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Complement abnormalities in multiple myeloma.

J J Zurlo1, G P Schechter, L F Fries

  • 1Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.

The American Journal of Medicine
|October 1, 1989
PubMed
Summary
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Multiple myeloma patients exhibit defective complement component C3 activation and deposition due to heterogeneous abnormalities, impacting host defense. This study investigated the underlying mechanisms of this complement deficiency.

Area of Science:

  • Immunology
  • Hematology
  • Biochemistry

Background:

  • Patients with multiple myeloma often display impaired opsonization and complement component C3 deposition.
  • Previous research suggests a link between defective C3 deposition and a failure of C3 activation in myeloma serum, though the exact mechanism remains unclear.

Purpose of the Study:

  • To investigate the underlying mechanisms responsible for the observed failure in complement component C3 activation and deposition in multiple myeloma patients.
  • To evaluate the kinetics of C3 deposition and measure serum levels of complement components in vitro.

Main Methods:

  • In vitro analysis of C3 deposition kinetics onto zymosan using radiolabeled C3 in serum from 10 multiple myeloma patients and healthy donors.
  • Measurement of serum levels for various complement pathway components using standard assays.

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Main Results:

  • Five out of ten patients showed poor C3 deposition, with two others exhibiting transient defects.
  • Decreased levels of classical and alternative complement pathway components were observed, particularly in patients with the most severe C3 deposition defects.
  • Elevated Bb fragment levels indicated in vivo activation of the alternative pathway, while classical pathway abnormalities were less clear. Paraprotein concentration inversely correlated with abnormal C3 deposition and C3/C4 levels.

Conclusions:

  • The defect in C3 activation and deposition in multiple myeloma is attributed to a heterogeneous group of complement abnormalities, not a single deficiency.
  • While no direct correlation with clinical status was found in this small cohort, these complement defects likely contribute to compromised host defense in multiple myeloma.