Pruritus Secondary to Primary Biliary Cholangitis

A Review of the Pathophysiology and Management With Phototherapy

A.B. Hussain; R. Samuel; V.S. Hegade; D.E. Jones; N.J. Reynolds


The British Journal of Dermatology. 2019;181(6):1138-1145. 

In This Article

Receptor Expression Theory

Knowledge continues to grow regarding the actions of UVB phototherapy at a molecular and cellular level.[75–77] Phototherapy and UV radiation are known to have an effect on the expression and function of various proteins and receptors in the skin, including adhesion molecules, cytokines, prostaglandins and growth factor receptors.[78–82] In atopic dermatitis, narrowband UVB is thought to induce apoptosis of epidermal T cells by damaging DNA and activating death receptors, subsequently reducing T-cell-mediated inflammation in the skin.[83] Other examples include vitiligo, where higher vitamin D receptor expression is seen in those undergoing UVB therapy.[55] These findings clearly support the role of UVB in receptor modulation in both inflammatory and noninflammatory skin diseases.

As previously discussed, TRPA1 is a recognized chemosensitive, thermosensitive and mechanosensitive receptor on the membrane of afferent neurons and is necessary for the activation of the bile salt TGR5 and TSLPR pruritus pathways.[38,47,61] It is possible that narrowband UVB reduces expression of a combination of TGR5, TSLPR and TRPA1 without altering bile salt or LPA/ATX concentrations, thus reducing pruritus. This receptor expression theory is further supported by the previously discussed observation that bile acid levels often do not correlate with itch intensity.[30]