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Treatment of Autonomic Disorders of Familial Amyloid Polyneuropathy with L-Threo-3,4-Dihydroxyphenyserine

  • Takako Kikkawa
  • Shu-ichi Ikeda
  • Nobuo Yanagisawa
  • Masanobu Yazawa
  • Norinao Hanyu
Chapter

Abstract

Familial amyloid polyneuropathy (FAP) is a hereditary systemic amyloidosis characterized by polyneuropathy and severe autonomic disorders1. Autonomic disorders of FAP include orthostatic hypotension, gastrointestinal symptoms, urinary disturbance and impotence. Among them, orthostatic hypotension restricts activities of patients, but there has been no beneficial treatment. Recent reports showed6,7 that the intravenous or oral administration either of L-or DL-threo-3,4-dihydroxyphenylserine (L-,DL-DOPS) had a short term effect on orthostatic hypotension of FAP. In this paper we evaluated the effet of the oral administration of L-DOPS on the orthostatic hypotension and the gastrointestinal symptoms in FAP.

Keywords

Gastrointestinal Symptom Orthostatic Hypotension Nagano Prefecture Familial Amyloid Polyneuropathy Clin Neurol 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Andrade C. A peculiar form of peripheral neuropathy, familiar atypical generalized amyloidsis with special involvement of the peripheral nerves. Brain, 75: 408–428, 1952.CrossRefGoogle Scholar
  2. 2.
    Ikeda S, Koh CS, Miyasaka M, Yanagisawa N and Tsukagoshi H. Familial amyloid neuropathy with late onset and benign course. Clin Neurol, 21: 135–142, 1981.Google Scholar
  3. 3.
    Ikeda S, Hanyu N, Hongo M, Yoshioka J, Oguchi H, Yanagisawa N, Kobayashi T, Tsukagoshi H, Ito N and Yokota T. Hereditary generalized amyloidosis with polyneuropathy. Brain, 110: 315–337, 1987.CrossRefGoogle Scholar
  4. 4.
    Kito S, Itoga E, Kamiya K, Kishida T and Yamamura Y. Studies on familial amyloid polyneuropathy in Ogawa village, Japan. Eur. Neurol., 19: 141–151, 1980.CrossRefGoogle Scholar
  5. 5.
    Shirabe T, Hashimoto M, Araki S, Mawatari S and Kuroiwa Y. Two autopsy cases of familial polyneuritic amyloidosis. Adv Neurol Sci (Tokyo), 13: 206–215, 1969.Google Scholar
  6. 6.
    Suzuki T, Higa S, Tsuge I, Sakoda S, Hayashi A, Yamamura Y, Takaba Y and Nakajima A. Orthostatic hypotension in familial amyloid polyneuropathy: Treatment with DL-threo-3,4-dihydroxyphenylserine. Neurology (Ny), 31: 1323–1326, 1981.CrossRefGoogle Scholar
  7. 7.
    Suzuki T, Higa S, Tsuge I, Sakoda S, Hayashi A, Yamamura Y, Takaba Y and Nakajima A. Effect of infused L-threo-3,4-dihydroxyphenylserine on adre-nergic activity in patients with familial amyloid polyneuropathy. Eur. J. Clin. Pharmacol., 17: 429–435, 1980.CrossRefGoogle Scholar
  8. 8.
    Suzuki T, Tsuge I, Higa S, Hayashi A, Yamamura Y, Takaba Y and Nakajima A. Catecholamine metabolism in familial amyloid polyneuropathy. Clin. Genet., 16: 117–124, 1979.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1988

Authors and Affiliations

  • Takako Kikkawa
    • 1
  • Shu-ichi Ikeda
    • 1
  • Nobuo Yanagisawa
    • 1
  • Masanobu Yazawa
    • 2
  • Norinao Hanyu
    • 2
  1. 1.Department of Medicine (Neurology)Shinshu University School of MedicineMatsumotoJapan
  2. 2.Department of NeurologyNagano Red Cross HospitalNaganoJapan

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