scholarly journals Spontaneous Regression of Palmar Warts after Suffering from Diffuse Contact Dermatitis against Alkyl Bromide

2021 ◽  
pp. 54-57
Author(s):  
Gyohei Egawa ◽  
Tetsuya Honda ◽  
Kenji Kabashima

Contact immunotherapy with several sensitizing chemicals such as diphenylcyclopropenone (DPCP) or squaric acid dibutyl ester (SADBE) have been used for the treatment of recalcitrant or multiple warts. Here, we report a case of multiple verrucae vulgaris (VV) on the palm which spontaneously resolved after the development of systemic contact dermatitis against alkyl bromide. We considered that our case accidentally mimics contact immunotherapy against multiple VV. VV sometimes regress spontaneously, which may be triggered by accidental contact dermatitis, as shown in our case.

2021 ◽  
Author(s):  
Zhouxian Pan ◽  
Juncai Dong ◽  
Jinlyu Sun ◽  
Jing Zhang ◽  
Christopher Chang ◽  
...  

2009 ◽  
Vol 27 (3) ◽  
pp. 355-364 ◽  
Author(s):  
Rajiv I. Nijhawan ◽  
Matthew Molenda ◽  
Matthew J. Zirwas ◽  
Sharon E. Jacob

2011 ◽  
Vol 23 (1) ◽  
pp. 85 ◽  
Author(s):  
Eujin Cho ◽  
Jeong Deuk Lee ◽  
Sang Hyun Cho

2004 ◽  
pp. 285-319
Author(s):  
Torkil Menn√â ◽  
Howard Maibach ◽  
Niels Veien

2017 ◽  
Vol 118 (1) ◽  
pp. 619-624 ◽  
Author(s):  
Lintao Qu ◽  
Kai Fu ◽  
Steven G. Shimada ◽  
Robert H. LaMotte

Persistent itch often accompanies allergic contact dermatitis (ACD), but the underlying mechanisms remain largely unexplored. We previously demonstrated that CXCL10/CXCR3 signaling activated a subpopulation of cutaneous primary sensory neurons and mediated itch response after contact hypersensitivity (CHS), a murine model of ACD, induced by squaric acid dibutylester. The purpose of this study was to determine the ionic mechanisms underlying CXCL10-induced neuronal activation and allergic itch. In whole cell recordings, CXCL10 triggered a current in dorsal root ganglion (DRG) neurons innervating the area of CHS. This current was modulated by intracellular Cl− and blocked by the general Cl− channel inhibitors. Moreover, increasing Ca2+ buffering capacity reduced this current. In addition, blockade of Cl− channels significantly suppressed CXCL10-induced Ca2+ response. In behavioral tests, injection of CXCL10 into CHS site exacerbated itch-related scratching behaviors. Moreover, the potentiating behavioral effects of CXCL10 were attenuated by either of two Cl− channel blockers. Thus we suggest that the Cl− channel acts as a downstream target mediating the excitatory and pruritic behavioral effects of CXCL10. Cl− channels may provide a promising therapeutic target for the treatment of allergic itch in which CXCL10/CXCR3 signaling may participate. NEW & NOTEWORTHY The ionic mechanisms underlying CXCL10-induced neuronal activation and allergic itch are largely unexplored. This study revealed that CXCL10 evoked an ionic current mainly carried by Cl− channels. We suggest that Cl− channels are likely key molecular candidates responsible for the CXCL10-evoked neuronal activation and itch-like behaviors in a murine model of allergic contact dermatitis induced by the antigen squaric acid dibutylester. Cl− channels may emerge as a promising drug target for the treatment of allergic itch in which CXCL10/CXCR3 signaling may participate.


2018 ◽  
Vol 56 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Marcella Aquino ◽  
Greg Rosner

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