Plasma α-Glutathione S-Transferase in Patients with Chronic Mesenteric Ischemia and Median Arcuate Ligament Syndrome.

Background: Chronic mesenteric ischemia (CMI) due to either atherosclerosis of the mesenteric arteries or median arcuate ligament syndrome (MALS) is an underdiagnosed entity. The etiology of MALS and its existence have been debated and questioned. We aimed to identify plasma biomarkers indicating mesenteric ischemia in patients with CMI and MALS. Methods: Plasma α-glutathione S-transferase (α-GST), intestinal fatty acid-binding protein (I-FABP), citrulline, and ischemia modified albumin (IMA) were analyzed in fifty-eight patients with CMI (Group A, n=44) and MALS (Group B, n=14) before and after revascularization. The plasma levels of these potential biomarkers were compared with those of healthy individuals (Group C, n=16). Group comparison was performed with the Mann-Whitney U-test. Cross-tabulation and its derivatives were obtained. Receiver operating characteristic (ROC) curves and area under the curve (AUC) were calculated. Results: Plasma levels of α-GST were significantly raised in the patients with CMI (7.8 ng/mL, p<0.001) and MALS (8.4 ng/mL, p<0.001), as compared with the control Group C (3.3 ng/mL). The threshold for normal median plasma α-GST levels of 4 ng/mL yielded a sensitivity of 93% and 86%, specificity of 86% and 88%, respectively, for the diagnosis of CMI due to atherosclerosis and MALS. AUC of ROC curves was 0.96 (p<0.0001) for CMI and 0.85 (p<0.002) for MALS. The patient groups did not differ from the healthy controls in any other biomarkers. Conclusion: Plasma α-GST levels are elevated in CMI and MALS patients. Elevated plasma levels of α-GST suggest ischemia as the etiology of MALS.

Early Identification of Chronic Mesenteric Ischemia with Endoscopic Duplex Ultrasound.

Introduction: Due to diagnostic delay, chronic mesenteric ischemia (CMI) is underdiagnosed. We assumed that the patients suspected of CMI of the atherosclerotic origin or median arcuate ligament syndrome (MALS) could be identified earlier with endoscopic duplex ultrasound (E-DUS). Patients and Methods: Fifty CMI patients with CTA-verified stenosis of either ≥50% and ≥70% of celiac artery (CA) and superior mesenteric artery (SMA) were examined with E-DUS and transabdominal duplex ultrasound (TA-DUS). Peak systolic velocities (PSV) of ≥200cm/s and ≥275cm/s for CA and SMA, respectively, were compared with CTA. Subgroup analysis was performed for the patients with (n=21) and without (n=29) prior revascularization treatment of CMI. The diagnostic ability of E-DUS and TA-DUS was tested with crosstabulation analysis. Receiver operating characteristics (ROC) curve analysis was performed, and the area under the curve (AUC) was calculated to investigate the test accuracy. Results: In the patients with ≥70% stenosis, E-DUS had higher sensitivity than TA-DUS (91% vs 81% for CA and 100% vs 92% for SMA). AUC for SMA ≥70% in E-DUS was 0.75 and with TA-DUS 0.68. The sensitivity of E-DUS for CTA-verified stenosis ≥70% for CA was 100% in the patients without prior treatment. E-DUS demonstrated higher sensitivity than TA-DUS for both arteries with stenosis ≥50% and ≥70% in the treatment-naive patients. Conclusion: E-DUS is equally valid as TA-DUS for the investigation of CMI patients and should be used as an initial diagnostic tool for patients suspected of CMI.

[A 68-year-old woman with iron deficiency anemia]. / En 68 år gammel kvinne med blødningsanemi.

A 68-year-old woman with iron deficiency anemia (due to gastrointestinal bleeding) was evaluated. Over a period of two years she received iron supplementation perorally and intravenously, as well as multiple blood transfusions, but the hemoglobin level did not exceed 10 g/dL. The investigations included upper endoscopy, duodenoscopy with side optical view, ileocolonoscopy, capsule endoscopy, antegrad single-balloon enteroscopy and conventional angiography of the abdominal vessels. Upper and lower endoscopies were performed repeatedly. The only consistent finding was linear erosions of the gastric mucosa in a large hiatal hernia at the level of the diaphragm. The association between large hiatal hernias and iron deficiency anemia was first described in the 1930s. The bleeding source is thought to be erosions or ulcerations in the hiatal hernia, as described by Cameron & Higgins in 1986. These lesions are analogous to the finding in our patient. The recognized treatment options are iron supplementation, proton pump inhibition and fundoplication. In our case we decided to start treatment with pantoprazole. Her hemoglobin level had normalized within an observational period of three months.