Role of adenosine deaminase and the influence of age on the diagnosis of pleural tuberculosis

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art_ABRAO_Role_of_adenosine_deaminase_and_the_influence_of_2014.PDF (617.97 KB)
Citações na Scopus
35
Tipo de produção
article
Data de publicação
2014
Editora
INT UNION AGAINST TUBERCULOSIS LUNG DISEASE (I U A T L D)
DOI
Indexadores
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Autores
ABRAO, F. C.
ABREU, I. R. L. Bruno de
MIYAKI, D. H.
BUSICO, M. A. M.
Autor de Grupo de pesquisa
Editores
Coordenadores
Organizadores
Citação
INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE, v.18, n.11, p.1363-1369, 2014
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
OBJECTIVE: 1) To determine factors affecting adenosine deaminase (ADA) levels in pleural fluid (PF), and 2) to establish the optimal ADA cut-off level for a Brazilian population. DESIGN: ADA levels in PF of 309 patients were analysed to investigate pleural effusion. All patients were evaluated for age, sex and presence of tuberculosis (TB) based on a positive pleural biopsy. Differences in ADA levels between groups were analysed using Kruskal-Wallis one-way analysis of variance. Logistic regression analysis was also carried out to predict the occurrence of TB. ADA cut-off levels were selected using the receiver operating characteristic (ROC) curve. RESULTS: The mean PF ADA level was significantly higher in the tuberculous pleural group than in non-tuberculous pleural patients (63.3 +/- 29 IU/l vs. 19 +/- 31 IU/l, P < 0.001). There was a significant correlation between PF ADA levels and age: for patients aged >= 45 years, the ROC curve for ADA had an area under the curve of 0.91. An ADA level of 29 IU/l resulted in a sensitivity of 88.6% and specificity of 91.5%. CONCLUSIONS: There is a significant negative correlation between PF ADA level and age. The use of a lower ADA cut-off reduces the number of false-negative results.
Palavras-chave
pleural effusion, biological markers, pleura
URI
https://observatorio.fm.usp.br/handle/OPI/16041
Referências
  1. Baumann MH, 2007, CHEST, V131, P1125, DOI 10.1378/chest.06-2352
  2. Conde MB, 2009, J BRAS PNEUMOL, V35, P1018, DOI 10.1590/S1806-37132009001000011
  3. Garcia-Zamalloa A, 2012, PLOS ONE, V7, DOI 10.1371/journal.pone.0038729
  4. Bergmemyer H. V., 1974, METHOD ENZYMAT AN, P1092
  5. Gopi A, 2007, CHEST, V131, P880, DOI 10.1378/chest.06-2063
  6. Greco S, 2003, INT J TUBERC LUNG D, V7, P777
  7. Krenke R, 2010, CURR OPIN PULM MED, V16, P367, DOI 10.1097/MCP.0b013e32833a7154
  8. Light RW, 2010, RESPIROLOGY, V15, P451, DOI 10.1111/j.1440-1843.2010.01723.x
  9. Light R W, 2007, PLEURAL DIS
  10. Merino JM, 1999, CHEST, V115, P26, DOI 10.1378/chest.115.1.26
  11. Morisson Patrizio, 2008, J. bras. pneumol., V34, P217, DOI 10.1590/S1806-37132008000400006
  12. NIWA Y, 1985, CHEST, V87, P351, DOI 10.1378/chest.87.3.351
  13. Porcel JM, 2009, LUNG, V187, P263, DOI 10.1007/s00408-009-9165-3
  14. Sharma SK, 2005, J CLIN LAB ANAL, V19, P40, DOI 10.1002/jcla.20054
  15. Tay TR, 2013, BMC INFECT DIS, V13, DOI 10.1186/1471-2334-13-546
  16. Tobias-Machado M, 2013, INT BRAZ J UROL, V39, P328, DOI 10.1590/S1677-5538.IBJU.2013.03.05
  17. Udwadia ZF, 2010, CURR OPIN PULM MED, V16, P399, DOI 10.1097/MCP.0b013e328339cf6e
  18. Valdes L, 1998, ARCH INTERN MED, V158, P2017, DOI 10.1001/archinte.158.18.2017
  19. VALDES L, 1995, THORAX, V50, P600, DOI 10.1136/thx.50.6.600
  20. Yeon K M, 2002, TUBERCULOSIS RESP DI, V53, P530

Coleções
Artigos e Materiais de Revistas Científicas - LIM/62
Artigos e Materiais de Revistas Científicas - ODS/03