Pustular psoriasis is a group of rare, severe and sometimes life threatening skin conditions in which the skin becomes sore and red, and pustules appear. Most forms of pustular psoriasis affect the hands and feet, so called palmo-plantar pustulosis (PPP), making walking and manual work difficult. Treatment options are limited and unsatisfactory. Even the recent, ‘biologic’ treatments that have been developed for the common form of psoriasis (plaque psoriasis) are usually ineffective.

Very recently, our research group and others have shown that the biological processes underlying PPP are very different from plaque psoriasis. This may explain the lack of response of PPP to standard treatments. These studies indicate that a group of proteins belonging to the interleukin (IL)-1 family are central to the disease. This concept is supported by case reports of anakinra, an IL-1 blocker developed for other diseases such as arthritis, being effective for the treatment of PPP.

Our laboratory at King’s College London has been involved in this research looking at the pathways behind the causes of PPP and we are excited to now be leading a large clinical trial investigating the effectiveness of IL-1 blockers as a treatment for PPP, bringing our work from the bench to bedside.

Results from this trial, if successful, will investigate if anakinra is helpful to treat people with PPP and other forms of pustular psoriasis.

***October 2019 Update***

The team led by Dr Capon is investigating genes that influence IL-1 production to establish whether they are malfunctioning in individuals affected by PPP.

In the last 12 months, they concentrated on a gene called CARD14, which has been linked to various proteins of the IL-1 family. The team examined the DNA of 160 individuals with PPP, who were recruited through the APRICOT and PLUM studies. They found that 14 of these study participants carried CARD14 DNA changes. They are now investigating whether these changes can enhance the production of IL-1. This will shed new light on the mechanisms contributing to the accumulation of IL-1 and the onset of PPP.