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Titolo:
A case of late onset cardiac amyloidosis with a new transthyretin variant (lysine 92)
Autore:
Saito, F; Nakazato, M; Akiyama, H; Kitahara, Y; Date, Y; Iwasaki, Y; Harasawa, S; Hisaki, R; Hori, T; Kinukawa, N; Watanabe, T; Sakamaki, T; Yagi, H; Hoshii, Y; Yutani, C; Kanmatsuse, K;
Indirizzi:
Surugadai Nihon Univ Hosp, Dept Cardiol, Chiyoda Ku, Tokyo 1018309, Japan Surugadai Nihon Univ Hosp Tokyo Japan 1018309 a Ku, Tokyo 1018309, Japan Surugadai Nihon Univ Hosp, Dept Pathol, Tokyo 1018309, Japan Surugadai Nihon Univ Hosp Tokyo Japan 1018309 thol, Tokyo 1018309, Japan Miyazaki Med Coll, Dept Internal Med 3, Miyazaki 88916, Japan Miyazaki MedColl Miyazaki Japan 88916 rnal Med 3, Miyazaki 88916, Japan Yamaguchi Univ, Sch Med, Dept Pathol 1, Ube, Yamaguchi 755, Japan Yamaguchi Univ Ube Yamaguchi Japan 755 athol 1, Ube, Yamaguchi 755, Japan Natl Cardiovasc Ctr, Div Pathol, Osaka, Japan Natl Cardiovasc Ctr Osaka Japan ardiovasc Ctr, Div Pathol, Osaka, Japan
Titolo Testata:
HUMAN PATHOLOGY
fascicolo: 2, volume: 32, anno: 2001,
pagine: 237 - 239
SICI:
0046-8177(200102)32:2<237:ACOLOC>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
POLYNEUROPATHY; CARDIOMYOPATHY;
Keywords:
cardiac amyloidosis; transthyetin variant; DNA sequencing;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
10
Recensione:
Indirizzi per estratti:
Indirizzo: Saito, F Surugadai Nihon Univ Hosp, Dept Cardiol, Chiyoda Ku, 1-8-13 KandaSurugadai, Tokyo 1018309, Japan Surugadai Nihon Univ Hosp 1-8-13 Kanda Surugadai Tokyo Japan 1018309
Citazione:
F. Saito et al., "A case of late onset cardiac amyloidosis with a new transthyretin variant (lysine 92)", HUMAN PATH, 32(2), 2001, pp. 237-239

Abstract

A new transthyretin (TTR) variant (lysine 92), which causes late onset cardiac amyloidosis, is described in a 71-year-old man. The patient at first had syncope due to ventricular tachycardia and was admitted our hospital. Typical findings of cardiac amyloidosis were observed by echocardiography, and a diagnosis of systemic amyloidosis was made by rectal biopsy. The man died approximately 3 years and 6 months after first admission, with graduallyworsening congestive heart failure. Pathological examination showed prominent amyloid deposits in the heart and the vascular wall of many organs including the liver, pancreas, kidney, lung, and gastrointestinal tracts. Amyloid protein of transthyretin type was indicated by immunohistochemical study, and DNA sequencing identified a novel mutation in the transthyretin gene encoding 92 glutamine --> lysine. A polymerase chain reaction-induced mutation restriction analysis with a mismatched antisense primer showed that thepatient was heterozygous for the TTR Lys92 allele. HUM PATHOL 32:237-239. Copyright (C) 2001 by W.B. Saunders Company.

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Documento generato il 28/03/20 alle ore 13:54:31