الفهرس 
TITLEOnly 14 pages are availabe for public view
 |  | from | 83 |  |  |
| | | from | 83 | | |
Abstract
Pemphigus is a rare auto-immune disease present worldwide. It is considered to be one of the auto-immune bullous diseases. Pemphigus has different subtypes including pemphigus vulgaris, pemphigus foliaceus, IgA pemphigus, paraneoplastic pemphigus and pemphigus vegetans.The most common of which is pemphigus vulgaris representing about 73% ofpemphigus patients.
P38 MAPK is a protein kinase involved in various cellular processes in response to stress stimuli, thus it is incriminated in many auto-immune pro-inflammatory diseases with many evidence .The commercially available inhibitor of P38 MAPK was used in a number of studies to stop or decelerate different auto-immune diseases.
The aim of the study is to investigate the role of P38 MAPK in pemphigus supported by a previous study that used its inhibitor to stop function of caspases, leading to cessation of acantholysis. Thus P38 MAPK is potentially involved in the disease pathology and its inhibitor can be used to ameliorate disease activity together with corticosteroids.
The current study was conducted on 50 subjects who were classified into 25 pemphigus patient and 25 age and sex matched healthy controls. The 25 patients were 19 pemphigus vulgaris patient, 4 pemphigus foliaceus and 2 IgA pemphigus patients.
Keratinocyte sampling was done via simple skin curettage in a previously locally anesthetized patient. The sample was then transported in the appropriate non supplemented culture media. This was followed by propagating the keratinocytes in the suitable keratinocyte culture media conditions for about 7-10 days. Cells were then collected from the culture and the adherent rest of the cells were trypsinized.The cells were then stored until the next step which was performing electrophoresis on SDS-PAGE to the keratinocyte crude extract and transfer on the membrane .
Then immunoblotting was performed by using a primary, secondary antibodies and visualized using the substrate. Various bands were scanned and quantified using the Canon CamScan euro-immune Germany.
By comparing P38 MAPK values between cases and controls, it showed statistical significant difference towards the controls; however 3 cases were double the control. The reason why we thought P38 MAPK ought to have been elevated in all cases because they were on corticosteroids which was proved in a study to both directly and indirectly inhibit P38 MAPK. The marker was found to be elevated in patients who were in relapse and one of which was tapered which may indicate early regaining of pemphigus activity. P38 MAPK was found to be elevated in patients with long disease history and a patient with recent diagnosis indicating that the patient may develop long standing disease and needs follow up.
Statistical correlation of the marker with the different disease subtypes, and clinical indices including activity index, severity index, damage index and treatment duration showed no significance.