主页 > 医学前沿 >
【medical-news】脊椎关节病的anti-TNF治疗策略所存在
Public release date: 30-Jan-2007
The problem with treating spondylarthritis with anti-TNF strategies
Joint fusion and joint inflammation are separate processes, study suggests, and should be considered separate therapeutic targets
Any form of arthritis that affects one or more vertebral joints, spondylarthritis (SpA) represents a group of closely related disorders, including ankylosing spondylitis (AS), psoriatic arthritis (PsA), and arthritis associated with inflammatory bowel disease. Aside from chronic inflammation, these conditions are all characterized by ankylosis, stiffness and fusion of bone in the spine and peripheral joints, provoked by abnormal cartilage and bone formation. What triggers ankylosis remains unknown. Currently, inhibition of tumor necrosis factor ?(TNF? is the most effective strategy for controlling the painful symptoms of SpA and slowing vertebral joint destruction. But does anti-TNF therapy do anything to reduce the incidence or severity of ankylosis?
To answer this critical question, a quartet of researchers led by Dr. Frank P. Luyten, Division of Rheumatology, University Hospitals, Leuven, Belgium, tested the effectiveness of etanercept, an established TNF receptor, on animal models of arthritis. Their findings, highlighted in the February 2007 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), cast doubts on the feasibility of preventing joint and spine ankylosis with anti-TNF strategies while shedding light on the process of SpA.
A sample of male mice with spontaneous arthritis were caged together and observed from the age of 10 weeks. From week 12 to week 25, the mice were treated twice weekly with etanercept, in a strength comparable to standard dosage for human patients, or a placebo. Mice were also scored twice weekly for signs of arthritis, including cartilage formation, bone formation, and joint ankylosis. The mice were killed at age 25 weeks, autopsied, and analyzed, through cell population staining, for the presence of TNF?
In a complementary experiment, another sample of mice was induced with arthritis, using methylated bovine serum albumin. Four days later, these mice were given a single injection of etanercept. Three days later, on day seven, they were killed. Signs of arthritis were assessed and graded for cartilage destruction and bone erosion.
For the mice with induced arthritis, etanercept had a significant impact on disease severity, inhibiting inflammation and cartilage and bone destruction. For the mice with spontaneous arthritis, however, etanercept proved no more effective than placebo at inhibiting new cartilage or bone formation or ankylosis. What's more, TNF?positive cells were observed in the joint capsule, adjacent blood vessels and in new cartilage.
"Our observations strengthen our hypothesis that new bone formation in SpA is clinically relevant and largely independent of inflammation," Dr. Luyten states. "Long-term results from clinical trials are required to corroborate this hypothesis in patients with SpA," he acknowledges, "and to define whether the process of ankylosis should become a separate therapeutic target." 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。
Public release date: 30-Jan-2007
公开发表时间：2007年1月30日
The problem with treating spondylarthritis with anti-TNF strategies
治疗(脊)椎关节炎时抗－TNF策略存在的问题
Joint fusion and joint inflammation are separate processes, study suggests, and should be considered separate therapeutic targets
研究显示关节融合术和关节感染是各自独立的过程，在治疗中应分别对待．
Any form of arthritis that affects one or more vertebral joints, spondylarthritis (SpA) represents a group of closely related disorders, including ankylosing spondylitis (AS), psoriatic arthritis (PsA), and arthritis associated with inflammatory bowel disease. 凡是影响一个或更多椎骨连结，(脊)椎关节的关节炎都显示出一组紧密相关的症状，包括强制性脊柱炎，银屑病关节炎和肠炎引起的关节炎．Aside from chronic inflammation, these conditions are all characterized by ankylosis, stiffness and fusion of bone in the spine and peripheral joints, provoked by abnormal cartilage and bone formation. 除去慢性炎症，当异常软骨和骨形成时，这些疾病都很表现出关节强直，四肢强直，脊柱和周围关节融合．What triggers ankylosis remains unknown. 引起关节强直的诱因还未找出．Currently, inhibition of tumor necrosis factor ?(TNF?) is the most effective strategy for controlling the painful symptoms of SpA and slowing vertebral joint destruction. But does anti-TNF therapy do anything to reduce the incidence or severity of ankylosis?关节强硬性脊椎炎和慢性椎关节破坏会引起疼痛，当前抑制肿瘤坏死因子是控制它们引起疼痛症状最有效的治疗．To answer this critical question, a quartet of researchers led by Dr. Frank P. Luyten, Division of Rheumatology, University Hospitals, Leuven, Belgium, tested the effectiveness of etanercept, an established TNF receptor, on animal models of arthritis. 为了回答解决这个问题，由Frank P. Luyten 博士领导的四组研究员在动物关节炎模型上检测了依那西普的效果．Frank P. Luyten 博士在比利时列弗大学医院风湿病区就职．依那西普是一种已经证实的肿瘤坏死因子受体．Their findings, highlighted in the February 2007 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), cast doubts on the feasibility of preventing joint and spine ankylosis with anti-TNF strategies while shedding light on the process of SpA.他们的发现在2007年二月刊的《关节炎和风湿病》(http://www.interscience.wiley.com/journal/arthritis)上发表．当了解关节强硬性脊椎炎发病过程中，研究怀疑使用抗肿瘤坏死策略预防关节和脊柱关节强直的可行性．
阅读本文的人还阅读：
作者:admin@医学,生命科学 2011-02-24 05:12
医学,生命科学网