Pemphigoid, Bullous Clinical Trial
Official title:
Evaluation of Cytokines and Immunoglobulins in Serum and Blister Fluids Appeared Before Treatment and Subsequently Under Treatment in Bullous Pemphigoid
This study investigates the differences of Eosinophil Cationic Protein, Tumor Necrosis Factor-alpha and Anti-BP180-NC16A IgG levels of blister fluids in Bullous Pemphigoid patients which appeared before and under treatment subsequently. These molecules will also be measured in blood serum before and under treatment. Changes of titers in serum and differences between blister fluids will be compared to observe whether correlation exists between them. These measures will also be compared between groups of responders and non-responders to the first-line treatment options to analyze correlation with treatment success.
Bullous Pemphigoid is an auto-immune bullous disorder in which auto-antibodies to
hemidesmosomes, complement pathway, inflammatory cells and mediators play a crucial roles for
disease pathogenesis.
Anti-BP180-NC16A IgG is an antibody that it primarily triggers inflammatory reactions and
complement cascade in bullae development and plays major roles in disease pathogenesis. It is
secreted by plasma cells which is induced by T-helper 2 cells and their cytokines in serum
and lesional tissue. Anti-BP180 antibody detection in serum is very important in diagnosis
and titers correlate with disease activity. Anti-BP180 antibody can also be detected in
blister fluids and it may aid diagnosis.
Eosinophil cationic Protein is a cytokine and secreted by Eosinophil which is found in
abundant numbers and correlated with tissue damage in Bullous Pemphigoid lesions. Serum
titers of Eosinophil Cationic Protein has a correlation with disease activity and it is
higher in blister fluid than serum. Tumor Necrosis Factor-alpha is an another cytokine which
is secreted from inflammatory cells initially after inflammatory cascade is triggered. It is
also found increased in serum blister fluids. Tumor necrosis factor-alpha is associated with
clinical severity in bullous pemphigoid.
In Bullous Pemphigoid, development of bulla is required to be stopped if treatment will be
considered as successful. Nevertheless smaller, more rapidly healing vesicles and bullae
appear under treatment which are not regarded as findings of treatment failure. In this study
we will measure Eosinophil Cationic Protein, Tumor Necrosis Factor-alpha and Anti-BP180-NC16A
IgG levels with E.L.I.S.A. technique in these subsequently appeared blisters if they will
appear and compare them with pretreatment blisters. We will also measure levels of these
molecules in blood serum before and under treatment. We will analyze corralation between
blood serum and blister fluids. Also we will compare responder patients and non-responder
patients to first-line treatment options to observe correlation of changes and differences in
these body fluids with treatment success.
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