Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission

The recruitment status of this study is unknown because the information has not been verified recently.
Verified December 2010 by National Taiwan University Hospital.
Recruitment status was  Active, not recruiting
Sponsor:
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT01265082
First received: December 21, 2010
Last updated: NA
Last verified: December 2010
History: No changes posted
  Purpose

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.


Condition
Bullous Pemphigoid
Pruritus

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Prospective
Official Title: Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission

Resource links provided by NLM:


Further study details as provided by National Taiwan University Hospital:

Estimated Enrollment: 40
Study Start Date: December 2010
Groups/Cohorts
Patients in remission with pruritus
Patients in remission without pruritus

Detailed 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.

  Eligibility

Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population

primary care clinic,

Criteria

Inclusion Criteria:

  • Patients with bullous pemphigoid

Exclusion Criteria:

  • Patients have other disorders which can lead to itching sensation
  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT01265082

Locations
Taiwan
Department of Dermatology, National Taiwan University Hospital
Taipei, Taiwan
Sponsors and Collaborators
National Taiwan University Hospital
Investigators
Study Director: Yung-Tsu Cho, M.D. Department of Dermatology, National Taiwan University Hospital
  More Information

No publications provided

Responsible Party: Li-Fang, Wang, Department of Dermatology, National Taiwan University Hospital
ClinicalTrials.gov Identifier: NCT01265082     History of Changes
Other Study ID Numbers: 201006012R
Study First Received: December 21, 2010
Last Updated: December 21, 2010
Health Authority: Taiwan: Department of Health

Additional relevant MeSH terms:
Pemphigoid, Bullous
Pruritus
Skin Diseases, Vesiculobullous
Skin Diseases
Autoimmune Diseases
Immune System Diseases
Skin Manifestations
Signs and Symptoms

ClinicalTrials.gov processed this record on April 17, 2014