LAUSR

was commenced on a tapering dose of prednisolone. The systemic symptoms resolved, but he still had marked palmoplantar involvement which is currently being treated with methotrexate and acitretin. The pathophysiology of palmoplantar psoriasis, PPPP and PPP is thought to be different to chronic plaque-type psoriasis with different cytokines such as IL-36 and IL-17 playing a role. Ustekinumab, an IL-12/23 inhibitor, is effective in treating PPP, PPPP and paradoxical reactions secondary to TNF inhibitors and can be used as a first-line biologic agent for PPP. At least six cases have been published suggesting a temporal association of PPPP/PPP and ustekinumab (Table 1). Pustules tend to form within days to months of starting ustekinumab. Another two reports describe worsening of chronic plaque psoriasis or development of inverse psoriasis with ustekinumab. An increase in IFN-alpha due to blocking IL-23, TNFalpha and the Th-17 pathway may be responsible for paradoxical reactions. Though alternative explanations for clinical deterioration including infections (bacterial, viral), lack of response to biologic or natural disease fluctuation were considered in our three cases, temporality similar to the published case reports supports a paradoxical reaction. A preferred treatment option for paradoxical reactions cannot be extrapolated from the small number of case reports. Cases typically improved with switching biologic agent or adding a topical or oral corticosteroid. Further research is required to determine why this paradoxical reaction occurs, which subsets of patients are at risk, the reason for a predominant pustular presentation and appropriate therapy.