| Autor: |
Fiz, Ivana, Antonopoulos, Wiebke, Kölmel, Jan-Constantin, Rüller, Karina, Fiz, Francesco, Piazza, Cesare, Peretti, Giorgio, Flechtenmacher, Christa, Schirmacher, Peter, Sittel, Christian |
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| Zdroj: |
European Archives of Oto-Rhino-Laryngology; Feb2023, Vol. 280 Issue 2, p775-780, 6p |
| Abstrakt: |
Purpose: Our previous study on the idiopathic progressive subglottic stenosis (IPSS) highlighted a possible hormonal mechanism, with over-expression of estrogen receptors alpha (ER-α) and progesterone receptors (PR). We tested whether such over-expression take place in non-idiopathic subglottic stenosis (NISS) as well. Methods: 37 specimens of iatrogenic NISS were analyzed (20 females; mean age, 59 ± 12 years; range 41–85). Immunoreactivity of ER-α and PR was calculated as the product of intensity (1 = weak, 2 = moderate, 3 = strong) and positive cells percentage (1 to 4, for < 10%, 10–50%, 50–80%, and > 80%). This score was calculated on the stenotic tissue (ST), and stenosis margins (SM). Results: The expression of PR was significantly higher in ST of IPSS compared with female and male NISS patients (8.7 ± 3.1 vs. 4.9 ± 3.2, p < 0.001 for IPSS vs. female and 8.7 ± 3.1 vs. 2.1 ± 2.7, p < 0.01 for IPSS vs. male NISS patients). Contrarily, ER-α showed gender differences, as both IPSS and female NISS patients had similar, yet higher ER-α expression compared with male NISS patients (7.0 ± 4.2 vs. 6.5 ± 2.5, p = NS for IPSS vs. female and 7.0 ± 4.2 vs. 3.4 ± 2.0, p < 0.02 for IPSS vs. male NISS patients). There was no difference in fibroblast receptor expression between ST and SM. However, ER-α and PR expression was significantly lower in marginal mucous glands when compared with ST. Conclusions: The IPSS pathogenesis appears to be driven by hormonal mechanisms, in particular, by over-expression of PR. Marginal cells display a reduced hormone receptor density. This finding could be interpreted as a compensatory mechanism. These findings could open up for targeted IPSS treatment. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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