Wolfgang Miesbach: Moving from Bleed Control to Comprehensive Joint Health
Wolfgang Miesbach, Head of Hemostasis/Hemophilia Center at Medical Clinic 2 at University Hospital Frankfurt, shared a post on LinkedIn about a recent article by Padmavathi Kavadipula and L. Vijaya Mohan Rao, published in Journal of Thrombosis and Haemostasis, adding:
“Zero bleeds is not zero joint damage
Annualised bleeding rates have fallen to levels we would not have predicted ten years ago.
Haemophilic arthropathy has not fallen with them.
It remains the most visible long-term burden our patients carry, and a new paper explains why:
The joint is not only a bleeding problem.
Iron and free haem act as danger signals:
TLR4/NF-κB signalling, M1 macrophage polarisation, IL-1β, IL-6 and TNF-α, VEGF-driven neoangiogenesis.
The new vessels are fragile, they bleed again.
By the time structural change is visible on imaging, this has been running for years.
Where the field is heading
- Single-target blockade (IL-1β, IL-6R, TNF-α, IL-33/ST2) attenuates part of the pathology, never all of it.
- Extracellular vesicles, in particular FVIIa-released endothelial EVs enriched in miR-10a, act on several pathways at once and are mechanistically better matched to a multifactorial disease.
Two qualifications of equal weight
- Nearly all of this evidence rests on single needle-puncture murine models, which do not reproduce the recurrent, cumulative injury our patients sustain.
- Anti-inflammatory treatment does not stop bleeding. These are adjuncts to haemostatic protection, not alternatives to it.
The question for the coming decade is whether bleed protection alone is sufficient, or whether joint protection will require a second, independent therapeutic axis.”
Title: Pathogenic mechanisms and novel experimental anti-inflammatory therapies in hemophilic arthropathy
Authors: Padmavathi Kavadipula, L. Vijaya Mohan Rao
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