Early inflammatory response in ischemic stroke.
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Biomedical subjects
Publications and source records attributed to M Di Napoli.
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BACKGROUND AND PURPOSE: The prognostic influences of fibrinogen and C-reactive protein (CRP) levels and their relations in ischemic stroke have not been well described. The aim of this study was to investigate and compare the 1-year prognostic influences of fibrinogen and CRP levels on outcome in ischemic stroke. METHODS: Fibrinogen and CRP were determined within 24 hours after stroke and related to 1-year outcome in 128 patients with first-ever ischemic stroke. The Kaplan-Meier technique was applied in survival analysis. Multiple logistic regression analysis was used to evaluate the associations between risk factors and outcome. RESULTS: The probabilities of death or new vascular event were 21.1%, 27.9%, and 51.7% (P:=0.0172, chi(2) for trend), respectively, in patients stratified by tertiles of fibrinogen (<3.78, 3.78 to 6.17, and >6.17 g/L). The probabilities of a primary end point were 12.1%, 29.7%, and 54.8% (P:=0.0004), respectively, after stratification of patient data by tertiles of CRP level (<5, 5 to 33, and >33 mg/L). In multiple logistic regression analysis, higher CRP levels (odds ratio, 2.39; 95% CI, 1.28 to 4.49; P:=0.0066) and stroke severity on the Canadian Neurological Stroke Scale (odds ratio, 2.37; 95% CI, 1.01 to 5.58; P:=0.0472) were independently associated with death or new vascular event. CONCLUSIONS: Increased levels of CRP are associated with a worse outcome in patients with ischemic stroke. The increased risk associated with elevated CRP levels is independent of the prognostic influence of fibrinogen.
BACKGROUND AND PURPOSE: There is growing evidence of the prognostic importance of C-reactive protein (CRP) in ischemic stroke. However, the independent value of CRP at different stages after stroke has not been established. Therefore, we assessed the prognostic values of CRP in ischemic stroke. We also compared the relation of CRP at admission and discharge with 1-year outcome. METHODS: One hundred ninety-three patients were included in a derivation set (n=128) and a validation set (n=65). Serum CRP was measured, within 24 hours after index ischemic stroke, within 48 to 72 hours, and at hospital discharge. We examined the association between the level of CRP at different stages after stroke and outcome. We adjusted for the possible confounding effect using a multivariate Cox proportional hazard model. RESULTS: A cutoff point of 1.5 mg/dL for CRP at discharge provided optimum sensitivity and specificity for adverse outcome, based on the receiver operator curves. CRP at admission (hazard ratio [HR] 2.78, 95% CI 1.45 to 5.33; P=0.0021) and discharge (HR 9.42, 95% CI 4.27 to 19.05; P<0.0001) were predictors of the combined end point of new vascular events or death at 1 year. CRP at hospital discharge was the strongest independent marker of adverse outcome (HR 7.42, 95% CI 2.75 to 20.03; P=0.0001). These results were confirmed in the validation set (HR 15.66, 95% CI 3.36 to 72.97; P=0.0005). CONCLUSIONS: CRP is a marker of increased 1-year risk in ischemic stroke. CRP at discharge is better related to later outcome and could be of greater utility for risk stratification. These findings are consistent with the hypothesis that elevated CRP may predict future cardiovascular events or death.
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Alterations of intracranial vessel tone have been implicated in the pathophysiology of migraine. The cerebrovascular reactivity was measured by means of transcranial Doppler in 60 migraine patients with (n = 30) or without aura (n = 30) during the headache-free interval and in 30 healthy controls. The vasomotor response was evaluated during hypercapnia induced by inhalation of a mixture of CO2 5% and O2 95% and during hypocapnia obtained after voluntary hyperventilation. To improve the power of the study in detecting possible abnormalities of cerebrovascular reactivity, two different measures were performed at 1 week intervals in migraine patients and controls. Reactivity index values during CO2 inhalation were significantly different (p = 0.01) among the three groups during the first and second measurements; in particular, lower values were found in patients suffering from migraine without aura with respect to controls (p < 0.05, Scheffé's test). Values of reactivity index obtained following induction of hypocapnia did not differ between migraine patients and controls (all p values > 0.05). Our data suggest a reduced vasodilatory response to hypercapnia of cerebral arterioles in patients suffering from migraine without aura with respect to controls that might be related to baseline arteriolar vasodilation.
BACKGROUND AND PURPOSE: Changes in stroke incidence are likely to occur as a consequence of aging of the population, but evidence for this hypothesis is lacking. METHODS: A prospective community-based registry of first-ever strokes (1994 to 1998) classified according to the International Classification of Diseases, 9th Revision (ICD-9) was established in the L'Aquila district, central Italy, with a total population of 297,838 (1991 census). Patients were identified by active monitoring of multiple sources, including general practitioners. RESULTS: In 1994, 819 patients (398 men and 421 women; mean +/- SD age, 74.8 +/- 11.3 years) suffered from a first-ever stroke. Eighty-nine percent of the patients had neuroimaging studies of the brain and were reclassified with the recent Application of the International Classification of Diseases to Neurology (ICD-10 NA). The occurrence of subarachnoid hemorrhage, intracerebral hemorrhage, cerebral infarction, and ill-defined events was 2.9%, 14.9%, 80.2%, and 2.0%, respectively. Crude annual incidence of first-ever stroke was 2.75/1000 (95% confidence interval [CI], 2.57 to 2.94) and 24.23/1000 (95% CI, 21.65 to 27.10) in patients older than 80 years. Incidence rates were higher in men and steeply increased with age. The standardized rate was 2.37/1000 for the Italian and 2.28/1000 for the European population. The 30-day case-fatality rate was 25.6% (95% CI, 22.8% to 28.7%). The occurrence of death, disability, and full recovery at 1 year was 36.9%, 38.9%, and 24.2%, respectively. No differences were found in stroke incidence and case-fatality according to income and urban or rural residences. CONCLUSIONS: In our population-based study, we found a high stroke incidence notably in the older age subgroups, suggesting that rather than declining, stroke is only being postponed until later in life.
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The paper reports a case of acute hepatitis C (HCV) in a patient who was a chronic carrier of hepatitis B virus (HBV) during the course of which the authors observed a transient HBsAg clearance. The 53-year-old patient was a carrier of chronic HBV infection in an integrated minus variant phase. The patient presented an abrupt increment in aminotransferase (ALT) which was not compatible with the typical "a poussée" progress of atypical chronic HBV hepatitis in that it was associated with HbsAg clearance in the absence of signs of superinfection by delta hepatitis virus (HDV), with subsequent repositivisation of HBsAg and contemporary anti-HCV seroconversion (RIBA positive for C-22, C-33, C-100, 5-1-1) on clinical remission. Polymerase chain reaction (PCR) was negative on remission for both HBV DNA and HCV. RNA became positive six months afterwards for HCV RNA alone; moreover HBsAg, anti-HCV, RIBA C-22, C-33, C-100, 5-1-1 were constantly positive, thus further confirming the inhibitory capacity of HCV towards HBV and not vice versa, as also shown by the chronic nature of infection and deterioration of clinical conditions. The authors conclude by underlining the need to assay for HCV RNA using a PCR method in alla cases of re-acutisation of chronic hepatitis due to both wild virus B and the domestic virus during the course of which HBsAg becomes negative, even transiently, in the absence of Delta superinfection.
In this paper the authors have evaluated the incidence and the clinical implications of sick euthyroid syndrome (SES) in a group of 144 patients in a department of internal medicine. SES is an alteration of thyroid hormone values in the absence of a thyroid disease, which is seen in patients suffering from serious diseases. Having classified SES into 3 subgroups according to the different alterations seen in the values of T3, T4, FT3, FT4, TSH, rT3 and TBG, they show the hypotheses that explain the biochemical mechanisms which are at the basis of these hormonal alterations. Fourteen of the 144 patients under observation were excluded as they were suffering from ascertained or subclinical thyroid disease. Thirty (23% of cases) of the remaining 130 patients had alterations of the thyroid hormones in accordance with SES diagnosis. Of these 30 patients, 19 had hormone values found in SES type I (63%), 2 in SES type II (6.5%) and 9 in SES type III (30.5%). In SES type I the diseases seen, in order of frequency, were: obstructive chronic bronchopneumopathy with acute respiratory failure, diabetic ketoacidosis, neoplasms, ischemic heart disease, cardiac failure, chronic renal failure, liver diseases, acute cerebral vasculopathies, sepsis and collagenopathies. The disease seen in the 2 cases of SES type II was obstructive chronic bronchopneumopathy with acute respiratory failure. In SES type III the diseases seen were, in order of frequency: diabetic ketoacidosis, lung diseases, ischemic heart disease, cardiac failure, peripheral arteriopathies, acute cerebral vasculopathies, neoplasms, liver diseases, acute renal failure. The incidence of SES in 23% of the admitted to hospital patients was found to be slightly higher than in other studies; this could be explained by a stricter selection of inpatients: in fact self-sufficient patients or those not needing urgent admission, were sent to an efficient out patient clinic where necessary examinations were quickly carried out, hospitalization being reserved for patients with more serious illnesses. We would like to underline how the incidence of SES is much greater than that of what is known as thyroid disease (23% compared to 5%), thereby confirming that it is the most frequent cause of alterations of thyroid hormones. With regard to the pathogenetical hypotheses, it is confirmed that in SES, the reduction of T3 values is accompanied by an increase in the values of rT3 as for reduced activity of 5-desiodinasis enzyme. In SES type III the increase of T4 values is due to the increase of TBG resulting in an increase in the link for T4 and therefore a reduced peripheral hormone activity.(ABSTRACT TRUNCATED AT 400 WORDS)
The type of small-vessel disease in small deep (lacunar) infarcts (SDIs) remains contentious as opposed to that in primary intracerebral haemorrhage (PICH), which is lipohyalinosis in most cases. Therefore, we compared risk factor profiles as indicators of underlying vessel pathology, between patients with SDI and patients with PICH, and those with a non-cardio-embolic infarct involving the cortex (CORTI). Multivariate regression analysis showed the diabetes mellitus [odds ratio (OR) 0.56; 95% confidence interval (CI) 0.34-0.90] and hypercholesterolaemia (OR 0.63; 95% CI 0.40-0.99) were more strongly associated with CORTI than with SDI. Carotid stenosis was associated with SDI in comparison with PICH (OR 7.5; 95% CI 1.02-54.94). Compared with PICH, CORTI was more strongly associated with diabetes mellitus (OR 3.27; 95% CI 1.38-7.76), carotid stenosis (OR 24.42; 95% CI 4.99-119.45), and hypercholesterolaemia (OR 3.12; 95% CI 1.47-6.65), whereas hypertension was associated with PICH (OR 0.37; 95% CI 0.18-0.79). These data support the hypothesis that small-vessel atheromatosis rather than small-vessel lipohyalinosis underlies lacunar infarcts in most cases.