Clinicopathological and biochemical findings of thyroid amyloid in hereditary transthyretin amyloidosis with and without liver transplantation

  • Guannan Huang
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Mitsuharu Ueda
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Masayoshi Tasaki
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Taro Yamashita
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Yohei Misumi
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Teruaki Masuda
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Genki Suenaga
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Yasuteru Inoue
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Yumiko Kinoshita
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Sayaka Matsumoto
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Mayumi Mizukami
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Yukimoto Tsuda
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Toshiya Nomura
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and
  • Konen Obayashi
    Department of Morphological and Physiological Sciences, Graduate School of Health Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan
  • Yukio Ando
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Chuo-ku, Kumamoto, Japan and

書誌事項

公開日
2017-01-02
資源種別
journal article
DOI
  • 10.1080/13506129.2016.1276440
  • 10.6084/m9.figshare.4546864.v1
  • 10.6084/m9.figshare.4546864
公開者
Informa UK Limited

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説明

Hereditary transthyretin (TTR) amyloidosis is a fatal disease causing systemic organ dysfunctions. Histopathological studies revealed that thyroid glands are major target tissues. However, details about thyroid functions remain to be fully elucidated in this disease. For patient treatment, liver transplantation (LT) reportedly prolongs patient survival, but thyroid gland function after LT still remains poorly understood. In this study, we investigated the thyroid functions in 101 patients with hereditary TTR amyloidosis and the effects of LT on thyroid functions in those patients. In addition, we investigated histopathological and biochemical findings of thyroid specimens obtained at autopsy. Disease duration and age at examination inversely correlated with serum levels of free triiodothyronine (fT3) in hereditary TTR amyloidosis. On the contrary, in patients who underwent transplantation, time from disease onset to transplantation and age at transplantation clearly correlated with serum fT3and thyroid stimulating hormone (TSH) levels. In autopsy studies, amounts of thyroid amyloid deposits in patients with transplantation were significantly lower than those in patients without transplantation. Mass spectrometric analyzes also revealed that proportions of wild-type (WT) TTR in thyroid amyloid deposits in patients with hereditary TTR amyloidosis who underwent transplantations were higher than those in patients without transplantation. Thyroid hormone functions may diminish according to the disease progression. LT could prevent thyroid dysfunction in hereditary TTR amyloidosis.

収録刊行物

  • Amyloid

    Amyloid 24 (1), 24-29, 2017-01-02

    Informa UK Limited

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