统性疾病。它的病因学和发病机制至今未明。近年来 ,人们注意到逆转录病毒与类风湿性关节炎的发病密切相关。1　逆转录病毒在类风湿性关节炎病因学上的地位类风湿性关节炎的病因可能与某些细菌和病毒相关 ,如ＥＢ病毒、结核杆菌等。推测类风湿性关节炎是某种感染因素在遗传易感个体中触发的自身免疫性疾病。人们发现羊感染慢病毒后出现关节炎 ,其病理特点与人类风湿性关节炎的病理改变极相似。 1 993年Ｓａｔｏ等[1 ] 报道1 0例感染人类Ｔ淋巴细胞白血病病毒(ＨＴＬＶ)的患者…     

类风湿性关节炎临床治疗方案的研究进展

类风湿性关节炎(RA)是一种临床上常见的全身性自身免疫性疾病,患者临床表现主要为对称性、涉及多个关节、慢性的关节疾病和滑膜关节炎,其发病相关因素主要涉及遗传、滑膜中T细胞、B细胞及细胞因子等免疫细胞等,但具体机制现仍不完全明确。目前,RA的临床治疗效果尚不理想,主要的治疗方法为常规药物、中医中药、外科手术及新技术疗法等。     

α1-酸性糖蛋白在类风湿性关节炎诊断中的价值

类风湿性关节炎(rheumatoid arthritis,RA)是一种病因尚未明了的慢性全身性炎症性疾病,以慢性、对称性、多滑膜关节炎和关节外病变为主要临床表现,属于自身免疫炎性疾病,与环境、细胞、病毒、遗传、性激素及神经精神状态等因素密切相关.该病具有较高的致残率,发病2年之内即可出现不可逆性骨关节破坏,故早期诊断、早期治疗对控制其病情非常重要.α1-酸性糖蛋白(AAG)是一种急性时相蛋白,在一些炎症性和自身免疫性疾病中,常有较大的变化[1],本文讨论AAG与CRP、RF以及类风湿性关节炎病情之间的相关性,以了解该指标在类风湿性关节炎诊断中的价值.     

治疗类风湿性关节炎中药的研究概况

类风湿性关节炎是一种以关节病变为主的慢性全身性自身免疫疾病，中药在治疗类风湿性关节炎方面有着独特的优势。从传统的中药中寻找有效部位或有效成分治疗类风湿性关节炎已成为研究的热点。该文概述了治疗类风湿性关节炎单味中药及有效成分的研究进展。     

抗风湿性关节炎的中药及作用机制研究进展

类风湿性关节炎是一种与自身免疫相关的难以治愈的疾病,本文总结了近5年公开发表的治疗类风湿性关节炎的中药复方及单体,并综述了其作用机制,为类风湿性关节炎治疗药物的研发提供研究方向。     

治疗类风湿性关节炎的中药及活性成分研究进展

类风湿性关节炎是一种慢性免疫性疾病。它以关节滑膜炎为特征,表现为对称性多发性关节炎,并伴有软骨和骨质破坏。近几年中药对类风湿性关节炎的治疗已经取得了实质性的进展。现对中药治疗类风湿性关节炎的研究做一简要综述。     

TNF-α抑制剂的研究进展

类风湿性关节炎(RA)是一种发病率很高的自身免疫性疾病,至今还没有理想的治疗药物。TNF-α抑制剂的研究近年来倍受关注,现已成为抗类风湿药物的一个热门研究方向。TNF-α等一系列促炎因子水平的上升已被证明会引起一系列的炎性感染、自身免疫性疾病,如类风湿性关节炎（RA）、脓毒性颤振、充血性心脏衰竭、牙周疾病等。抑制TNF-α的产生或降低TNF-α的浓度现已成为类风湿性关节炎的一种有效治疗途径。本文综述近年来TNF-α抑制剂的研究进展。     

加味桂枝芍药知母汤治疗类风湿性关节炎的临床价值

目的对应用加味桂枝芍药知母汤对患有类风湿性关节炎疾病的患者实施治疗的临床效果进行研究。方法将我院收治的92例患有类风湿性关节炎疾病的患者随机分为对照组和治疗组,平均每组46例。采用布洛芬与甲氨蝶呤联合对对照组惠者实施治疗;在对照组的西药治疗方案基础上加用加味桂枝芍药知母汤对治疗组患者实施治疗。结果治疗组患者类风湿性关节炎疾病治疗效果明显优于对照组;类风湿症状表现消失时间和接受临床药物治疗总时间明显短于对照组;出现药物不良反应的人数明显少于对照组;停药后类风湿性关节炎病情再次复发率明显低于对照组。结论应用加味桂枝芍药知母汤对患有类风湿性关节炎疾病的患者实施治疗的临床效果非常明显。     

人工膝关节置换术后的康复护理

人工膝关节置换手术是治疗膝关节严重骨性关节炎、类风湿性关节炎等疾病的有效手段,目的是解除患者病痛、纠正畸形、恢复膝关节功能及提高日常生活质量[1],而术后康复锻炼是保证手术成功的重要因素.     

类风湿性关节炎与细胞凋亡

类风湿性关节炎(rheumatoid arthritis，RA)是一种慢性、全身炎症性自身免疫疾病，主要累及小关节，可伴有心、肺、血管、神经和眼等结缔组织炎性损伤。其病理特征主要为滑膜慢性炎症性增厚、骨与软骨组织的受损，最后导致关节的破坏。RA发病机制较为复杂，包括感染、遗传等因素。近年来发现细胞凋亡异常可导致滑膜组织过度增生、肥厚，从     

Lymphoma in patients with rheumatoid arthritis: what is the evidence of a link with methotrexate?

An increasing number of instances of lymphoma in patients with rheumatoid arthritis who are treated with methotrexate continue to appear. The majority of patients with lymphoproliferation have features of immunosuppression-associated lymphoma. Rheumatoid arthritis itself and the actions of methotrexate concur in leading to a immunosuppressed state. Possible oncogenic mechanisms and the risk factors for patients with rheumatoid arthritis to develop lymphoma while receiving methotrexate include: (i) intense immunosuppression and severe disease in combination with genetic predisposition and; (ii) an increased frequency of latent infection with prooncogenic viruses like Epstein-Barr virus. The aetiological role of methotrexate in the development of these lymphomas is supported by the spontaneous remission of these malignancies in some of patients with rheumatoid arthritis after methotrexate has been stopped. The physicians caring for patients with rheumatoid arthritis receiving methotrexate should be vigilant about signs and symptoms suggestive of lymphoma, mostly in those patients with significant comorbidity, long standing and severe disease who are more likely to be immunosuppressed. If a lymphoma appears in these patients, methotrexate should be stopped. Spontaneous remission may occur and a period of observation is advisable when clinically possible. If functional deterioration appears or there are signs of lymphoproliferative organ invasion after several months then specific antineoplastic treatment should be instituted.     

The role of coagulation in chronic inflammatory disorders: a jack of all trades

Chronic inflammatory disorders constitute a heterogeneous group of complex and multifactorial diseases, which are often associated with increased cardiovascular morbidity and mortality, independent of the established cardiovascular risk factors. In keeping with this observation, hypercoagulability is frequently observed in patients suffering from atherosclerosis, chronic obstructive pulmonary disease and rheumatoid arthritis although the physiological significance of activated coagulation remained elusive. However, the identification of protease activated receptors (PAR) seem to provide a link between coagulation activation and disease progression as their activation by coagulation factors triggers a broad range of signaling pathways relevant for chronic inflammatory disorders. In experimental animal models, anticoagulation and/or genetic ablation of PAR signaling affords protection against the perpetuation of atherosclerosis, chronic obstructive pulmonary disease and rheumatoid arthritis. It is thus tempting to speculate that targeting the coagulation-PAR axis might have clinical relevance in the setting of chronic inflammatory disorders. In the current review, we discuss the current knowledge on coagulation activation in inflammatory disorders, we discuss the relationship between atherosclerosis, chronic obstructive pulmonary disease and rheumatoid arthritis and we review the current knowledge on PAR signaling in these disorders.     

Possible role of microbial IgG Fc-binding proteins in rheumatoid arthritis

IgG Fc binding substances (receptors) are widespread among pathogenic microorganisms. The receptors from Staphylococcus aureus, streptococci of group A, C and G as well as Herpes-infected cells bind to the interface between the CH2 and CH3 domains i.e. to His 435, Tyr 436 and possibly also His 433 and/or 310. Most rheumatoid factors (RF) from patients with rheumatoid arthritis show a similar binding pattern. Hence, it has been shown that antibodies to microbial IgG Fc receptors (S. aureus and group A streptococci type M15) and RF are idiotypic-anti-idiotypic antibody "partners" i.e. that RF are the "internal images" of microbial IgG Fc binding proteins. Group A streptococci possessing IgG Fc receptors elicit higher titres of RF when injected in rabbits as compared to group A streptococci without IgG Fc receptors. The streptococcal IgG Fc receptors exhibit a diversity of preferences for subclasses of human IgG, some of them showing allotype preferences. Such allotypes are also recognized by certain RF. IgG RF are able to self-associate thereby forming immune complexes which can activate the complement cascade as well as stimulate release of prostaglandins and (probably) interleukin-1. Since these factors have been assigned an important pathogenic role in rheumatoid arthritis, self-aggregating IgG RF, proposed to be induced by microbial IgG Fc receptors might be an important pathogenic factor in rheumatoid arthritis because rheumatoid arthritis is the only known condition where synthesis of RF takes place in the synovia.     

Eradication of Helicobacter pylori may reduce disease severity in rheumatoid arthritis

BACKGROUND: A triggering infectious agent has long been postulated in rheumatoid arthritis. Data on the possible role of Helicobacter pylori infection are lacking. AIM: To assess the effect of H. pylori eradication in patients with rheumatoid arthritis. METHODS: Fifty-eight adult patients with established rheumatoid arthritis and dyspeptic symptoms were recruited - 28 were H. pylori-positive and 30 were H. pylori-negative on the basis of invasive tests. All infected patients were treated successfully. We evaluated the disease activity using clinical and laboratory parameters at baseline and every 4 months during 2 years, and compared the variations in the two subgroups. RESULTS: H. pylori-eradicated rheumatoid arthritis patients showed progressive improvement over time (P < 0.0001) of all clinical indices compared with baseline, whereas H. pylori-negative rheumatoid arthritis patients remained substantially unchanged. After 2 years, H. pylori-eradicated rheumatoid arthritis patients differed significantly (P < 0.04-0.0001) from patients without H. pylori infection in terms of improvement of all clinical parameters. At the same time point, several laboratory indices (erythrocyte sedimentation rate, fibrinogen, alpha2-globulins and antinuclear antibody) showed significantly lower values (P < 0.02-0.0003) in the H. pylori-eradicated subgroup compared to the H. pylori-negative subgroup. CONCLUSIONS: Our data suggest that H. pylori infection is implicated in the pathogenesis of rheumatoid arthritis, in that its eradication may induce a significant improvement of disease activity over 24 months. H. pylori eradication seems to be advantageous in infected rheumatoid arthritis patients, but controlled studies are needed.     

小剂量来氟米特治疗类风湿性关节炎合并乙肝病毒携带者的疗效及安全性观察

目的探讨小剂量来氟米特治疗类风湿性关节炎合并乙肝病毒（HBV）携带者的疗效和安全性。方法将115例确诊活动期类风湿性关节炎患者按乙肝患病情况分为3组,均给予来氟米特抗风湿治疗,观察疗效及HBV激活情况。结果治疗后各组患者的疾病活动性评分等疗效指标与治疗前相比皆有明显改善（P〈0．05）,有79．13％（91／115）患者疗效达ACR20;有15例（13．0％）患者治疗后出现肝功能异常,5例（4．3％）患者出现HBV再激活来自HBV携带者组,既往HBV感染组及无感染组患者治疗后均未出现HVB再激活：多元回归模型显示．使用来氟米特治疗的RA患者发生HBV再激活受基础乙肝患病情况、治疗前谷丙转氨酶（ALT）和关节肿胀数（SJC28）情况的影响,三者可使HBV再激活的风险增加约30％。结论来氟米特治疗类风湿性关节炎具有较好的临床疗效,但治疗前应检查肝脏疾病、肝功能及HBV—DNA载量,乙肝病毒携带者存在HBV再激活风险,应慎重选择。     

基因工程药物临床应用分析

基因工程药物带来了治疗学的新突破，在临床治疗中日益发挥举足轻重的作用。为了适应现代生物技术的发展，掌握基因工程药物的有关知识，促进基因工程药物合理用药。对该院1999～2002年基因工程药物的临床应用进行了统计分析。基因工程药物临床应用品种逐年增加，销售金额不断增长，临床用途越来越广泛。基因工程药物疗效确切、使用安全、不良反应少，在糖尿病、心血管疾病、病毒感染性疾病、类风湿性关节炎、创面修复和抗肿瘤等方面具有广泛的应用前景。     

类风湿关节炎发病危险因素及治疗依从性的调查研究

目的探讨类风湿关节炎患者发病危险因素及影响其治疗依从性的原因。方法采用1：1匹配的方法，收集病例和对照各100例，进行单因素分析和多因素Logistic回归分析。结果与类风湿关节炎发病危险性增加相关的因素有：阳性家族史、既往结核病史、曾在阴冷潮湿的环境中生活等。影响其治疗依从性的相关因素有：患者本人对该病基本知识了解甚少、经济困难、药物毒副作用等。结论类风湿关节炎的发病与治疗和多因素相关，避免一些不利因素，可减少类风湿关节炎的发生及提高其治疗依从性。     

慢性病病人药物治疗依从性调查及影响因素分析

目的:调查新疆维吾尔自治区冠心病、高血压、糖尿病、类风湿性关节炎及哮喘这5种慢性病病人药物治疗依从性。方法:对600例慢性病病人进行问卷调查,并对用药依从性的影响因素进行分析,回收有效答卷452份,回收率75.3%。结果:哮喘病人依从性为32%,类风湿性关节炎病人依从性为67.2%,冠心病、高血压及糖尿病病人依从性在前两者之间。影响药物治疗依从性的因素包括老年病人、低文化层次、低收入、不同职业、哮喘病人、不规律复诊、药品种类、药品数量及其不良反应等。结论:多种因素可影响慢性病病人药物治疗依从性。     

Psoriatic arthritis-new insights give new options for treatment

Psoriatic arthritis (PsA), an inflammatory joint disease associated with psoriasis of the skin, has a heterogeneous pattern expressed by different manifestations, such as mild mono-oligoarthritis, a very severe, erosive and destructive polyarthritis indistinguishable from rheumatoid arthritis, and spondylarthropathy with axial involvement or enthesitis. The disease pattern often differs between patients as well as within the same patient over time. Measurable inflammatory activity is not always evident. Early detection of inflamed joints or axial involvement in patients with PsA is important in order to reduce the inflammation and prevent destruction, deformity and functional disability in the joints involved. Several factors, e.g., genetic, immunological, environmental and vascular, have been proposed to be of importance for the aetiology, the expression and prognosis of PsA. The basic treatment for PsA has been administration of non-steroid anti-inflammatory drugs (NSAIDs). Few disease modifying anti-rheumatic drugs (DMARDs) have been available due to a lack of efficacy of most of the DMARDs used for other rheumatic diseases. New insights into genetic, immunological and vascular factors in PsA are of interest as possible targets for future therapy and will be discussed in this review.     

The MDR1 3435 polymorphism in patients with rheumatoid arthritis

OBJECTIVE: Rheumatoid arthritis (RA) is a multifactorial disease, the pathogenesis of which involves immunological, genetic and environmental factors. P-glycoprotein (P-gp) encoded by the MDR1 gene, is an important transporter for many drugs, xenobiotics and cytokines and may be associated with many immunological processes and apoptosis. The activity of P-gp is genetically determined. Naturally occurring MDR1 polymorphisms have been described and correlated with potential clinical effects. Several mutations in the MDR1 gene have been recognized, but only some of them are associated with P-gp expression. The C3435T polymorphism was found to correlate with the activity of P-glycoprotein. The aim of the study was to evaluate the C3435T MDR1 polymorphism in patients with rheumatoid arthritis and to investigate a possible correlation with disease susceptibility, activity and severity. METHODS: The study was carried out in 92 patients with rheumatoid arthritis and 97 healthy subjects as a control group. The C3435T polymorphism was determined using the PCR-RFLP method. RESULTS: The distribution of C3435TT MDR1 genotypes in RA patients did not differ significantly from that in a control group and was as follows: 3435CC in 25 (26.9%) subjects, 3435CT in 50 (53.8%) and 3435TT in 17 (18.3%). The probability of remission of RA symptoms after therapy with methotrexate and glucocorticosteroids however, was 2.89-fold greater in patients with the 3435TT genotype compared to patients with the genotypes 3435CC and 3435CT. The risk of having an active form of rheumatoid arthritis resistant to therapy with disease-modifying antirheumatic drugs in patients with 3435CC and 3435CT genotypes was 2.89 times greater than in homozygous 3435TT subjects. CONCLUSION: We suggest that the C3435T MDR1 polymorphism is not an important genetic risk factor for RA susceptibility, but that this polymorphism may have an influence on the activity of the disease and its response to therapy with disease-modifying antirheumatic drugs.