The utility of high-resolution impedance manometry (HRIM) for evaluating oropharyngeal dysphagia (OPD) has been investigated. These approaches are limited because of the sophisticated methodology. A method of transforming HRIM into a simple and useful diagnostic tool for evaluating OPD is needed. A videofluoroscopic swallowing study (VFSS) and HRIM were performed by independent blinded examiners in 26 consecutive healthy volunteers (12 men; median age, 56.5 years) and 10 OPD patients (five men; median age, 59.5 years). Upper esophageal sphincter (UES) relaxation parameters were measured using a standard HRIM protocol. Peristalsis and bolus transit of the pharyngoesophageal (PE) segment were assessed using an HRIM-modified protocol in which the catheter was pulled back 10 cm. PE bolus transits were evaluated with an impedance contour pattern (linear vs. stasis) method. A significant difference was observed between the manometric measures of healthy volunteers and OPD patients for only the duration of pharyngeal contraction (0.49 ± 0.19 vs. 0.76 ± 0.33 s, P = 0.04). The percentage agreement and kappa value for detecting pharyngeal residue between the VFSS and the impedance analysis were 100% and 1.00, respectively. HRIM allowed for comprehensive assessment of abnormal pharyngeal components that caused pharyngeal residue on VFSS in two patients; reduced base of the tongue versus weak pharyngeal contraction in one, and reduced relaxation of the UES versus reduced laryngeal elevation in the remaining patient. Our findings demonstrated that HRIM using a simple methodology (i.e., pull-back of the catheter) detected pharyngeal residue through a simple analysis of the impedance contour pattern (linear vs. stasis). Furthermore, HRIM facilitated a comprehensive assessment of OPD mechanisms and recognition of subtle abnormalities not yet visible to the naked eye on VFSS.

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Collectively, our data show that expression of Nrf2 is clearly downregulated in diabetic skin tissue, and suggest that Nrf2 may be necessary for protection against glucose-induced oxidative stress.