克拉迪宾和S1P受体调节器在未接受治疗的复发性复发性多发性硬化症中的比较有效性
Shalom Haggiag1, Luca Prosperini1, Massimo Filippi2
1Centro Sclerosi Multipla, Dipartimento di Neuroscienze, Azienda Ospedaliera San Camillo-Forlanini, Rome, Italy.
JAMA network open
|November 3, 2025
概括
与S1PRMs相比,克拉迪宾在25个月内在未经治疗的复发性复发性多发性硬化症 (RRMS) 患者中降低残疾进展方面表现出更高的有效性. 然而,它的复发预防效益在36个月后减少,需要潜在的再治疗.
科学领域:
- 神经学 神经学
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 早期治疗选择对于管理复发性复发性多发性硬化症 (RRMS) 是至关重要的.
- 在未接受治疗的RRMS患者中,对克拉迪宾与-1酸盐受体调节剂 (S1PRMs) 的比较数据有限.
- 了解治疗有效性对于优化患者的治疗结果至关重要.
研究的目的:
- 为了比较cladribine与S1PRMs在未经治疗的RRMS患者中的临床有效性.
- 评估疾病活动,残疾累积和治疗反应的差异.
- 为RRMS管理提供早期治疗决策的信息.
主要方法:
- 一项比较有效性研究,利用来自108个意大利多发性硬化中心的数据.
- 包括从未接受过治疗的RRMS患者,在2011-2021年期间开始使用克拉迪宾或S1PRMs (fingolimod,ozanimod,ponesimod),随访时间≥12个月.
- 倾向性得分匹配和对对审查被用来平衡基线特征和随访时间; 考克斯比例危险模型被用于结果比较.
主要成果:
- 在最初的25个月随访期间,在克拉迪宾和S1PRM组之间没有观察到复发率,MRI活性或NEDA-3损失的显著差异.
- 克拉德里宾显示残疾恶化的风险较低,主要是由于独立于复发活动 (PIRA) 的进展减少.
- 36个月后,克拉迪宾与更高的复发风险和增加的NEDA-3损失有关,而停药率相似.
结论:
- 克拉迪宾在25个月的时间内在减少残疾进展方面表现出优异的有效性,这可能是由于PIRA减少,尽管短期NEDA-3结果相似.
- 克拉德里宾的复发预防效果在36个月后减少,这表明需要重新治疗或修改治疗以持续长期控制疾病.
- 这些发现强调了考虑早期RRMS治疗的时间依赖性疗效的重要性.
相关概念视频
01:29Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents
475
Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
475
01:24Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
476
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
476
01:20Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein
804
Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
804
01:21Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids
423
Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
423
01:27Pharmaceutical Alternatives: Polymorphic Form-Related and Particle Size-Related Therapeutic Nonequivalence
142
Changes in polymorphic forms can significantly influence the bioavailability of poorly soluble drugs. Although the FDA defines pharmaceutical equivalence based on having the same active ingredient, dosage form, and route of administration, it does not automatically disqualify products with different polymorphic forms. This means two products with different polymorphs can still be deemed pharmaceutically equivalent. However, polymorphic differences can affect properties like wettability,...
142