Barzegari Massoume; Valikhani Mahin; Esmaili Nafiseh; Naraghi Zahra; Nikoo Azita; Kamyab Kambiz; Ghanadan Ali; Tamizifar Banafshe
Volume 11, Issue 2 , 2008, , Pages 64-66
Abstract
Background: Pemphigus vulgaris (PV) is an autoimmune blistering disease, caused by autoantibodies against desmoglein (Dsg) 3 and / or Dsg1 which induce the loss of adhesion between keratinocytes. Nikolsky's sign is the ability to induce peripheral extension of a blister as a consequence of applying lateral ...
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Background: Pemphigus vulgaris (PV) is an autoimmune blistering disease, caused by autoantibodies against desmoglein (Dsg) 3 and / or Dsg1 which induce the loss of adhesion between keratinocytes. Nikolsky's sign is the ability to induce peripheral extension of a blister as a consequence of applying lateral pressure to the border of an intact blister. If the weakening of the intercellular adhesion is present but not marked, then the damage may be demonstrated only microscopically (microscopic Nikolsky’s sign and can increase the sensitivity of the histopathological studies. Methods: We studied 40 patients and divided them randomly into two groups (A, B). Group A were subjected to the tangential pressure over the perilesional skin before a biopsy specimen was taken from that site; group B patients were subjected to a biopsy without the tangential pressure technique. Results: Histopathological changes of pemphigus vulgaris were present in 30% of the patients in group A and 5% of the patients in group B. They were not statistically different. The presence of microscopic Nikolsky’s sign was significantly higher in patients with generalized disease. Conclusion: Microscopic Nikolsky sign can increase the sensitivity of histologic diagnosis of PV.
Mortazavi Hossein; Amirzargar Ali Akbar; Valikhani Mahin; Hallaji Zahra; Daneshpazhouh Maryam; Tabrizi Mohammad Javad Nazemi; Seirafi Hassan; Nikbin Behrouz; Khosravi Farideh; Toosi Siyavash; Chams-Davatchi Cheida
Volume 11, Issue 1 , 2008, , Pages 11-16
Abstract
Background: In addition to humoral immunity associated with anti-desmoglein antibodies, cellular immunity and mediators including cytokines are involved in the pathogenesis of pemphigus vulgaris. In this study we evaluated the level of IL-2, IFN-γ, TNF-α, IL-4, and IL-10 in the sera of patients ...
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Background: In addition to humoral immunity associated with anti-desmoglein antibodies, cellular immunity and mediators including cytokines are involved in the pathogenesis of pemphigus vulgaris. In this study we evaluated the level of IL-2, IFN-γ, TNF-α, IL-4, and IL-10 in the sera of patients with pemphigus vulgaris before and after treatment.Methods: A total number of 71 new patients with pemphigus vulgaris were included in the study. The above mentioned cytokines were measured in patients with a mild disease (20 bullae or less) and a severe disease (60 bullae or more) using ELISA method before and 4 weeks after treatment with 2 mg/kg/day prednisolone and 2mg/kg/day azathioprine. We also measured IL-4 and IL-10 in 69 mildly and 70 severely affected patients only at the beginning of the study. All patients had muco-cutaneous phenotype. Patients with a mild disease had mild mucosal involvement and patients with a severe disease had moderate to severe mucosal involvement. Serum levels of IL-2 and IFN-γ were also measured in 27 normal controls.Results: In the total study population, the level of IL-2 decreased from 103.9 pg/ml to 82.79 pg/ml after treatment (p=0.05). Comparing cytokines between 2 groups (severe and mild), the level of IL-2 before treatment showed significantly lower figures in severe patients (147.27 versus 67.38, p=0.04). On the other hand, IFN-γ after treatment was significantly higher in severe patients (0.75 versus 0.42, p=0.04).Conclusion: Mean level of IL-2 is lower in severe pemphigus vulgaris patients than that of mild disease. This finding indicates that, in pemphigus vulgaris, IL-2 level negatively correlates with the severity of the disease and widespread underlying autoimmune process. The data also suggests that the level of IFN-γ directly correlates with the severity of the disease.