Clinical ahd immunologicai studies of polyneuropathy associated with monoclonal gammopathy

被引用文献2件
  • SAITO T
    Department of Internal Medicine, Kitasato University School of Medicine
  • Irie Sachiko
    Department of Internal Medicine, Kitasato University School of Medicine
  • Ogino Mieko
    Department of Internal Medicine, Kitasato University School of Medicine
  • Ogino Yutaka
    Department of Internal Medicine, Kitasato University School of Medicine
  • Kyuno Katsuhiro
    Department of Internal Medicine, Kitasato University School of Medicine
  • Ito Hiroaki
    Department of Internal Medicine, Kitasato University School of Medicine
  • Kanazawa Naomi
    Research Division of East Hospital, Kitasato University School of Medicine
  • Kowa Hisayuki
    Department of Internal Medicine, Kitasato University School of Medicine

この論文をさがす

抄録

We studied 36 patients with polyneuropathy and monoclonal gammopathies, of whom, 16 had an IgM, 11 had an IgG, and 7 had an IgA monoclonal gammopathy. The two remaining patients had a biclonal (IgM, IgG) gammopathy. Tweleve patients (65%) with monoclonal gammopathy of undetermined significance (MGUS) or nonmalignant IgM monoclonal gammopathy had high titers of myelin-associated glycoprotein (MAG) IgM antibodies by enzyme-linked immunosorbent assay and reacted with MAG by immunoblot. Morphological studies of affected sural nerves typically show the characteristics features of chronic demyelination in patients with IgM MGUS. The neuropathy in patients with anti-MAG IgM M-proteins is probably caused by M-protein autoantibody activity. Patients with IgG, IgA of MGUS had symmetrical sensorimotor polyneuropathy, and sural nerve biopsy in these patients showed axonal degeneration. M-protein autoantibody activity to peripheral nerve tissue was not observed by immunoblot in this group. M-proteins in patients with IgG, IgA of MGUS may have a different peripheral nerve tissue target.

収録刊行物

被引用文献 (2)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ