Journal of cosmetic dermatology · 2020
Smad7 in psoriasis vulgaris patients: A clinical and immunohistochemical study.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Hemida Aiat Shaban, Hammam Mostafa Ahmed, Salman Arwa Tawfik Ahmed, Shehata Wafaa Ahmed
Аннотация
BACKGROUND: Psoriasis is an inflammatory disease that is mostly immune-derived. It causes proliferation of skin cells, forming plaques. Psoriasis etiology is unknown. It might be multifactorial.
AIMS: This work aimed to study Smad7 expression in psoriasis vulgaris patients in comparison with normal skin.
PATIENTS/METHODS: Thirty patients with psoriasis vulgaris in comparison with 20 age- and sex-matched seemingly healthy individuals were selected. We used psoriasis area and severity index (PASI) to evaluate psoriasis severity. Skin biopsies were prepared from skin lesions (30), perilesions (30) and control (20) groups for histopathological and immunostaining evaluation of Smad7.
RESULTS: Smad7 was progressively upregulated in proliferating keratinocytes from controls (58.18 ± 30.93) to perilesional (106 ± 38.93) and lesional (156.33 ± 62.01) skin (P < .001). Also, dermal inflammatory cells showed upregulation of Smad7 expression from control skin (40 ± 28.28) to skin lesions (137.33 ± 73.86) (P < .010). Smad7 expression showed a positive significant correlation with psoriasis severity (r = .452; P < .012).
CONCLUSION: Smad7 may be involved in increased keratinocyte proliferation as well as skin inflammation in psoriasis vulgaris patients.
AIMS: This work aimed to study Smad7 expression in psoriasis vulgaris patients in comparison with normal skin.
PATIENTS/METHODS: Thirty patients with psoriasis vulgaris in comparison with 20 age- and sex-matched seemingly healthy individuals were selected. We used psoriasis area and severity index (PASI) to evaluate psoriasis severity. Skin biopsies were prepared from skin lesions (30), perilesions (30) and control (20) groups for histopathological and immunostaining evaluation of Smad7.
RESULTS: Smad7 was progressively upregulated in proliferating keratinocytes from controls (58.18 ± 30.93) to perilesional (106 ± 38.93) and lesional (156.33 ± 62.01) skin (P < .001). Also, dermal inflammatory cells showed upregulation of Smad7 expression from control skin (40 ± 28.28) to skin lesions (137.33 ± 73.86) (P < .010). Smad7 expression showed a positive significant correlation with psoriasis severity (r = .452; P < .012).
CONCLUSION: Smad7 may be involved in increased keratinocyte proliferation as well as skin inflammation in psoriasis vulgaris patients.