The increasing use of the D-dimer assay in clinical practice could be extended to patients presenting with acute cerebrovascular ischemic events to help predict stroke subtype.
PCT may be a useful marker to predict which patients subsequently have early VAP. The CPIS could help as an early way to detect the patients with early VAP and who need further diagnostic testing.
While additional powered studies are needed, the present results suggest that the prevalence of undiagnosed CD in the mothers of SGA infants is higher than in the general female population.
Recent evidence indicates a possible role of D-dimer in the early diagnosis of ischemic stroke subtypes. Whether D-dimer can also predict the long-term outcome following ischemic stroke is controversial. To define the prognostic role of D-dimer, patients hospitalized after an acute ischemic cerebrovascular event underwent D-dimer measurement (Liatest D-D; normal level < 0.50 microg/ml) on admission and were followed up for recurrent cerebrovascular events, occurrence of other cardiovascular events, and mortality. We enrolled 96 patients (mean age 74.9 years, 42 men). Mean follow-up was 61.5 months; 47 (48.5%) patients died, 23 (48.9%) because of a vascular event. There was no difference in mean D-dimer levels between dead patients and survivors (1.68 and 1.63 microg/ml, P = NS), but the mortality risk was higher with D-dimer of at least 0.50 microg/ml (odds ratio, 5.32; 95% confidence interval, 1.79-15.84). After adjustment for age and stroke subtype, the odds ratio was not significant. Mean D-dimer was similar between patients with and without a new vascular event (1.43 and 1.68 microg/ml, P = NS), and D-dimer of at least 0.50 microg/ml was not predictive of an increased risk of subsequent events. D-dimer levels measured in the acute phase after an acute cerebrovascular event probably do not predict the long-term clinical outcome.
Context The usefulness of stool calprotectin determination in diagnosis of inflammatory disease of the colon has been reported; information about its usefulness for patients with polyposis are scarce, however. Objective To evaluate the significance of stool calprotectin concentrations for patients affected by colonic polyposis. Patients Sixty-three consecutive patients (35 males, 28 females, mean age 60.3 years, range 39-78 years) were enrolled: 26 patients (41.3%) with polyps, 17 patients (27.0%) with asymptomatic diverticular disease, and 20 subjects (31.7%) with normal endoscopic appearance of the colon. Results Stool calprotectin concentrations were 17.4 ± 24.5 lg g -1 for patients with colonic polyposis, significantly higher than concentrations for patients with diverticulosis (7.1 ± 5.7 lg g -1 ; P = 0.026) or for patients with normal appearance of the colon (calprotectin 6.0 ± 5.8 lg g -1 ; P = 0.003). For patients with a single polyp, stool calprotectin concentrations were similar to those for patients with multiple polyps. Calprotectin fecal concentrations for patients with sessile polyps and those with flat polyps were not significantly different. Calprotectin concentrations were not significantly related to the size of the polyps. Conclusion Our data show that colonic polyposis may cause an increase in stool calprotectin values and that these colonic lesions should be suspected when elevated stool calprotectin concentrations are found.
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