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Evaluation of the −26G>A CC16 polymorphism in acute respiratory distress syndrome*

Frerking, Ilka; Sengler, Claudia; Günther, Andreas; Walmrath, Hans-Dieter; Stevens, Paul; Witt, Heiko; Landt, Olfert; Pison, Ulrich; Nickel, Renate

doi: 10.1097/01.CCM.0000181526.24809.3E
Brief Report
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Objective: Different risk factors are presumably involved in the pathogenesis of acute respiratory distress syndrome (ARDS) including genetic factors. Clara cell protein 16 (CC16) is a potential candidate gene for ARDS susceptibility because reduced levels of the anti-inflammatory CC16 have been observed in bronchoalveolar lavage fluids or serum of patients with different inflammatory lung diseases. Furthermore, CC16 potently inhibits phospholipase A2, which plays a major role in ARDS pathophysiology. A functional polymorphism (−26G>A) was previously identified and related to decreased CC16 levels, asthma, and asthma severity.

Design: Observational study.

Settings: Adults with ARDS were recruited from intensive care units in two university medical centers.

Subjects: We evaluated the role of this genetic variant in 117 German patients with ARDS and 373 German controls.

Measurements: The CC16 −26G>A polymorphism was analyzed by melting-curve analysis using a pair of fluorescence resonance energy transfer probes.

Main Results: CC16 genotype frequencies in ARDS patients did not differ from those seen in controls. Also, the allele frequencies were identical in patients compared with controls (0.66 and 0.34). Moreover, only one of the patients who died (n = 27) was homozygous for the −26A allele.

Conclusions: The CC16 −26G>A polymorphism does not affect the susceptibility to and the outcome of ARDS.

From the Departments of Anesthesiology (IF, UP), Pediatrics (CS, HW, RN), and Neonatology (PS), Charité, Universitätsmedizin Berlin, Berlin, Germany; the Department of Medicine (AG, HDW), Justus–Liebig University, Giessen, Germany; and TIB MOLBIOL, Berlin, Germany (OL).

Supported, in part, by the Deutsche Forschungsgemeinschaft (Pi 165/8, Ste 459/4-4) and Sonnenfeld-Stiftung, Berlin, Germany (Witt 2000, Nickel 2001, Frerking 2003).

The authors have no financial associations or conflicts of interest.

© 2005 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins