Early diagnosis of acute mesenteric ischemia (AMI) remains a clinical challenge, and no biomarker has been consistently validated. We aimed to assess the accuracy of three promising circulating biomarkers for diagnosing AMI—citrulline, intestinal fatty acid-binding protein (I-FABP), and d-lactate. A cross-sectional diagnostic study enrolled AMI patients admitted to the intestinal stroke center and controls with acute abdominal pain of another origin. We included 129 patients—50 AMI and 79 controls. Plasma citrulline concentrations were significantly lower in AMI patients compared to the controls [15.3 μmol/L (12.0–26.0) vs. 23.3 μmol/L (18.3–29.8), p = 0.001]. However, the area under the receiver operating curves (AUROC) for the diagnosis of AMI by Citrulline was low: 0.68 (95% confidence interval = 0.58–0.78). No statistical difference was found in plasma I-FABP and plasma d-lactate concentrations between the AMI and control groups, with an AUROC of 0.44, and 0.40, respectively. In this large cross-sectional study, citrulline, I-FABP, and d-lactate failed to differentiate patients with AMI from patients with acute abdominal pain of another origin. Further research should focus on the discovery of new biomarkers.
Background
Data about reperfusion injury (RI) following acute arterial mesenteric ischemia (AAMI) in humans are scarce. We aimed to assess the prevalence and risk factors of RI following endovascular revascularization of AMI and evaluate its impact on patient outcomes.
Methods
Patients with AAMI who underwent endovascular revascularization (2016–2021) were included in this retrospective cohort. CT performed < 7 days after treatment was reviewed to identify features of RI (bowel wall hypoattenuation, mucosal hyperenhancement). Clinical, laboratory, imaging, and treatments were compared between RI and non-RI patients to identify factors associated with RI. Resection rate and survival were also compared.
Results
Fifty patients (23 men, median 72-yrs [IQR 60–77]) were included, and 22 were diagnosed with RI (44%) after a median 28 h (22–48). Bowel wall hypoattenuation and mucosal hyperenhancement were found in 95% and 91% of patients with post-interventional RI, respectively. Patients with RI had a greater increase of CRP levels after endovascular treatment (p = 0.01). On multivariate analysis, a decreased bowel wall enhancement on baseline CT (HR = 8.2), an embolic cause (HR = 7.4), complete SMA occlusion (HR = 7.0), and higher serum lactate levels (HR = 1.4) were associated with RI. The three-month survival rate was 78%, with no difference between subgroups (p = 0.99). However, the resection rate was higher in patients with RI (32% versus 7%; p = 0.03).
Conclusion
RI is frequent after endovascular revascularization of AAMI, especially in patients who present with decreased bowel wall enhancement on pre-treatment CT, an embolic cause, and a complete occlusion of the SMA. However, its occurrence does not seem to negatively impact short-term survival.
Introduction
Multiple chronic ulcers of small intestine are mainly ascribed to Crohn’s disease. Among possible differential diagnoses are chronic ulcers of small bowel caused by abnormal activation of the prostaglandin pathway either in the archetypal but uncommon non-steroidal anti-inflammatory drug (NSAID)-induced enteropathy, or in rare monogenic disorders due to PLA2G4A and SLCO2A1 mutations. SLCO2A1 variants are responsible for CEAS (Chronic enteropathy associated with SLCO2A1), a syndrome which was exclusively reported in patients of Asian origin. Herein, we report the case of two French female siblings with CEAS.
Case report
P1 underwent iterative bowel resections (removing 1 meter of small bowel in total) for recurrent strictures and perforations. Her sister P2 had a tight duodenal stricture which required partial duodenectomy. Next-generation sequencing was performed on P1’s DNA and identified 2 compound heterozygous variants in exon 12 in SLCO2A1, which were also present in P2.
Conclusion
CEAS can be detected within the European population and raise the question of its incidence and recognition outside Asia. Presence of intractable recurrent ulcerations of the small intestine mimicking Crohn’s disease with concentric stricture should motivate a genetic search for SLCO2A1 mutations, particularly in the context of family history or consanguinity.
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