Background Bile acid malabsorption is common in microscopic colitis, irritable bowel syndrome with diarrhea, and inflammatory bowel disease. We investigated the diagnostic accuracy of 7-alfa-hydroxy-4-cholesten-3-one and compared it with fibroblast growth factor-19 as biomarkers for bile acid malabsorption. Methods We enrolled consecutively 109 chronic diarrhea patients with standard laboratory tests, fecal calprotectin, and endoscopy separated into six groups: n = 30 with active inflammatory bowel disease, n = 21 with inflammatory bowel disease in remission reporting >3 bowel movements per day, n = 21 with inflammatory bowel disease after surgery, n = 23 with irritable bowel syndrome with diarrhea, n = 14 with microscopic colitis and 11 healthy subjects (controls). We defined bile acid malabsorption as >3 bowel movements and lower fibroblast growth factor-19 (<60 pg/ml). Results Median levels of 7-alfa-hydroxy-4-cholesten-3-one in inflammatory bowel disease active were 53.1 ng/ml, inflammatory bowel disease remission were 52.2 ng/ml, inflammatory bowel disease after surgery were 85.7 ng/ml, irritable bowel syndrome with diarrhea were 7.5 ng/ml, microscopic colitis were 69.3 ng/ml, and healthy controls were 3.7 ng/ml. We estimate a 7-alfa-hydroxy-4-cholesten-3-one cutoff of 48.9 ng/ml with 82.6% sensitivity and 84.3% specificity for detecting bile acid malabsorption. Both 7-alfa-hydroxy-4-cholesten-3-one >48.9 ng/ml and fibroblast growth factor-19 (<60 pg/ml) were found in 52% of the patients, compared with those 8% of patients below this 7-alfa-hydroxy-4-cholesten-3-one cutoff (P < 0.001). Serum 7-alfa-hydroxy-4-cholesten-3-one correlated with the number of bowel movements/day (r = −0.709; P < 0.001) and correlated inversely with fibroblast growth factor-19 (r = −0.741; P < 0.001). Conclusions Serum 7-alfa-hydroxy-4-cholesten-3-one above 48.9 ng/ml and fibroblast growth factor-19 below 60 pg/ml identify patients with diarrhea likely attributable to bile acid malabsorption with high diagnostic accuracy and they can be used as screening biomarkers for bile acid malabsorption in microscopic colitis and inflammatory bowel disease.

Background Oxidative stress and inflammation have been implicated in the pathogenesis of diastolic dysfunction (DD) and are both present in chronic obstructive pulmonary disease (COPD). Purpose To evaluate the role of oxidative stress markers (8-isoprostane) and inflammation (prostaglandin E2, resistin) in the pathogenesis of stress induced left ventricular diastolic dysfunction (LVDD) in non-severe COPD. Materials and methods 104 patients with non-severe COPD (FEV1 &gt; 50%) and preserved left ventricular ejection fraction &gt;50% underwent incremental cardio-pulmonary exercise testing (CPET). Echocardiography was performed before CPET and 1-2 minutes after peak exercise. Peak E/e’ ratio &gt;15 was a marker for stress LVDD. Urine concentration of 8-isoprostanes was assumed as surrogate marker for oxidative stress; urine concentration of prostaglandine-E2 and plasma resistin levels as inflammatory markers. Mass spectrometry was applied for 8-isoprostane and prostglandine E2 (Cayman. Chemical) measurement. Values were normalised to urine creatinine (µmol/l/cre). ELISA was applied for resistin measurement (Raybio_Human) (ng/ml). Results Patients were divided into two groups: subjects with stress LVDD (67) and subjects without stress LVDD (37). 8-isoprostane levels were higher in subjects with LVDD vs those without LVDD (32.9 vs 29.67µmol/l/cre; p&lt; 0.05). The same is observed regarding resistin plasma levels (22.51 vs 15.68ng/ml). Urine concentrations of prostaglandin E2 did not differ between the two groups (50.76 vs 51.07 µmol/l/cre) Conclusions In non-severe COPD patients the levels of oxidative stress (8-isoprostanes) and inflammation (resistin) seem to be associated with stress induced left ventricular diastolic dysfunction.

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Background Oxidative stress and inflammation have been implicated in the pathogenesis of diastolic dysfunction (DD) and are both present in chronic obstructive pulmonary disease (COPD). Aim To evaluate the role of oxidative stress markers (8-isoprostane) and inflammation (prostaglandin E2, resistin) in the pathogenesis of stress induced right ventricular diastolic dysfunction (RVDD) in non-severe COPD. Materials and methods 104 patients with non-severe COPD (FEV1 &gt; 50%) and preserved left ventricular ejection fraction &gt;50% underwent incremental cardio-pulmonary exercise testing (CPET). Echocardiography was performed before CPET and 1-2 minutes after peak exercise. Peak E/e’ ratio &gt; 6 was a marker for stress induced RVDD. Urine concentration of 8-isoprostanes was assumed as surrogate marker for oxidative stress; urine concentration of prostaglandine-E2 and plasma resistin levels as inflammatory markers. Mass spectrometry was applied for 8-isoprostane and prostglandine E2 (Cayman. Chemical) measurement. Values were normalised to urine creatinine (µmol/l/cre). ELISA was applied for resistin measurement (Raybio_Human) (ng/ml). Results Patients were divided into two groups: subjects with stress RVDD (82) and those without stress RVDD (22). In patients with and without RVDD the levels of 8-isoprostane were similar (30.78 vs 30.41µmol/l/cre). The urine concentration of prostaglandin E2 in patients with and without RVDD significantly differed (49.73 vs 62. 19µmol/l/cre; p &lt; 0.05). The same is observed regarding resistin plasma levels - in patients with and without RVDD (18.91 vs 5.47ng/ml). Conclusions In non-severe COPD patients oxidative stress levels are similar in the studied groups. Inflammation (resistin) seems to be the predominant pathogenetic factor, associated with stress induced RVDD. The exact role of prostaglandine E2 for RVDD remains elusive.