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