Validation of the Swedish translation of LPR-HRQL.

BACKGROUND: The aim of this study was to adapt the Laryngopharyngeal Reflux Health- Related Quality of Life questionnaire (LPR-HRQL) to Swedish and evaluate its psychometric properties in patients with suspected laryngopharyngeal reflux (LPR). MATERIAL/METHODS: The psychometric validation included 228 patients with suspected LPR who had previously undergone a 2-level 24-hour pH examination and who answered a mail-distributed set of questionnaires. The patients were divided into 2 comparable groups according to the Reflux Symptom Index (RSI) cut-off score: 126 patients with RSI score between 0-13 (defined as normal) and 102 patients with RSI score >13 (defined as abnormal, i.e. having LPR disease). RESULTS: LPR-HRQL was adapted to Swedish using a formal forward-backward translation method with input from expert groups (patients and physicians). Psychometric properties of the Swedish version of LPR-HRQL were evaluated by using factor analysis to explore the factor structure. Convergent and discriminant validity was determined by using the questionnaires RSI and Short Form-36 (SF-36). The psychometric tests performed fulfilled the criteria for structural integrity, validity and reliability, mostly confirming the results obtained in the original LPR-HRQL version. CONCLUSIONS: The Swedish translated version of LPR-HRQL proved to be a statistically valid instrument with which to assess HRQL in patients with LPR disease, and will be further tested in prospective studies.

Gene expression changes of inflammatory mediators in posterior laryngitis due to laryngopharyngeal reflux and evolution with PPI treatment: a preliminary study.

HYPOTHESIS: Standard of care in laryngopharyngeal reflux (LPR) is acid suppression therapy. Its treatment efficacy and mechanism of action are not well documented. No objective study investigating the molecular patterns of inflammation in LPR or in response to proton pump inhibitor (PPI) treatment has been accomplished. We hypothesized that gene expression levels of mediators of inflammation -- interleukin 6 (IL6), interleukin 8 (IL8), interleukin 1a (IL1a), interleukin 1b (IL1b), transforming growth factor beta 1 (TGFbeta1), vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF2), and tumor necrosis factor alpha (TNFalpha) -- in posterior larynx tissue would be increased in those with diagnosed LPR and would be then reduced with PPI treatment. STUDY DESIGN: Prospective uncontrolled trial. METHODS: Biopsies from the posterior larynx were taken from 25 participants with LPR before and after a 10-week period with rabeprazole (40 mg). RNA isolation and real-time PCR was used to measure gene expression levels. RESULTS: No significant differences were measured for any of the cytokines, either for the entire participant group (n = 25) or for the subset of participants who did not have a previous history of PPI usage (n = 15). In those participants who had a history of PPI usage (n = 10), a significant increase in gene expression levels post medication was measured for TGFbeta1 (P = .0396), VEGF (P = .0216), IL8 (P = .0297), after adjusting for compliance, subjective improvement, and reflux severity. CONCLUSIONS: Our findings are provocative and speak to the unresolved understanding of the pathophysiology of LPR, its diagnosis, and its differences from gastroesophageal reflux disease.