Overview

This trial is active, not recruiting.

Conditions bullous pemphigoid, pruritus
Sponsor National Taiwan University Hospital
Start date December 2010
Trial size 40 participants
Trial identifier NCT01265082, 201006012R

Summary

The following is the investigators hypothesis regarding the pruritus of BP patients during remission. Anti-BP 180 IgE binds to dermal mast cells, inducing their activation and secretion of mediators after being cross-linked by antigens. Among mediators, histamine directly induces itching and vessel changes, whereas tryptase potentiates itching and vessel changes in an indirect way through the actions of neuropeptides. Tryptase stimulates neurons which in turn secrete neuropeptides.

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Observational model case control
Time perspective prospective
Arm

Eligibility Criteria

Male or female participants of any age.

Inclusion Criteria: - Patients with bullous pemphigoid Exclusion Criteria: - Patients have other disorders which can lead to itching sensation

Additional Information

Official title Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission
Description Bullous pemphigoid(BP) is a cutaneous autoimmune blister disease. In addition to blisters formation which disrupt skin barrier and result in high mortality, erythematous edematous plaques often develop on skin of bullous pemphigoid patients accompanied with intensive pruritus. As regard with the pathogenesis of BP, it is generally accepted that anti-BP180 IgG is the most important pathogenic factor for blister formation, whereas anti-BP180 IgE which binds to mast cells and induces their activation results in erythematous edematous plaques. Quite a few bullous pemphigoid patients suffer from intensive pruritus even during clinical remission period that means blisters or plaques are no longer on their skin. The reasons why pruritus persists during this period are still obscure. Pruritus is the most common symptom of cutaneous diseases. Our understanding regarding pathophysiology of "pruritus" has made a remarkable progress in the past decade. Now, it is known that there are various kinds of substances that induce pruritus (pruritus mediators) and different combinations of these mediators are involved in different itching diseases. Moreover, neuropeptides secreted by stimulated neurons can in turn induce neurogenic inflammation. The following is our hypothesis regarding the pruritus of BP patients during remission. Anti-BP 180 IgE binds to dermal mast cells, inducing their activation and secretion of mediators after being cross-linked by antigens. Among mediators, histamine directly induces itching and vessel changes, whereas tryptase potentiates itching and vessel changes in an indirect way through the actions of neuropeptides. Tryptase stimulates neurons which in turn secrete neuropeptides. Thus, in order to test our hypothesis, the strategy of this study is to compare parameters between two groups of patients, bullous pemphigoid patients in remission with pruritus and without pruritus. The following parameters in serum and skin will be measured: total IgE, anti-BP 180 IgE, the number and activated status of mast cells, the amount of some mediators and neuropeptides produced by mast cells and neurons, respectively. In addition, these parameters in active stage will also be measured for reference and with a hope to find useful parameters for predicting the persistence of pruritus in remission.
Trial information was received from ClinicalTrials.gov and was last updated in December 2010.
Information provided to ClinicalTrials.gov by National Taiwan University Hospital.