The Epidemiology of Monoclonal Gammopathy of Unknown Significance: A Review

  • L. J. Herrinton
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 210)


The transient production of monoclonal components of immunoglobulins (M-components) occurs normally in response to trauma, particular drug treatments, and infection with specific antigens (Haas et cd. 1990; Merlini and Aguzzi 1988). Chronic production can occur with malignancy (B cell, colon, prostate, and breast) and with rheumatoid arthritis, tuberculosis, cirrhosis, and several other chronic inflammatory and infectious processes (Merlini and Aguzzi 1988; Saleun et cd. 1982). However, in approximately 60–90% of persons identified with elevated M-components in community-based surveys, the elevation is chronic and unexplained (Saleun et cd. 1982; Axelsson et cd. 1966; Kyle et cd. 1972). These persons are given a diagnosis of monoclonal gammopathy of unknown significance (MGUS). Although MGUS is itself benign, it can evolve to amyloidosis, myeloma, or macroglobulinemia (Kyle 1993). To better understand the significance and consequences of MGUS, the author conducted a literature review. Two methodological issues that affect the interpretation of the literature are discussed first.


Cellulose Acetate Monoclonal Gammopathy Hematology Patient Monoclonal Protein Plasma Cell Dyscrasia 
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  1. Axelsson U (1986) A 20-year follow-up study of 64 subjects with M-components. Acta Med Scand 219:519–22.PubMedCrossRefGoogle Scholar
  2. Axelsson U, Bachmann R, Hallen J (1966) Frequency of pathological proteins (M-components) in 6,995 sera from an adult population. Acta Med Scand 179:235–247.PubMedCrossRefGoogle Scholar
  3. Blade J, Lopez-Guillermo A, Rozman C, Cervantes F, Salgado C, Aguilar JL, Vives-Corrons JL, Montserrat E (1992) Malignant transformation and life expectancy in monoclonal gammopathy of undetermined significance. Br J Haematol 81;391–394.PubMedCrossRefGoogle Scholar
  4. Bowden M, Crawford J, Cohen HJ, Noyama O (1993) A comparative study of monoclonal gammopathies and immunoglobulin levels in Japanese and United States elderly. J Am Geriatr Soc 41:11–14.PubMedGoogle Scholar
  5. Carter A, Tatarsky I (1980) The physiopathological significance of benign monoclonal gammopathy: a study of 64 cases. Br J Haematol 46:565–574.PubMedCrossRefGoogle Scholar
  6. Fine JM, Lambin P, Leroux P (1972) Frequency of monoclonal gammopathy (‘M components’) in 13,400 sera from blood donors. Vox Sang 23:336–343.PubMedCrossRefGoogle Scholar
  7. Fine JM, Lambin P, Muller JY (1979) The evolution of asymptomatic monoclonal gammopathies. Acta Med Scand 205:339–341.PubMedCrossRefGoogle Scholar
  8. Haas H, Anders S, Bornkamm G, Mannweiler E, Schmitz H, Radl J, Schlaak M. (1990) Do infections induce monoclonal immunoglobulin components? Clin Exp Immunol 81:435–440.PubMedCrossRefGoogle Scholar
  9. Herrinton LJ, Weiss NS, Olshan AF(1994) Epidemiology of myeloma. In: Malpas JS, Bergsagel DE, and Kyle RA (eds) Myeloma: biology and management. Oxford Medical, Oxford, pp 127–168.Google Scholar
  10. Kleinbaum DG, Kupper LL, Morgenstern H (1982) Epidemiologic research. Lifetime Learning, Belmont, CA, p 161.Google Scholar
  11. Kyle RA (1993) “Benign” monoclonal gammopathy-after 20 to 35 years of follow-up. Mayo Clin Proc 68:26–36.PubMedGoogle Scholar
  12. Kyle RA, Greipp PA (1988) Plasma cell dyscrasias: current status. CRC Crit Rev Oncol Hematol 8:93–152.CrossRefGoogle Scholar
  13. Kyle RA, Finkelstein S, Elveback LR, Kurland LT (1972) Incidence of monoclonal proteins in a Minnesota community with a cluster of multiple myeloma. Blood 40:719–724.PubMedGoogle Scholar
  14. Manthorne LA, Dudley RW, Case CD, Turgeon WP, Ritchie RF (1988) A longitudinal study of monoclonal gammopathy of undetermined signficance (MGUS). Clin Res 36:414A.Google Scholar
  15. Merlini G, Aguzzi F (1988) The laboratory investigation of monoclonal components. Haematol 73:79–85.Google Scholar
  16. Papadopoulos NM, Elin RJ, Wilson DM (1982) Incidence of γ-globulin banding in a healthy population by high-resolution electrophoresis. Clin Chem 28:707–708.PubMedGoogle Scholar
  17. Pick AI, Shoenfeld Y, Skvaril F, Schreibman S, Frohlichman R, Weiss H, Pinkhas J. (1977) Asymptomatic (benign) monoclonal gammopathy-a study of 100 patients. Ann Clin Lab Sci 7;335–343.PubMedGoogle Scholar
  18. ei]Ries LAG, Miller BA, Hankey BF, Kosary CL, Harras A, Edwards BK (eds) (1994) SEER cancer statistics review, 1973-1991: tables and graphs. National Cancer Institute, Bethesda, p 301.Google Scholar
  19. Saleun JP, Vicariot M, Deroff P, Morin JF (1982) Monoclonal gammopathies in the adult population of Finistère, France. J Clin Pathol 35:63–68.PubMedCrossRefGoogle Scholar
  20. Schechter GP, Shoff N, Chan C, McManus CD, Hawley HP (1990) The frequency of monoclonal gammopathy of unknown significance in black and white veterans in a hospital population. In: Obrams GI and Potter M (eds) Epidemiology and biology of multiple myeloma. Springer-Verlag, New York, pp 83–85.Google Scholar
  21. Singh J, Dudley AW, Kulig KA (1990) Increased incidence of monoclonal gammopathy of undetermined significance in blacks and its age-related differences with whites on the basis of a study of 397 men and one woman in a hospital setting. J Lab Clin Med 116:785–789.PubMedGoogle Scholar
  22. Ucci G, Riccardi A, Luoni R, Ascari E (19993) Presenting features of monoclonal gammopathies: an analysis of 684 newly diagnosed cases. J Int Med 234:165–173.CrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1996

Authors and Affiliations

  • L. J. Herrinton
    • 1
  1. 1.Division of Research, Kaiser PermanenteOaklandUSA

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