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. 1984 Mar;39(3):196–200. doi: 10.1136/thx.39.3.196

Serum amyloid A protein and C-reactive protein levels in pulmonary tuberculosis: relationship to amyloidosis.

F C de Beer, A E Nel, R P Gie, P R Donald, A F Strachan
PMCID: PMC459761  PMID: 6710428

Abstract

C-reactive protein and serum amyloid A protein levels were measured in 54 patients with pulmonary tuberculosis. The primary tuberculous complex was associated with an insignificant acute phase response, while post-primary tuberculosis without evidence of lung destruction caused modest increases in C-reactive protein and serum amyloid A protein. In most patients with post-primary pulmonary tuberculosis with significant pulmonary destruction there was a major acute phase response, with very high serum amyloid A protein and C-reactive protein levels. The response in these patients is most likely to be due to secondary bacterial infection in addition to infection by Mycobacterium tuberculosis. Patients with miliary tuberculosis showed a major acute phase response. Serum amyloid A protein and C-reactive protein levels decreased rapidly after initiation of treatment in the patients with post-primary tuberculosis without significant pulmonary destruction.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Benditt E. P., Eriksen N. Amyloid protein SAA is associated with high density lipoprotein from human serum. Proc Natl Acad Sci U S A. 1977 Sep;74(9):4025–4028. doi: 10.1073/pnas.74.9.4025. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. De Beer F. C., Mallya R. K., Fagan E. A., Lanham J. G., Hughes G. R., Pepys M. B. Serum amyloid-A protein concentration in inflammatory diseases and its relationship to the incidence of reactive systemic amyloidosis. Lancet. 1982 Jul 31;2(8292):231–234. doi: 10.1016/s0140-6736(82)90321-x. [DOI] [PubMed] [Google Scholar]
  3. Glenner G. G. Amyloid deposits and amyloidosis: the beta-fibrilloses (second of two parts). N Engl J Med. 1980 Jun 12;302(24):1333–1343. doi: 10.1056/NEJM198006123022403. [DOI] [PubMed] [Google Scholar]
  4. Lavie G., Zucker-Franklin D., Franklin E. C. Degradation of serum amyloid A protein by surface-associated enzymes of human blood monocytes. J Exp Med. 1978 Oct 1;148(4):1020–1031. doi: 10.1084/jem.148.4.1020. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Pepys M. B. C-reactive protein fifty years on. Lancet. 1981 Mar 21;1(8221):653–657. doi: 10.1016/s0140-6736(81)91565-8. [DOI] [PubMed] [Google Scholar]
  6. ROANTREE R. J., RANTZ L. A. Clinical experience with the C-reactive protein test. AMA Arch Intern Med. 1955 Nov;96(5):674–682. doi: 10.1001/archinte.1955.00250160116009. [DOI] [PubMed] [Google Scholar]
  7. Shine B., de Beer F. C., Pepys M. B. Solid phase radioimmunoassays for human C-reactive protein. Clin Chim Acta. 1981 Nov 25;117(1):13–23. doi: 10.1016/0009-8981(81)90005-x. [DOI] [PubMed] [Google Scholar]
  8. Skogen B., Natvig J. B., Bøorresen A. L., Berg K. Degradation of amyloid-related serum protein SAA by a component present in rabbit and human serum. Scand J Immunol. 1980;11(6):643–648. doi: 10.1111/j.1365-3083.1980.tb00033.x. [DOI] [PubMed] [Google Scholar]

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