Soluble terminal complement components in human myasthenia gravis

Richard J. Barohn, Robin L. Brey

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


The loss of membrane acetylcholine receptor (AChR) leading to muscle weakness and impaired neuromuscular junction (NMJ) transmission in human myasthenia gravis (MG) is in part due to complement mediated muscle membrane damage. This has been supported by the histologic finding of C9 at the NMJ in human MG. We evaluated for evidence of terminal complement components in plasma by using an ELISA for SC5b-9 in 42 separate plasma samples from 31 patients with MG and from healthy controls. Abnormal elevations of SC5b-9 was found in 18 of 31 patients (58%) at one or more time points when plotted on a standard positive dilution curve. Multiple samples were available from 8 patients over time. Clinical deterioration in some, but not all, was accompanied by an increase in SC5b-9 values. There was no clear distinction in the group as a whole between MG severity or AChR antibody levels and SC5b-9 values. This supports the potential role of complement-mediated muscle membrane damage in the pathogenesis of human MG, but also demonstrates that plasma levels as measured by ELISA do not always correlate with disease activity.

Original languageEnglish (US)
Pages (from-to)285-290
Number of pages6
JournalClinical Neurology and Neurosurgery
Issue number4
StatePublished - Dec 1993


  • Complement
  • Experimental allergic myasthenia gravis
  • Membrane attack complex
  • Myasthenia gravis
  • Terminal complement components

ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology


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