Background and Aims

Introduction

Immune checkpoints such as PD-1 and PDL-1 inhibitors ensure the immunologic homeostasis by blocking excessive T cell activation. Tumors also use these checkpoints to evade recognition by the immune system. In recent years, immune checkpoint blockade has shown to have a potent anti-tumor effect, by shifting the immune system towards anti-tumor activity. Due to their specific mechanism of action, immune checkpoint inhibitors have specific immune-related adverse events. The most frequent irAEs are cutaneous.

Methods

Several cases of psoriasis induced by PD(L)-1 inhibitors:

A 75-year old woman with renal cell carcinoma presented with a psoriasis exacerbation after one month of Nivolumab. A 59-year old man with Non-Small Cell Lung Cancer developed a de novo psoriasis after one month of Nivolumab. A 30-year old man developed a de novo psoriasis guttata after one year of Nivolumab. A 67-year old man was treated with pembrolizumab and developed a de novo psoriasis guttata after two months. A 59-year old man was treated with avelumab for a glioblastoma and developed a psoriasis exacerbation after three months.

Results

Discussion:

While psoriasis exacerbation during immune checkpoint blockade is a well-described irAE, development of de novo psoriasis is less frequently observed. Pathogenesis is poorly understood, but it has been shown that the Th1/Th17 pathway is upregulated. Treating the psoriasis can be challenging, since the use of immunosuppressive treatment is fairly restricted because of the concomitant cancer. The development of psoriasis however should usually never be the sole reason to stop the checkpoint inhibitor.

Conclusions

See discussion