Lupus erythematosus:
Systemic lupus erythematosus (SLE) is a complex prototypic autoimmune disease associated with the presence of anti-nuclear autoantibodies (ANAs) related to chronic immune system activation. Immune irregulation is the significant characteristic of lupus erythematosus. However, it also includes the abnormal T-cell activation, hyperactivity of B-cells, inappropriate management of immune complexes, and cellular debris by the innate immune system 120.
Pathogenesis: The pathological mechanism of lupus erythematosus is unclear, but patients with systemic lupus erythematosus have shown decreased expression of PD-1 on T-cells and a higher frequency of neutrophils expressed by PD-L1. Therefore, activation of auto-reactive T-cells and over-activity of B-cells leads to the production of pathogenic autoantibodies and thus causing tissue injury120.
Clinical incidence: A total of eleven cases of lupus erythematosus were reported with anti-PD-1 therapy. Six cases were reported with pembrolizumab121-124 and five with nivolumab113, 125-127 immune checkpoint inhibitors. Histological and clinical diagnosis of lupus erythematosus and lichenoid reactions in some cases is difficult to differentiate113. In several reported cases, the skin lesions appeared to be pruritic nummular erythematous papules and plaques122 and annular papulosquamous plaques121, 125. One patient presented with fever, arthralgia, asthenia, and bullous lupus erythematosus127.
Treatment: The symptoms of cutaneous lesions were controlled with high potency topical and systematic corticosteroid treatment (prednisolone)121, 127. Other treatments initiated were tacrolimus (1mg/day)123, triamcinolone 0.1% ointment, sun protection, and hydroxychloroquine113, 125. In one such reported case, the skin rash of the patient resolved without treatment within one month after interruption of pembrolizumab therapy122.
Life-threatening cutaneous drug reactions