Environment. Spain's prestige oil spill resurfaces.
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Biomedical subjects
Publications and source records attributed to Xavier Bosch.
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Little is known about the prognostic value of leukocyte count on admission for patients with chest pain. In total, 1,461 patients who presented to the emergency department with non-ST-segment elevation chest pain were studied by clinical history, electrocardiography, serial troponin I determination, and leukocyte count on admission. End points were 1-year mortality and major events (mortality or infarction). Overall patient distribution by quartiles of leukocyte count showed increased mortality (6%, 7%, 6%, and 17%, p = 0.0001) and major events (13%, 13%, 15%, and 24%, p = 0.0001) in the fourth quartile. After adjustment for other risk factors, the fourth quartile cut-off value (>10,000 cells/ml) predicted mortality (hazard ratio 2.0, 95% confidence interval 1.4 to 2.8, p = 0.0001) but not major events (p = 0.07). When analysis was performed to assess troponin status, in the subgroup with increased troponin (n = 634, 16% mortality), a leukocyte count >10,000 cells/ml was related to mortality (hazard ratio 2.2, 95% confidence interval 1.5 to 3.4, p = 0.0001). However, in the subgroup with normal troponin levels (n = 827, 4.2% mortality), there were no differences in mortality between patients with or without a leukocyte count >10,000 cells/ml (4.4% vs 4.2%, p = 0.8), with survival curves showing a tight overlap (p = 0.9). Further, in the subgroup with normal troponin levels, leukocyte count was not significantly different between patients with or without ST depression (7,969 +/- 2,171 vs 8,108 +/- 2,356 cells/ml, p = 0.6) and was not associated with mortality in patients with ST depression (p = 0.7). In conclusion, leukocyte count on admission is predictive of mortality in patients with chest pain and non-ST-segment elevation myocardial infarction. However, in the absence of myocardial necrosis, leukocyte count lacks prognostic value.
Much like other autoantibodies (eg, anti-double stranded DNA in systemic lupus erythematosus or antiglomerular basement membrane antibodies in Goodpasture's syndrome), antineutrophil cytoplasmic antibodies (ANCA) have provided doctors with a useful serological test to assist in diagnosis of small-vessel vasculitides, including Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome, and their localised forms (eg, pauci-immune necrotising and crescentic glomerulonephritis). 85-95% of patients with Wegener's granulomatosis, microscopic polyangiitis, and pauci-immune necrotising and crescentic glomerulonephritis have serum ANCA. ANCA directed to either proteinase 3 or myeloperoxidase are clinically relevant, yet the relevance of other ANCA remains unknown. Besides their diagnostic potential, ANCA might be valuable in disease monitoring. In addition, data seem to confirm the long-disputed pathogenic role of these antibodies. Present treatments for ANCA-associated vasculitis are not free from side-effects and as many as 50% of patients relapse within 5 years. Accurate understanding of the key pathogenic points of ANCA-associated vasculitis can undoubtedly provide a more rational therapeutic approach.
Apoptosis is a mechanism of cell death implicated in the pathogenesis of alcohol-induced organ damage. Experimental studies have suggested alcohol-mediated apoptosis in the cardiac muscle, and there is evidence of skeletal muscle apoptosis in long-term high-dose alcohol consumers. The relation between skeletal and cardiac muscle damage in alcoholism led us to consider the pathogenic role of apoptosis in alcoholic dilated cardiomyopathy. We evaluated apoptosis in the hearts of individuals with long-term alcoholism (n = 19), of those with long-standing hypertension (n = 20), and of those with no known disease as control subjects (n = 7). Alcohol consumption measurement, heart function evaluation, and myocardial immunohistochemical and morphometric analysis were performed. Apoptosis was evaluated with deoxyribonucleotidyl transferase-mediated dUTP-biotin nick end-labeling assay, and BAX and BCL-2 expressions were used to detect induction of and protection from proapoptotic mechanisms, respectively. Hearts from patients with a history of alcoholism showed apoptotic indexes similar to those of organs from hypertensive donors. Subjects with structural heart damage of alcoholic or hypertensive origin showed higher apoptotic indexes in deoxyribonucleotidyl transferase-mediated dUTP-biotin nick end-labeling, BAX, and BCL-2 assays as compared with control subjects (P < .001 for all). Moreover, New York Heart Association class I alcoholic patients displayed higher BAX and BCL-2 expressions as compared with control subjects. We conclude that apoptosis is present to a similar degree in the heart muscle of high-dose alcohol consumers and long-standing hypertensive subjects and is related to structural damage. Proapoptotic mechanisms are activated in alcoholic patients without heart damage.
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Kikuchi-Fujimoto disease (KFD) is a benign and self-limited disorder, characterized by regional cervical lymphadenopathy with tenderness, usually accompanied with mild fever and night sweats. Less frequent symptoms include weight loss, nausea, vomiting, sore throat. Kikuchi-Fujimoto disease is an extremely rare disease known to have a worldwide distribution with higher prevalence among Japanese and other Asiatic individuals. The clinical, histopathological and immunohistochemical features appear to point to a viral etiology, a hypothesis that still has not been proven. KFD is generally diagnosed on the basis of an excisional biopsy of affected lymph nodes. Its recognition is crucial especially because this disease can be mistaken for systemic lupus erythematosus, malignant lymphoma or even, though rarely, for adenocarcinoma. Clinicians' and pathologists' awareness of this disorder may help prevent misdiagnosis and inappropriate treatment. The diagnosis of KFD merits active consideration in any nodal biopsy showing fragmentation, necrosis and karyorrhexis, especially in young individuals presenting with posterior cervical lymphadenopathy. Treatment is symptomatic (analgesics-antipyretics, non-steroidal anti-inflammatory drugs and, rarely, corticosteroids). Spontaneous recovery occurs in 1 to 4 months. Patients with Kikuchi-Fujimoto disease should be followed-up for several years to survey the possibility of the development of systemic lupus erythematosus.
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We investigated whether the result of early exercise testing yields prognostic information in addition to that afforded by a clinical risk score in patients who present with chest pain in the emergency department. The study group consisted of 340 patients without preexisting evidence of myocardial ischemia. A clinical risk score was calculated. Primary (mortality or myocardial infarction) and secondary (mortality, myocardial infarction, or rehospitalization due to unstable angina) end points at 1 year were defined. Patients with a positive exercise test result underwent invasive management. Frequencies of primary (7.4% vs 2.1%, p = 0.06) and secondary (9.3% vs 2.8%, p = 0.04) end points and risk score (1.6 +/- 1.0 vs 1.0 +/- 0.9 points, p = 0.0001) were higher in patients with a positive exercise test result. However, in multivariate analysis, clinical risk score was the only independent predictor for the primary (hazard ratio 2.0, 95% confidence interval 1.2 to 3.2, p = 0.004) and secondary (hazard ratio 1.9, 95% confidence interval 1.2 to 2.9, p = 0.003) end points. In conclusion, if a policy of invasive management is implemented for patients with positive exercise test results, the clinical risk score constitutes the main prognostic predictor of 1-year outcome.
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INTRODUCTION AND OBJECTIVES: To assess recent changes in the management of patients with acute myocardial infarction (AMI) and their impact on mortality using data from the PRIAMHO I and II registries (1995 and 2000). PATIENTS AND METHOD: Of the 168 public hospitals in Spain, 24 and 58 contributed to the 1995 and 2000 PRIAMHO registries, respectively. RESULTS: Patients in the PRIAMHO II registry (n=6221) were significantly older, more often female, and proportionally more likely to have coronary risk factors or a previous myocardial infarction, or to have undergone revascularization than those in PRIAMHO I (n=5242). Reperfusion therapy was administered more often (46.9% vs 41.9%, P<.001) and earlier (48 min vs 60 min, P<.001). Antiplatelet drugs were given to 96.1% vs 89.1% of patients, beta-blockers to 51.1% vs 30.1%, and ACE inhibitors to 41.6% vs 24.9% (P<.001 for all comparisons). In addition, 28-day mortality was 11.3% and 14.2% (P<.001), respectively, and one-year mortality, 16.4% and 18.5% (P<.001), respectively. The adjusted hazard ratio for mortality at one year in PRIAMHO II compared with PRIAMHO I was 0.78 (95% CI, 0.70-0.86, P<.001; adjusted for age, sex, diabetes, smoking, dyslipemia, hypertension, previous MI and CABG, ST-elevation status and Killip class at admission, and hospital characteristics). CONCLUSIONS: Even though patients registered in 2000 formed a higher risk group than those registered in 1995, one-year mortality after AMI decreased by 22% over the five-year period. This improvement was due to more frequent and earlier reperfusion therapy and better use of antithrombotics, beta-blockers and ACE inhibitors.
Our objective was to provide an update on recent epidemiologic evidence about the role of diet and nutrition on the risk of human papillomavirus (HPV) persistence and cervical neoplasia, taking HPV into account. We conducted a systematic review and qualitative classification of all observational studies controlling for HPV infection published between March 1995 and November 2003 and of all randomized clinical trials published between January 1991 and November 2003. Scientific evidence was classified as convincing, probable, possible or insufficient, as used in a previous study on diet and cancer. Thirty-three studies were eligible for this review (10 clinical trials, 8 observational prospective studies and 15 case-control studies). The few studies on HPV persistence showed a possible protective effect of fruits, vegetables, vitamins C and E, beta- and alpha-carotene, lycopene, luterin/zeaxanthin and cryptoxanthin. Evidence for a protective effect of cervical neoplasia was probable for folate, retinol and vitamin E and possible for vegetables, vitamins C and B12, alpha-carotene, beta-carotene, lycopene, lutein/zeaxanthin and cryptoxanthin. Evidence for an increased risk of cervical neoplasia associated with high blood homocysteine was probable. Results did not differ between studies looking at preneoplastic and invasive lesions or between retrospective and prospective studies. The available evidence for an association between diet and nutritional status and cervical carcinogenesis taking HPV infection into account is not yet convincing. Large cohort studies are needed to adequately assess the role of foods and nutrients in cervical HPV carcinogenesis.
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