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Báo cáo khoa hoc:" Accelerating restrictive cardiomyopathy after liver transplantation in a patient with familial amyloidotic polyneuropathy: a case report"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Accelerating restrictive cardiomyopathy after liver transplantation in a patient with familial amyloidotic polyneuropathy: a case report | Journal of Medical Case Reports BioMed Central Case report Open Access Accelerating restrictive cardiomyopathy after liver transplantation in a patient with familial amyloidotic polyneuropathy a case report Jason Robin 1 Sheridan Meyers1 Maher Nahlawi1 Jyothy Puthumana1 Jon Lomasney2 David Mehlman1 Vera Rigolin1 and Charles Davidson1 Address Department of Medicine Division of Cardiology Northwestern University Feinberg School of Medicine Chicago Illinois USA and 2Department of Pathology Northwestern University Feinberg School of Medicine Chicago Illinois USA Email Jason Robin - j-robin@md.northwestern.edu Sheridan Meyers - snm@northwestern.edu Maher Nahlawi - maher99@sbcglobal.net Jyothy Puthumana - jputhumana@nmff.org Jon Lomasney - j-lomasney@northwestern.edu David Mehlman - d-mehlman@northwestern.edu Vera Rigolin - v-rigolin@northwestern.edu Charles Davidson - cdavidso@nmh.org Corresponding author Published I February 2008 Received 15 August 2007 Journal of Medical Case Reports 2008 2 35 doi 10.1186 1752-1947-2-35 Accepted 1 February 2008 This article is available from http www.jmedicalcasereports.cOm content 2 1 35 2008 Robin et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Introduction Hereditary amyloidodis is a rare disease process with a propensity to cause polyneuropathies autonomic dysfunction and restrictive cardiomyopathy. It is transmitted in an autosomal dominant manner with disease onset usually in the 20s-40s. The most common hereditary amyloidogenic protein transthyretin is synthesized in the liver and lies on Chromosome 18. Over 80 amyloidogenic transthyretin mutations have been described the majority of which are neuropathic and hence the common name Familial Amyloidotic Polyneuropathy. .