Discussion & Conclusion
Psoriasis is a systemic immune-mediated and genetic disorder defined by
overgrowth and differentiation of keratinocytes. Environmental stimuli
trigger the process of disease in susceptible individuals. This
pathologic interaction occurs among skin cells, immunocytes and numerous
biologic signaling molecules. Through activation of TH1,
TH17, TH22 cells, these cells cause a
chronic inflammatory state, alter proliferation of keratinocytes and
release of several interleukins responsible for development of
psoriasis.1 Increased risk of malignant cancer
development in patients with psoriasis has been investigated recently.
In several studies, the total cancer incidence rate was higher than
general population. Subsequently SCC was the second most prevalent
cancer among psoriatic patients.2, 3 However it is
still unclear whether the correlation of SCC with psoriasis is due to
underlying genetic basis of disease or its treatments. Phototherapy,
immunosuppressive therapy and other well-known therapeutic methods have
made it challenging to estimate the baseline risk of SCC incidence in
psoriatic patients. So far several studies showed positive association
of such therapies on development of SCC. And the effect of certain
psoriasis treatments on incidence of SCC has been
proven.4 A systematic literature review conducted by
E. Archier et al. showed an increased risk of SCC following oral
psoralen and ultraviolet A (PUVA), a considerable and advantageous
therapeutic method.5 Systemic non-biologic therapies
such as methotrexate and cyclosporine have also been associated with
higher risk of malignancies. These two agents are associated with
increased risk of SCC in psoriatic patients, elevated by PUVA therapy.
Moreover tumor necrosis factor-a Inhibitors (anti-TNFa) were associated
with considerably higher risk of SCC development in psoriatic patients,
increased by primary PUVA exposure and/or immunosuppressive
therapy.4 However since most studies include treated
and untreated patients together, we have no available data on potential
risk of SCC development in patients without any well-defined therapy. In
this article we report a 45‑year‑old male patient with psoriasis who
have been treated with topical agents and multiple tumoral lesions
developed over his scalp eight years after his first initial diagnosis.
This case states that the potential risk of SCC development in patient
with psoriasis is probably not just due therapeutic side effects.
Further investigations are needed to clarify underlying pathobiology of
SCC development in these patients. Moreover periodic screening for
prevalent cancers such as SCC is warranted in patients with psoriasis.