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Amino Acids of Serum and Urine in Familial Amyloidotic Polyneuropathy
Shukuro Araki, MD;
Shiro Mawatari, MD;
Tetsuo Inokuchi, MD
Arch Neurol. 1970;23(1):9-13.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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AMYLOIDOSIS, a rare metabolic disorder of unknown etiology, is characterized by deposition of hyaline-like material in the connective tissue of various organs. In 1952, Andrade1 first clearly described a familial form of primary amyloidosis with polyneuropathy in Portugal. In 1956, Rukavina and his coworkers2 described another large family in North America. Subsequently, there were several reports of similar families throughout the countries.3-6 In Japan since 1966, Nakao et al7 and Araki et al8 first discovered two pedigrees of familial amyloidotic polyneuropathy; independently, two additional pedigrees have been reported from different areas of Japan.9,10 The clinical features and autosomal dominant pattern of inheritance were similar in almost all reported cases.
We have previously described the clinical manifestations, genetics, postmortem findings, and laboratory data in ten patients.11-13 We found no remarkable laboratory abnormalities, including serum proteins, electrolytes, and liver function tests. The purpose
. . . [Full Text PDF of this Article]
Author Affiliations
Fukuoka City, Japan
From the Department of Neurology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka City, Japan.
Footnotes
Submitted for publication Dec 4, 1969; accepted Feb 10.
Reprint requests to Department of Neurology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka City, Japan (Dr. Araki).
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