Background and Purpose-Because there is no biologic marker offering precise information about stroke etiology, many patients receive a diagnosis of undetermined stroke even after all available diagnostic tests are done, precluding correct treatment. Methods-To examine the diagnostic value of a panel of biochemical markers to differentiate stroke etiologies, consecutive acute stroke patients were prospectively evaluated. Brain computed tomography, ultrasonography, cardiac evaluations, and other tests were done to identify an etiologic diagnosis according to TOAST classification. Blood samples were drawn on Emergency Department arrival (Ͻ24 hours) to test selected biomarkers: C-reactive protein, D-dimer, soluble receptor for advanced glycation end products, matrix metalloproteinase-9, S-100b, brain natriuretic peptide (BNP), neurotrophin-3, caspase-3, chimerin, and secretagogin (assayed by ELISA). 6.7, PϽ0.001). A model combining clinical and biochemical data had a sensitivity of 66.5% and a specificity of 91.3% for predicting cardioembolism. Conclusions-Using a combination of biomarkers may be a feasible strategy to improve the diagnosis of cardioembolic stroke in the acute phase, thus rapidly guiding other diagnostic tests and accelerating the start of optimal secondary prevention. Results-Of

Background: At the present time, the determination of the outcome of stroke patients is based on the analysis of clinical and neuroimaging data. The use of prognostic blood biomarkers could aid in decision-making processes, e.g. admitting patients to specialized stroke units. Although the prognostic role of natriuretic peptides has been studied in heart failure and coronary diseases, the value of brain natriuretic peptide (BNP) is less known within the field of strokes. Objective: We aimed to study the relationship between plasma levels of BNP and acute neurological worsening or mortality after stroke in a large cohort of patients (investigating both ischemic and hemorrhagic disease). Methods: Consecutive stroke patients (ischemic and hemorrhagic) admitted to the Stroke Unit of our University Hospital within 24 h of the onset of symptoms were included. Stroke severity was assessed according to the National Institutes of Health Stroke Scale (NIHSS) at admission and at discharge. Neurological worsening was defined as an increase of 4 or more points in the NIHSS score or death during the patient’s stay at the Stroke Unit. Blood samples were drawn upon admission to measure plasma levels of BNP (Biosite Inc., San Diego, Calif., USA). Statistical analysis was performed using SPSS 15.0 and R software. Results: Altogether, 896 patients were included in the study. BNP plasma levels were higher among patients who deteriorated the most over time (n = 112; 90.5 vs. 61.2 ng/l; p = 0.006) or died (n = 83; 118.2 vs. 60.9 ng/l; p < 0.001). Multivariate logistic regression analysis indicated that plasma BNP level was an independent predictor of neurological worsening [BNP >56.7 ng/l; odds ratio (OR) = 1.64; p = 0.04] and death after stroke (BNP >65.3 ng/l; OR = 1.97; p = 0.034). Adding BNP level to other well-known clinical predictors of bad outcome did not significantly increase the predictive value. Conclusions: Plasma levels of BNP measured during the acute phase of stroke are associated both with early neurological worsening and mortality. However, this biological information does not supply prognostic information which would add to clinical variables, which limits its use as a biomarker. Further investigation and systematic reviews are needed to clarify the role of natriuretic peptides in stroke outcome.

Studies on head injury-induced pituitary dysfunction are limited in number and conflicting results have been reported. To further clarify this issue, 29 consecutive patients (24 males), with severe (n = 21) or moderate (n = 8) head trauma, having a mean age of 37 ± 17 years were investigated in the immediate post-trauma period. All patients required mechanical ventilatory support for 8-55 days and were enrolled in the study within a few days before ICU discharge. Basal hormonal assessment included measurement of cortisol, corticotropin, free thyroxine (fT4), thyrotropin (TSH), testosterone (T) in men, estradiol (E2) in women, prolactin (PRL), and growth hormone (GH). Cortisol and GH levels were measured also after stimulation with 100 µg human corticotropin releasing hormone (hCRH) and 100 µg growth hormone releasing hormone (GHRH), respectively. Cortisol hyporesponsiveness was considered when peak cortisol concentration was less than 20 µg/dl following hCRH. TSH deficiency was diagnosed when a subnormal serum fT4 level was associated with a normal or low TSH. Hypogonadism was considered when T (males) or E2 (women) were below the local reference ranges, in the presence of normal PRL levels. Severe or partial GH deficiencies were defined as a peak GH below 3 µg/l or between 3 and 5 µg/l, respectively, after stimulation with GHRH. Twenty-one subnormal responses were found in 15 of the 29 patients (52%) tested; seven (24%) had hypogonadism, seven (24%) had cortisol hyporesponsiveness, five (17%) had hypothyroidism, and two patients (7%) had partial GH deficiency. These preliminary results suggest that a certain degree of hypopituitarism occurs in more than 50% of patients with moderate or severe head injury in the immediate post-trauma period, with cortisol hyporesponsiveness and hypogonadism being most common. Further studies are required to elucidate the pathogenesis of these abnormalities and to investigate whether they affect long-term morbidity. P2 Cortisol reserve in head trauma victims: evaluation with the low-dose (1 µ µg) corticotropin (ACTH) stimulation test

No abstract