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Liver Transplantation as a Treatment for Familial Amyloidotic Polyneuropathy

Martha Skinner, MD; W. David Lewis, MD; Lee Anna Jones, MD; Jessica Kasirsky, BA; Kelly Kane, BA; Shyr-Te Ju, PhD; Roger Jenkins, MD; Rodney H. Falk, MD; Robert W. Simms, MD; and Alan S. Cohen, MD
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From the Department of Medicine, Boston City Hospital; New England Deaconess Hospital, Boston, Massachusetts. Requests for Reprints: Martha Skinner, MD, Arthritis Center, Boston University School of Medicine, 71 East Concord Street, Boston, MA 02118. Acknowledgments: The authors thank Drs. Tsuranobu Shirahama and Orville Rodgers for help with the biopsy material and Ms. Barbara Jarvis for secretarial assistance. Grant Support: Supported by grants AR 40414, AR 20613, and RR 533 from the National Institutes of Health; grant IM 676 from the American Cancer Society; and a grant from the Arthritis Foundation.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;120(2):133-134. doi:10.7326/0003-4819-120-2-199401150-00006
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No definitive treatment exists for familial amyloidotic polyneuropathy (FAP), an autosomal dominant disease associated with a mutant form of the protein transthyretin (prealbumin) [1]. Symptoms usually begin in middle life with peripheral neuropathy, autonomic dysfunction, cardiomyopathy, vitreous opacities, and occasionally renal failure. Death results from cardiomyopathy, malnutrition, or complications of autonomic neuropathy about 10 years after the onset of disease.

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Figure 1.
Isoelectric focusing gels of the serum transthyretin proteins from five patients before and after liver transplantation.

Numbers 1, 3, and 4 are from patients with transthyretin methionine 30 (Met 30), and numbers 2 and 5 are from patients with glycine 42 and asparagine 90 (Gly 42 and Asn 90). In the B lanes, normal transthyretin is the top band and mutant transthyretin is in the lower band. In the A lanes, only normal transthyretin is seen. A = after; B = before.

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