Determination of circulating amyloid precursor protein in diagnosis and monitoring of disease progression in systemic amyloidosis

Abstract

Serum amyloid A (SAA) plasma level was measured at 43 patients with chronic inflammatory diseases, including 31 patients with reactive AA-amyloidosis and 12 patients not having amyloidosis (control group). SAA-protein concentration was measured with immune-enzyme analysis (ELISA) in laboratory, corresponding to European standards. The level of immunoglobulin light chains was measured at 31 patients with AL-amyloidosis. Low plasma concentration of immunoglobulin light chains, detected with Freelite method, or its decrease after treatment, indicates relatively favorable prognosis. In contrast, high plasma level of immunoglobulin light chains show very unfavorable outcome. Increase of SAA plasma level indicates risk of nephrotic syndrome development. Conclusion. Circulating amyloid precursor concentrations can be used in monitoring of disease progression.
Conclusion: plasma level measurement of amyloide's proteins-predecessors can be used for amyloidosis diagnostic and prognosis of outcomes

References

  1. Benditt E.P., Eriksen N. Chemical classes of amyloid substance. Am J Pathol 1971;65:231-52.
  2. Glenner G.G., Terry W., Harada M. et al. Amyloid fibril proteins: proof of homology with immunoglobulin light chains by sequence analysis. Science 1971;172:1150-51.
  3. Levin M., Pras M., Franklin E.C. Immunologic studies of the major nonimmunoglobulin protein of amyloid. I. Identification and partial characterization of a related serum component. J Exp Med 1973;138:373-80.
  4. Liepnieks J.J., Kluve-Beckerman B., Benson M.D. Characterization of amyloid A protein in human secondary amyloidosis: the predominant deposition of serum amyloid A1. Biochim Biophys Acta 1995;1270:81-86.
  5. Baba S., Takahashi T., Kasama T., Fujie M., Shirawasa H. A novel polymorphism of human serum amyloid A protein, SAA1, is characterized by alanines at both residues 52 and 57. Biochim Biophys Acta 1992;282:615-20.
  6. Baba S., Masago S.A., Takahashi T., et al. A novel allelic variant of serum amyloid A, SAA1 gamma: genomic evidence, evolution, frequency, and implication as a risk factor for reactive systemic AA-amyloidosis. Hum Mol Genet 1995;4:1083-87.
  7. Moriguchi M., Terai C., Koseki Y., et al. Influence of genotypes at SAA1 and SAA2 loci on the development and the length of latent period of secondary AA-amyloidosis in patients with rheumatoid arthritis. Hum Genet 1999;105:360-66.
  8. Moriguchi M., Terai C., Kaneko H., et al. A novel single-nucleotide polymorphism at the 5-lanking region of SAA1 associated with risk or type AA amyloidosis secondary to rheumatoid arthritis. Arthritis Rheum 2001;44:1266-72.
  9. Yamada T., Okuda Y., Takasugi K., et al. An allele of serum amyloid A1 associated with amyloidosis in both Japanese and Caucasians. Amyloid: J Protein Folding Disord 2003;10:7-11.
  10. Booth D.R., Booth S.E., Gillimore J.D., et al. SAA1 alleles as risk factors in reactive systemic amyloidosis. Amyloid: Int J Exp Clin Invest 1998;5:262-65.
  11. Cazeneuve, C., Ajrapetyan H., Papin S., et al. Identification of MEFV-independent modifying genetic factors for familial Mediterranean fever. Am J Hum Genet 2000;67:1136-43.
  12. Medlej-Hashim M., Delague V., Chouery E., et al. Amyloidosis in familial Mediterranean fever patients: correlation with MEFV genotype and SAA1 and MICA polymorphisms effects. BMC Med Genet 2004;5:4.
  13. Gershoni-Baruch R., Brik R., Zacks N., et al. The contribution of genotypes at the MEFV and SAA1 loci to amyloidosis and disease severity in patients with familial Mediterranean fever. Arthritis Rheum 2003;48:1149-55.
  14. Bakkaloglu, A., Duzova A., Ozen S., et al. Influence of serum amyloid A (SAA1) and SAA2 gene polymorphisms on renal amyloidosis, and on SAA/C-reactive protein values in patients with familial Mediterranean fever in the Turkish population. J Rheumatol 2004;31:1139-42.
  15. Akar N., Hasipek M., Akar E., et al. Serum amyloid A1 and tumor necrosis factor-alpha alleles in Turkish familial Mediterranean fever patients with and without amyloidosis. Amyloid: J Protein Folding Disord 2003;10:12-16.
  16. Sipe J.D. (ed.) Amyloid Proteins. The Beta Sheet Conformation and Disease 2005 WILEY-VCH.
  17. Bradwell A.R. Serum free light chain analysis, 4th edition, 2006, The Binding Site Ltd.
  18. Kyle R.A., Gertz M.A. Primary systemic amyloidosis: clinical and laboratory features in 474 cases. Semin. Hematol. 1995;32(1):45-59.
  19. Magy N., Benson M.D., Liepnieks J.J., et al. Cellular events associated with the initial phase of AA amyloidogenesis: insights from a human monocyte model. Amyloid. 2007;14(1):51-63.
  20. Gillmore J.D., Lovat L.B., Persey M.R., et al. Amyloid load and clinical outcome in AA amyloidosis in relation to circulating concentration of serum amyloid A protein. Lancet 2001;358:24-29.
  21. Финкельштейн А.В., Птицин О.Б. Физика белка. М., Книжный дом "Университет", 2002.
  22. Козловская Л.В., Рамеев В.В., Саркисова. И.А. Патогенез и клиническое значение анемии хронических заболеваний // Анемия. 2005. № 4. С. 22-31.

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