No abstract

Experimental studies suggest that the intestinal barrier is affected in ischemic stroke. D-Lactate and intestinal fatty acid-binding protein (IFABP) are markers of intestinal mucosa integrity and barrier function. Our purpose was to evaluate the serum concentrations of these markers in patients with acute ischemic stroke (AIS). We included patients with AIS and used healthy subjects as controls. Clinical, demographic and outcome measures were recorded. Blood was drawn within 24 h of symptom onset. Serum concentrations of D-Lactate and IFABP were determined using commercially available colorimetric and ELISA kits, respectively. We included a total of 61 patients (median age of 64 years). The majority of patients were male (57.4%). The most common cause of stroke was atherosclerosis (34.4%), followed by small-vessel disease and cardioembolic (32.7% each). Mean admission NIHSS score was 8. Median IFABP and D-Lactate concentrations were significantly higher in patients than in controls. Concentrations were not associated with stroke severity or 3-month outcome. Patients with large-artery atherosclerosis and cardioembolic etiology had higher D-Lactate values than patients with small-vessel disease. D-Lactate and IFABP were significantly elevated in patients with AIS. This suggests that there is disruption of the intestinal barrier in patients with AIS.

No abstract

Dear Editor, Reperfusion therapy using tissue plasminogen activator (tPA) improves the clinical outcome in stroke; however, it should be applied during the first 4.5 h. Only less than 30% of patients arrive at the hospital on time mainly due to a prehospital delay. 1,2 Prehospital delay is analyzed as onset-to-door time, which is divided into onset-to-alarm time (OAT), that corresponds to the time since the patient or the witness identified stroke symptoms until the decision to look for medical attention, and transfer time (Figure 1). More than 50% of the delay corresponds to OAT. 3 Factors associated to OAT vary in every population. We conducted a study to describe the OAT in our population and factors that contribute to a delay in hospital arrival. A retrospective, observational study was performed at the Department of Neurology of the University Hospital UANL in Monterrey, Mexico. Clinical and demographical data were obtained from a Stroke Clinical Registry (iReNe). 4 All patients diagnosed

Introduction: Ischemic stroke is associated with gastrointestinal complications such as constipation, dysphagia and fecal incontinence. However, the precise mechanisms involved have not been fully elucidated. D-Lactate and Intestinal Fatty-Acid Binding Protein (IFABP) are markers of intestinal mucosa integrity and barrier function. We evaluated serum concentrations of these markers in patients with acute ischemic stroke. Materials and methods: We included consecutive patients with ischemic stroke, and used healthy, age and sex-matched subjects as controls. We excluded cases determined to be of other or undetermined etiology according to the TOAST classification. Blood was drawn within 24 hours of symptom onset. Serum concentrations of D-Lactate and IFABP were determined using commercially available colorimetric and ELISA kits, respectively. Results: We included a total of 61 patients and 20 controls. The majority of patients were male (57.4%), and had a median age of 64 years. The most common cause of stroke was large-vessel atherosclerosis (34.4%), followed by small-vessel occlusion and cardioembolism (32.7% each). Mean admission NIHSS score was 8. IFABP and D-Lactate concentrations were significantly higher in patients than in controls (0.57±1 ng/ml vs. 1.84±2.7 ng/ml, p=0.04 and 0 nmol/μl vs. 0.38±0.66 nmol/μl, p=0.01, respectively). Concentrations were not associated with stroke severity or outcome. Patients with large-artery atherosclerosis and cardiombolic etiology had significantly higher D-Lactate values than patients with small-vessel disease. Conclusions: D-Lactate and IFABP were significantly elevated in patients with ischemic stroke. This provides, to our knowledge, for the first time in humans, evidence of intestinal barrier disruption. A stroke-associated systemic stress response could be responsible, but the lack of an association with stroke severity does not support this hypothesis. Embolic or atherosclerotic involvement of the mesenteric vasculature is another possibility. Further studies should aim at looking for a plausible mechanism as well as a possible association between intestinal barrier dysfunction and post-stroke gastrointestinal and infectious complications.