BACKGROUND AND OBJECTIVES:The expression of soluble adhesion molecules inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), besides activation of endothelial cells and transendothelial migration of leukocytes, play an important role in inflammation and progression of ischemic injury after acute stroke. The aim of this study was to determine serum levels of soluble ICAM-1 and VCAM-1 in patients with acute ischemic stroke and controls and correlate them according to etiological subtypes (thromboembolic or lacunar stroke), stroke severity and disability after acute stroke.PATIENTS AND METHODS:Hospital-based prospective study of acute stroke patients hospitalized between December 2008 and September 2009 at the University Hospital Sestre Milosrdnice in Zagreb, Croatia.METHODS:We enrolled 110 patients with acute ischemic stroke and 93 healthy individuals as controls. Serum concentrations of VCAM-1 and ICAM-1 were determined by means of quantitative sandwich enzyme immunoassay. Patients were classified according to etiological subtype, clinical severity of stroke and disability after stroke.RESULTS:There was no significant difference between levels of soluble adhesion molecules VCAM-1 and ICAM-1 in patients and in controls. Levels of VCAM-1 were significantly higher in patients with thromboembolic stroke than in controls. There was no significant correlation between levels of soluble adhesion molecules VCAM-1 and ICAM-1 and stroke severity and disability. There was marked biological interindividual variability in all patient groups.CONCLUSION:This study confirms the role of adhesion molecule VCAM-1 in the pathogenesis of acute thromboembolic stroke.

The aim of the study was to determine serum levels of selected matrix metalloproteinases (MMPs) and their natural inhibitors (TIMPs) in the acute phase of different stroke types subdivided according to the Oxfordshire Community Stroke Project (OCSP) classification and the possibility of discriminating stroke types according to their levels. The study included 126 patients with acute stroke within the first 24 h of symptom onset, and 124 healthy volunteers. The stroke group had lower MMP-2 concentrations and MMP-2/TIMP-2 ratios (p<0.001) but higher TIMP-2 (p<0.001) than controls. The level of MMP-9 and the MMP-9/TIMP-1 ratio were higher in patients with total anterior circulation infarct (TACI) than in patients with other stroke subtypes according to OCSP classification (p=0.0019, p=0.0065, respectively) or in controls (p<0.0001, p=0.0024, respectively). A negative correlation of MMP-2 levels with MMP-9 and MMP-9/TIMP-1 ratio was recorded in all stroke subtypes except for TACI. Receiver operating characteristic analysis showed similar discriminating power for MMP-9 levels and Barthel index in the differential diagnosis of TACI. High MMP-9/TIMP-1 ratio (odds ratio 3.263) was associated with TACI. Our results demonstrate that the MMP-9/TIMP-1 ratio may provide information to help in assessing stroke patients in the future as a baseline biomarker of infarct extent.

BIB treatment in our setting showed the best results for individuals with BMI from 35 to 40 kg/m(2). Our preliminary results showed that BIB is safe, well tolerated with minor side effects, and alters quality of life for the better. The complication rate was negligible, due to the detailed pretreatment examinations and follow-up.

The importance of ghrelin and leptin in treatment-induced changes was reaffirmed. Ghrelin hyper-response in non-morbidly obese subjects characterized greater short-term treatment efficiency and landmarked an inclination to weight regain. The results suggest a potential pattern of individualization between obese patients according to body mass index towards intragastric balloon or bariatric surgery. Further studies are needed in order to get better insights in the pathophysiologic mechanisms of obesity.

BACKGROUNDPrevious studies suggest that infarct expansion may be responsible for increased mortality after stroke onset in patients with prolonged stress hyperglycemia. Therefore, we evaluated the influence of prolonged stress hyperglycemia on stroke mortality in patients with and without diabetes.PATIENTS AND METHODSFor 630 stroke patients admitted to the neurological intensive care department within 24 hours of stroke onset, we correlated mean blood glucose levels (MBGL) at admission and 72 hours after admission in diabetic and non-diabetic patients with final outcome. Blood glucose levels higher then 6.1 mmol/L (121 mg/dL) were treated as hyperglycemia.RESULTSOf 630 patients (mean age 71 ± 6), 410 were non-diabetic (mortality, 25%) and 220 patients were diabetic (mortality, 20%). All patients who died within 28 days of hospitalization had prolonged hyperglycemia (at admission and after 72 hours, despite insulin therapy). The unadjusted relative risk of in-hospital mortality within 28 days for all stroke patients was 0.68 (95% CI, 0.14–1.9) for non-diabetic patients and 0.39 (95% CI, 0.27–1.56) for diabetic patients. The unadjusted relative risk of in-hospital mortality within 28 days in ischemic stroke in patients with MBGL > 6.1–8.0 mmol/L (121–144 mg/dL) at admission and after 72 hours was 1.83 (95% CI, 0.41–5.5) for non-diabetic patients and 1.13 (95% CI, 0.78–4.5) for diabetic patients. Non-diabetic patients with hyperglycemia had a 1.7 times higher relative risk of in-hospital 28-day mortality than patients with diabetes.CONCLUSIONProlonged stress hyperglycemia in ischemic stroke patients increases the risk of in-hospital 28-day mortality, especially in non-diabetic patients.