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Rheopheresis as a causal therapy option for systemic scleroderma (SSc)
Stine Lutze1, G Daeschlein1, W Konschake1
1Department of Dermatology, University Medicine Greifswald, Greifswald, Germany.
Systemic sclerosis involves vasculopathy, autoinflammation, and fibroblast dysfunction. Apheresis therapies targeting plasma proteins, like interleukin-6, show promise for treating this collagenosis.
Area of Science:
- Rheumatology
- Immunology
- Vascular Biology
Background:
- Systemic sclerosis is a complex collagenosis characterized by vasculopathy, autoinflammation, and fibroblast dysfunction.
- Vasculopathy is clinically more significant in systemic sclerosis than autoinflammation, unlike other collagenoses such as Lupus erythematosus.
Observation:
- Classical immunosuppressants show limited efficacy, suggesting autoinflammation is not the primary driver of systemic sclerosis.
- Therapeutic strategies focusing on vasculopathy demonstrate greater effectiveness.
Findings:
- Apheresis methods, such as plasmapheresis, reduce plasma proteins including fibrinogen, C-reactive protein, and cytokines.
- Interleukin-6, a key cytokine, is significantly reduced by apheresis, indicating its potential central role.
Implications:
- Targeting interleukin-6 and other plasma proteins via apheresis may offer a novel therapeutic approach for systemic sclerosis.
- Further research into apheresis mechanisms could elucidate the pathomechanism of systemic sclerosis and improve treatment outcomes.
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