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Tytuł pozycji:

Metabolic disorders/obesity is a primary risk factor in hidradenitis suppurativa : an immunohistochemical real-world approach

Tytuł:
Metabolic disorders/obesity is a primary risk factor in hidradenitis suppurativa : an immunohistochemical real-world approach
Autorzy:
Knolle, Jurgen
Zouboulis, Christos C.
Almansouri, Daifallah
Hossini, Amir M.
Balthasar, Ottfried
Wojas-Pelc, Anna
Vaiopoulos, Aristeidis
Kaleta, Katarzyna
Nikolakis, Georgios
Bogusławska, Anna
Data publikacji:
2022
Język:
angielski
ISBN, ISSN:
10188665
Linki:
https://www.karger.com/DOI/10.1159/000517017  Link otwiera się w nowym oknie
Dostawca treści:
Repozytorium Uniwersytetu Jagiellońskiego
Artykuł
Background: Hidradenitis suppurativa (HS) is an inflammatory, potentially scarring disease of the hair follicle, affecting the apocrine gland-bearing skin areas. The major comorbid disorders associated with the occurrence or the aggravation of the disease are obesity and smoking. Numerous efforts to dissociate these factors led to controversial results. Objectives: To assess the importance of metabolic disorders/obesity, smoking/environmental toxins, and inflammation in HS by utilizing the differential expression of major relevant protein markers in lesional skin of obese/smoking versus non-obese/non-smoking HS patients. Methods: Lesional skin specimens deriving from two groups of HS patients (BMI >30 and smokers, n = 12 vs. BMI <30 and non-smokers, n = 10) were stained with antibodies raised against irisin, PPARγ, and IGF-1R, which correlate with metabolic disorders/obesity, EGFR and AhR, associated with smoking, and IL-17, IL-17R, and S100A8, as markers of inflammation. Results: Metabolic disorders/obesity-related markers exhibited marked differential expression between the two groups, while smoking-associated markers a limited one. IL-17R expression was stronger in obese/smokers, and S100A8 staining exhibited intense strong immunoreactivity in both groups without significant difference. Conclusions: The notion that obesity plays a role in HS development appears to be supported by the prominent regulation of the associated lesional biomarkers. Tobacco smoking might contribute less to HS than previously suspected.

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