Hi-drad-uh-NIE-tis sup-yoo-ruh-TIE-vuh – also known as hidradenitis suppurutiva (HS) – is a pathologically complicated skin condition, where chronic skin inflammation leads to abscesses and scarring. It is a systemic disease with local manifestations, meaning that the chronic insult to the skin is systemic, but it is physically located where skin rubs against skin, such as the armpits, groins and under the breasts. It is well known that immune cells, such as neutrophils and mast cells are involved, but what do we know about tissue remodeling?
When the beautiful collagens of the skin become a part of disease pathogenesis
Patients with HS not only experience pain from the neutrophil-rich tunnels but also from excessive tissue remodeling that causes scarring of the skin. These patients have an imbalance in tissue formation and tissue repair, partly due to the excessive activity of immune cells, which release enzymes that degrade the skin.
One group of tissue-degrading enzymes are matrix metalloproteinases, abbreviated as MMPs. These are released by macrophages, the most numerous inflammatory cells found in HS patients. MMPs infiltrate and contribute to HS pathology, signaling that increased activity of MMPs degrades the proteins of the skin tissue, such as collagens. This process can be quantified by specific blood-based biomarker assays targeting this pathological process.
Pathological fragments in HS may be used to identify disease types
In HS, biomarkers of tissue remodeling such as type III collagen degraded by MMPs (C3M), are associated with disease severity (Hurley Staging).
C3M is released upon MMP activation and measures dermal tissue remodeling. This raises the question – can we use C3M to identify subtypes of patients based on their disease activity, and potentially molecular endotypes to help select the right treatment for the patients?
To address this, the levels of C3M are different depending on how active the disease is when divided into the Sartorious Score (HSS).
Finding the patients with high C3M levels reflects high disease activity, and may indicate a different subtype of patients needing a different treatment type.
