ABSTRACT
Background: Environmental factors, including virus infection, may play a role in the activation and/or exacerbation of pemphigus. However, it is still unclear whether human herpesvirus [HHV-8] is involved in pathogenesis of pemphigus or not
Objective: This study was undertaken to investigate the possible association of pemphigus with HHV-8
Methods: Polymerase chain reaction assay [PCR] was used for detection of HHV-8 DNA in lesional and nonlesional skin biopsy specimens of pemphigus patients. Restriction fragment length polymorphism was done on positive cases to confirm the PCR results. Twenty patients with pemphigus [14 with pemphigus vulgaris and 6 with pemphigus foliaceus] and ten control subjects were included in this study
Results: HHV-8 DNA was detected in lesional skin biopsy specimens of 8 out of 20 pemphigus patients [40%]. Biopsy specimens of non-lesional skin of the patients and of control subjects were all negative for HHV-8 DNA. There was no significant difference in HHV-8 prevalence among different types of pemphigus
Conclusion: Our results support the association of HHV-8 and pemphigus. HHV-8 infection might be a contributing factor in the development of pemphigus
ABSTRACT
Background: there is a controversy about the role of beta-endorphin in the pathogenesis of psoriasis, some reports demonstrated elevated circulating beta-endorphin in psoriatic patients especially with actively spreading plaques while lesion-free patients showed reduction of this neuropeptide. On the other hand, the here is published data denoting that circulating beta endorphin has no primary importance in the manifestation of the psoriasis and that inflammation in psoriatic skin lesions is probably not mediated directly by circulating P-endorphin
Objective: to measure plasma beta-endorphin levels in psoriatic patients and demonstrate whether there are any changes of its peripheral blood levels correlating with the clinical improvement. This in order to determine whether and to which limit this neuropeptide is involved in psoriasis
Subjects and Methods: we measured plasma beta-endorphin concentration by enzyme immunoassay in 46 patients with psoriasis both during the presence of lesions and in symptom Free State. Then compared it with that of 18 non-psoriatic patients with T cell mediated inflammatory diseases [10 atopic dermatitis and 8 systemic sclerosis patients] as control. While 24 age and sex matched, healthy individuals were studied as a negative control
Results: the mean 8- endorphin level of psoriatic patients, atopic dermatitis and systemic sclerosis was significantly higher than healthy controls. After treatment, when the skin lesions cleared in the psoriatic patients there was statistically significant reduction of plasma beta-endorphin level. Significant elevation of beta endorphin was found in patients with long lasting lesions. However, there was no significant difference in P-endorphin levels among patients with and without pruritus, nor in those with and without history of major stress. No significant difference between wide and localized spread lesion. Similarly there was no significant difference between those with high and low PASI scores
Conclusion: beta-endorphin is involved in the pathogenesis of psoriasis. Elevated plasma beta-endorphin levels occurs in psoriasis and decline in these levels parallel to clinical improvement and clearance of psoriatic skin lesions. The increased P-endorphin level in psoriasis is not the results of activation of pituitary-adrenal axis by chronic stress, but is produced in psoriatic skin lesions by inflammatory cells. We hope that in the near future neuropeptides will represent a new approach to skin therapy