Discussion
The exact underlying mechanism for the association of psoriasis and pemphigus vulgaris is still unclear, but there are various hypotheses which could clarify the relationship to some extent. For example, Rituximab which is widely used for treatment of pemphigus vulgaris can be a potential contributing factor for development of psoriatic plaques in some patients.
In addition to rituximab-induced psoriasis in pemphigus vulgaris, several psoriasis cases has been also reported in patients with rheumatoid arthritis, non-Hodgkin’s lymphoma, systemic lupus erythematosus, granulomatosis with polyangiitis, idiopathic membranous glomerulopathy and chronic idiopathic demyelinating polyneuropathy disorder after receiving rituximab for controlling the underlying disorder.
Rituximab may induce psoriasis via a variety of mechanisms. First, rituximab leads to B-cell depletion resulting in elimination of B-cells regulation on T-cells and therefore T-cells activation (2, 3). Rituximab also has been shown to impair the response to infection leading to the psoriasis development (2). Since psoriasis has been regarded as a T-cell-driven disease, the T cell dysregulation after rituximab therapy might be responsible for development of psoriasis (3).
According to the literature, in patients with rituximab-induced psoriasis, nail changes, pustular and plantar psoriasis, and psoriatic arthritis, as well as all the plaque type psoriasis were detected in patients. Psoriasis onset varied between 10 days to 2 years after the first dose. In our case, psoriatic lesions developed 4 months after the second course of rituximab.
Several studies have shown a link between bullous disease and psoriasis. Bullous pemphigoid is known as the most common auto-immune bullous disease associated with
psoriasis (2), followed by pemphigus vulgaris, pemphigus foliaceous (2-6), and
herpetiform pemphigus (7). On the other hand, less commonly, there are some reports of development psoriasis in pemphigus vulgaris patients similar to our case (8, 9).
In a recent study recorded by Balighi et al, three patients with pemphigus vulgaris developed psoriasis, two of them did not receive rituximab. This may also highlight another contributing factor other than rituximab. For instant, the role of spreading epitope may be a suggested etiology for this coincidence. According to this model many proteins, which were not recognizable by immune system cells, become identifiable after activation of chronic autoimmune response that leads to a new autoimmune reaction (epitope phenomenon 1998)
In 1987 yokoo et al reported a case for pemphigus foliaceous coexistence with psoriasis in one patient, focusing on the fact that the activation of plasminogen is involved in acantholysis in pemphigus. Also, increased concentrations of plasminogen activator have been detected in psoriasis lesions.
Based on genome-wide association studies, psoriasis and pemphigus are both related to HLA DRB1 alleles. As a result, genetic factors may also play a remarkable role in association of these two auto-inflammatory skin diseases.
Table 1: Review of literature for rituximab-induced psoriasis for a variety of underlying disorders