Increased expression of 11 beta-hydroxysteroid dehydrogenase type 2 in the lungs of patients with acute respiratory distress syndrome
Autor: | Takashi Suzuki, Hironobu Sasano, Hiroyoshi Tsubochi, Takashi Kondo, Hironori Ishibashi, Satoshi Suzuki |
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Rok vydání: | 2003 |
Předmět: |
Adult
Male ARDS medicine.medical_specialty Pathology Pathology and Forensic Medicine Cytokeratin Internal medicine 11-beta-Hydroxysteroid Dehydrogenase Type 2 medicine Humans Diffuse alveolar damage Lung Dexamethasone Aged Alveolar Wall Aged 80 and over Respiratory Distress Syndrome business.industry General Medicine Middle Aged medicine.disease Immunohistochemistry medicine.anatomical_structure Endocrinology Prednisolone Female Autopsy business Glucocorticoid medicine.drug |
Zdroj: | Pathology international. 53(11) |
ISSN: | 1320-5463 |
Popis: | We examined the immunohistochemical distribution of 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-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 11 beta-HSD2 in 13 cases. The cells expressing 11 beta-HSD2 in the alveolar wall were positive for surfactant apoprotein-A as well as cytokeratin. Immunoreactivity for 11 beta-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 11 beta-HSD2 immunoreactivity 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 11 beta-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. |
Databáze: | OpenAIRE |
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