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2.
J Am Geriatr Soc ; 65(8): 1796-1801, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28407209

RESUMO

OBJECTIVES: To explore the performance of the neutrophil-to-lymphocyte ratio (NLR), an index of systemic inflammation that predicts prognosis of several diseases, in a cohort of elderly adults with community-acquired pneumonia (CAP). DESIGN: Prospective clinical study from January 2014 to July 2016. SETTING: Unit of Internal Medicine, University of Catania, Catania, Italy. PARTICIPANTS: Elderly adults admitted for CAP (N = 195). MEASUREMENTS: Clinical diagnosis of CAP was defined as the presence of a new infiltrate on plain chest radiography or chest computed tomography associated with one or more suggestive clinical features such as dyspnea, hypo- or hyperthermia, cough, sputum production, tachypnea (respiration rate >20 breaths per minute), altered breath sounds on physical examination, hypoxemia (partial pressure of oxygen <60 mmHg), leukocytosis (white blood cell count >10,000/µL). Clinical examination, traditional tests such as Pneumonia Severity Index (PSI); Confusion, Urea, Respiratory rate, Blood pressure, aged 65 and older (CURB-65), and NLR were evaluated at admission. The accuracy and predictive value for 30-day mortality of traditional scores and NLR were compared. RESULTS: NLR predicted 30-day mortality (P < .001) and performed better than PSI (P < .05), CURB-65, C-reactive protein, and white blood cell count (P < .001) to predict prognosis. No deaths occurred in participants with a NLR of less than 11.12. Thirty-day mortality was 30% in those with a NLR between 11.12% and 13.4% and 50% in those with a NLR between 13.4 and 28.3. All participants with a NLR greater than 28.3 died within 30 days. CONCLUSIONS: These results would encourage early discharge of individuals with a NLR of less than 11.12, short-term in-hospital care for those with a NLR between 11.12 and 13.4, middle-term hospitalization for those with a NLR between 13.4 and 28.3, and admission to a respiratory intensive care unit for those with a NLR greater than 28.3.


Assuntos
Infecções Comunitárias Adquiridas/mortalidade , Contagem de Linfócitos , Neutrófilos/citologia , Pneumonia/mortalidade , Idoso , Idoso de 80 Anos ou mais , Infecções Comunitárias Adquiridas/sangue , Infecções Comunitárias Adquiridas/terapia , Feminino , Hospitalização , Humanos , Itália , Masculino , Pneumonia/sangue , Pneumonia/terapia , Prognóstico
3.
Hepat Mon ; 12(10 HCC): e5943, 2012 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-23162599

RESUMO

CONTEXT: Studies on experimental animals have shown liver is a common target of chemical carcinogens; this might suggest that occupational exposure to chemicals is another risk factor for HCC. However, the relationship between occupation and liver cancer has not been extensively studied, with the exception of the known association between vinyl chloride and angiosarcoma of the liver. EVIDENCE ACQUISITION: A MEDLINE and conventional search of the past 50 years of the medical literature was performed to identify relevant articles on incidence and mechanisms of HCC due to occupational exposure to chemicals. Several important edited books and monographs were also identified and reviewed. RESULTS: While laboratory data clearly indicate that the liver is an important target of chemical carcinogenesis, epidemiological studies provide very limited evidence on occupational risk factors for HCC. Nevertheless, we found some case reports and epidemiological data showing a moderately increased risk of HCC development in people exposed to vinyl chloride, organic solvents, pesticides, polychlorinated biphenyls, and arsenic. CONCLUSIONS: Occupational exposure to chemicals may be another risk factor for HCC development, but the interpretation of currently available findings is limited by the small number of studies, questionable accuracy of the diagnosis of liver cancer, and potential confounding or modifying factors such as chronic hepatitis virus infection and alcohol consumption. Further relevant investigations are required for clarifying the actual contribution of occupational exposure to chemicals in HCC development.

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