“…• There has been significant decreased suppressor activity in psoriasis disease which results in increasing production of autoantibodies against skin antigens [9] • Plasminogen activator which has a major role in the induction of acantholysis has been increased in psoriatic lesions [8,9] • HLA-DR4 haplotype is a common HLA type in both diseases [8] • IgG autoantibodies could be able to induce Interleukin-8 (IL8) expression in keratinocytes; IL-8 has an important role in the production of neutrophilic pustules [4] • Corticosteroids which have been used for treatment of AIBD could be a trigger for pustular psoriasis [7] on the other hand phototherapy for psoriasis may be a trigger to produce endogenous pemphigus autoantibodies [3,10]; in addition heat and ultra violet (UV) radiation are exacerbating factors in PF [2]. Also interleukin-1 (IL-1) is a proinflammatory cytokine which has a major role in AIBD, psoriasis and UV damage [7] • Enalapril or penicillamin intake, topical dithranol or salicylic acid, transient hypo zincemia and potential infectious foci, all have been incriminated in previous case reports [5,11].…”