Background: Applications of potassium iodide (KI) to inflammatory skin diseases have not been prevalent, most likely because the mechanism of its therapeutic effects has been unknown. Currently, information on effects of KI on skin diseases is available only in case reports, and few studies report on its mechanism. Recently, we reported 25 cases of palmoplantar pustulosis (PPP) treated with KI and its success and effectiveness. PPP is a common, chronic and very refractory inflammatory skin disorder. However, none of the many different remedies that exist are generally accepted as being reliably effective, and almost all PPP cases are resistant to treatment. This old drug has been replaced by powerful and expensive new drugs, such as biological or immunosuppressive agents, in current dermatology practice. KI is inexpensive with few side effects and, although it has long been used as a drug, it has not been used frequently in clinical practice. Elucidation of the pharmacologic mechanism for the therapeutic effects of KI would lead to its wide use in clinical practice with high evidence, which also would be very cost-effective.
Methods: We applied 5% sodium dodecyl sulphate (SDS) and 3% KI to the shaved backs of BALB/C mice. In SDS-induced inflammatory murine skin, inflammatory leukocyte invasion is observed, such as macrophage and the neutrophilic permeation other than a lymphocyte. In addition, primary inflammatory cytokine such as TNF-α or IL-1 are increasing in this model mouse. We speculated that the effect of KI, a drug whose effectiveness is known for several diseases, can be easily verified using a simple dermatitis model. In addition, small interfering RNA (siRNA), which was designed to knockdown interleukin (IL)-10, was injected to same mice. Expressions of the genes encoding inflammatory cytokines and inflammatory cell counts were measured by real-time reverse transcription-polymerase chain reaction fluorescence-activated cell sorting analysis, respectively.

Anti-inflammatory effects of potassium iodide in sodium dodecyl sulphate-induced inflammatory murine skin through interleukin-10 regulation