Abstract
LES resting pressure compared to non-IPF patients (14.1 [4-32.5] vs. 16.7 [4-37.2]; p= 0.0999). Mean contraction amplitude in the distal and proximal esophagus were slightly higher in IPF compared to non-IPF patients (92.4 [40-190] vs. 84 [35-170] and 90.6 [10210] vs. 79.9 [10-210], respectively; p=ns), but the difference was not significant. In contrast, IPF patients had significantly higher (p<0.01) esophageal acid exposure (9.25[4.7-15.4] vs. 3.3[1.4-7.4] vs. 0.7[0-2.4.2]), number of acid (45[23-55] vs. 32[19-44] vs. 18[10-31]), weakly-acidic (34[19-43] vs. 21[11-33]) vs. 18[15-28]) and proximal reflux events (51[26.565.5] vs. 20[9.5-34.5] vs. 9[5-20]) compared to non-IPF patients and HVs. Pulmonary fibrosis HRCT-scores correlated well with reflux episodes in both distal (r2=0.567) and proximal (r2=0.6323) esophagus. Patients with IPF had more bile acids and pepsin (p<0.001) in BAL (62% and 67%) and saliva (61% and 68%) than non-IPF patients (40% and 40% in BAL, 33% and 36% in saliva) and controls (0% and 0% in both BAL and saliva). Conclusion: Increased acid and weakly acidic GER as well as more reflux reaching the proximal esophagus are prevalent in IPF. Patients with IPF have a relevant risk of gastric aspiration (increased bile acids and pepsin in saliva) or definite gastric aspiration (bile acids or pepsin in BAL). Outcome studies with intense anti-reflux therapy are needed to confirm the deleterious role of reflux in IPF progression.
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