Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission
|ClinicalTrials.gov Identifier: NCT01265082|
Recruitment Status : Unknown
Verified December 2010 by National Taiwan University Hospital.
Recruitment status was: Active, not recruiting
First Posted : December 22, 2010
Last Update Posted : December 22, 2010
|First Submitted Date||December 21, 2010|
|First Posted Date||December 22, 2010|
|Last Update Posted Date||December 22, 2010|
|Start Date||December 2010|
|Primary Completion Date||Not Provided|
|Current Primary Outcome Measures||Not Provided|
|Original Primary Outcome Measures||Not Provided|
|Change History||No Changes Posted|
|Current Secondary Outcome Measures||Not Provided|
|Original Secondary Outcome Measures||Not Provided|
|Current Other Outcome Measures||Not Provided|
|Original Other Outcome Measures||Not Provided|
|Brief Title||Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission|
|Official Title||Explore the Mechanisms of Pruritus in Bullous Pemphigoid Patients During Remission|
|Brief 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.|
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.
|Study Design||Observational Model: Case Control
Time Perspective: Prospective
|Target Follow-Up Duration||Not Provided|
|Sampling Method||Non-Probability Sample|
|Study Population||primary care clinic,|
|Publications *||Not Provided|
* Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
|Recruitment Status||Unknown status|
|Completion Date||Not Provided|
|Primary Completion Date||Not Provided|
|Ages||Child, Adult, Senior|
|Accepts Healthy Volunteers||No|
|Contacts||Contact information is only displayed when the study is recruiting subjects|
|Listed Location Countries||Taiwan|
|Removed Location Countries|
|Other Study ID Numbers||201006012R|
|Has Data Monitoring Committee||No|
|U.S. FDA-regulated Product||Not Provided|
|IPD Sharing Statement||Not Provided|
|Responsible Party||Li-Fang, Wang, Department of Dermatology, National Taiwan University Hospital|
|Study Sponsor||National Taiwan University Hospital|
|PRS Account||National Taiwan University Hospital|
|Verification Date||December 2010|