NDLI: Continued Deposition of Wild-Type Transthyretin in Cardiac Amyloid after Liver Transplantation

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Continued Deposition of Wild-Type Transthyretin in Cardiac Amyloid after Liver Transplantation

Content Provider	Scilit
Author	Liepnieks, J. J. Yazaki, M. Benson, M. D.
Copyright Year	2004
Description	Transthyretin (TTR) amyloidosis is the most prevalent type of hereditary systemic amyloidosis. The majority of the over 80 mutations in the TTR gene result in amyloid deposition in peripheral nerve that leads to progressive polyneuropathy. Amyloid cardiomyopathy, however, is the most common cause of death. Since plasma TTR is produced mainly in the liver, liver transplantation has been employed as a promising therapy for patients with hereditary TTR amyloidosis to stop synthesis of plasma variant TTR. Several studies of patients after liver transplantation have shown no further progression in neurological symptoms including autonomic dysfunction in many patients (1–4). A few clinical studies, however, have reported progression of cardiac amyloidosis and vitreous amyloidosis still occurs after liver transplantation (5–8). In order to assess the possible contribution of wild-type TTR to continuing amyloid deposition after liver transplant, we investigated the relative amounts of wild-type and variant TTR in the cardiac amyloid of patients who underwent liver transplant compared to that of patients without liver transplant. Book Name: Amyloid and Amyloidosis
Related Links	https://content.taylorfrancis.com/books/download?dac=C2010-0-33252-7&isbn=9780429125249&doi=10.1201/9781420037494-125&format=pdf
Ending Page	356
Page Count	3
Starting Page	354
DOI	10.1201/9781420037494-125
Language	English
Publisher	Informa UK Limited
Publisher Date	2004-11-29
Access Restriction	Open
Subject Keyword	Book Name: Amyloid and Amyloidosis Transplantation Amyloidosis Liver Transplant Transthyretin Wild Type Ttr Cardiac Amyloid
Content Type	Text
Resource Type	Chapter

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