Increased expression of 11β-hydroxysteroid dehydrogenase type 2 in the lungs of patients with acute respiratory distress syndrome

Satoshi Suzuki, Hiroyoshi Tsubochi, Hironori Ishibashi, Takashi Suzuki, Takashi Kondo, Hironobu Sasano

研究成果: Article査読

13 被引用数 (Scopus)

抄録

We examined the immunohistochemical distribution of 11β- hydroxysteroid dehydrogenase type 2 (11β-HSD2), the enzyme responsible for the conversion of bioactive glucocorticoids to their receptor-inactive forms, in lung tissue obtained at autopsy from 14 patients who had died due to acute respiratory distress syndrome (ARDS). We found positive immunoreactivity for 11β-HSD2 in 13 cases. The cells expressing 11β-HSD2 in the alveolar wall were positive for surfactant apoprotein-A as well as cytokeratin. Immunoreactivity for 11β-HSD2 was also detected in the CD68+ cells, which were found in the alveolar spaces. All patients had been treated with glucocorticoids for ARDS and/or the underlying diseases. There was no statistically significant correlation between the use of glucocorticoids and 11β-HSD2 immunoreactlvlty in the alveolar wall (P = 0.0729). However, expression of grade ++ was found in three out of five patients who received dexamethasone pulse therapy at relatively large doses, as well as in three other patients treated with prednisolone for a long period of time for the underlying disease. An increase in the expression of 11β-HSD2 may result in faster glucocorticoid breakdown in lung cells in patients with ARDS. Impaired glucocorticoid availability in the lungs of such patients may explain, in part, the fact that glucocorticoid therapy does not always rescue patients with ARDS.

本文言語English
ページ(範囲)751-756
ページ数6
ジャーナルPathology international
53
11
DOI
出版ステータスPublished - 2003 11 1

ASJC Scopus subject areas

  • 病理学および法医学

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