類風濕性關節炎 | Rheumatoid Arthritis (RA)

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類風濕性關節炎 / Rheumatoid arthritis (RA)

類風濕性關節炎（RA）是一種慢性全身性自身免疫性疾病，主要影響滑膜關節襯裡，與進行性殘疾、過早死亡和社會經濟負擔有關。迫切需要更好地理解病理機制是如何導致個體RA進展惡化的，以便開發出在疾病進展的每個階段有效治療患者的療法。在這裡，我們解剖了特定階段的病因和病理：（i）觸發，（ii）成熟，（iii）靶向，和（iv）暴發性階段，伴隨著滑膜增生，軟骨損傷，骨侵蝕和全身後果。現代藥物治療（包括傳統的、生物的和新的潜在的小分子疾病修飾的抗風濕藥物）仍然是RA治療的主流，並且在實現疾病緩解而無關節畸形方面取得了重大進展。儘管如此，相當一部分類風濕關節炎患者對現時的治療沒有有效的反應，因此迫切需要新的藥物。(1)

多靶點治療於類風濕性關節炎的作用:

  • EDTA治療類風濕性關節炎反應良好(2)
  • EDTA治療類風濕性關節炎症狀和氧化狀態得到改善(3)
  • 蛋白水解酶口服療法具有一定的鎮痛和抗炎作用(4)
  • 保護和保存關節軟骨(5)
  • 良好的免疫、抗炎、抗感染和抗腫瘤/抗轉移活性(6)

Rheumatoid arthritis (RA)

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that primarily affects the lining of the synovial joints and is associated with progressive disability, premature death, and socioeconomic burdens. A better understanding of how the pathological mechanisms drive the deterioration of RA progress in individuals is urgently required in order to develop therapies that will effectively treat patients at each stage of the disease progress. Here we dissect the etiology and pathology at specific stages: (i) triggering, (ii) maturation, (iii) targeting, and (iv) fulminant stage, concomitant with hyperplastic synovium, cartilage damage, bone erosion, and systemic consequences. Modern pharmacologic therapies (including conventional, biological, and novel potential small molecule disease-modifying anti-rheumatic drugs) remain the mainstay of RA treatment and there has been significant progress toward achieving disease remission without joint deformity. Despite this, a significant proportion of RA patients do not effectively respond to the current therapies and thus new drugs are urgently required.(1)

Refs
  1. Stotz HU, Pittendrigh BR, Kroymann J, et al. Induced plant defense responses against chewing insects. Ethylene signaling reduces resistance
    of Arabidopsis against Egyptian cotton worm but not diamondback moth [published correction appears in Plant Physiol 2001 Apr;125(4):2203]. Plant Physiol. 2000;124(3):1007-1018. doi:10.1104/pp.124.3.1007
  2. L.J. Leipzig, A.J. Boyle, D.S. McCann. Case histories of rheumatoid arthritis treated with sodium or magnesium EDTA. Volume 22, ISSUE 8-9, P553-563, February 01, 1970. DOI:https://doi.org/10.1016/0021-9681(70)90032-9
  3. Bamonti, F., Fulgenzi, A., Novembrino, C. et al. Metal chelation therapy in rheumathoid arthritis: a case report. Biometals 24, 1093–1098 (2011). https://doi.org/10.1007/s10534-011-9467-9
  4. Jörg Leipner, Felix Iten, Reinhard Saller. Therapy with Proteolytic Enzymes in Rheumatic Disorders. February 2001BioDrugs 15(12):779-89. DOI: 10.2165/00063030-200115120-00001
  5. S R Chintalacharuvu 1 , N Urankar-Nagy, C A Petersilge, F W Abdul-Karim, S N Emancipator. Treatment of collagen induced arthritis by proteolytic enzymes: immunomodulatory and disease modifying effects. Comparative Study. J Rheumatol. 2001 Sep;28(9):2049-59. PMID: 11550974
  6. Josef Beuth, MD. Proteolytic Enzyme Therapy in Evidence-Based Complementary Oncology: Fact or Fiction? https://doi.org/10.1177/1534735408327251
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