Plasma β-endorphin levels during liver transplantation in patients with familial amyloidotic polyneuropathy
✍ Scribed by Francisco Acosta; Julian Diaz; Teodomiro Fuente; Tomas Sansano; Ricardo Robles; Pablo Ramirez; Francisco S. Bueno; Pascal Parrilla
- Publisher
- Elsevier Science
- Year
- 1996
- Tongue
- English
- Weight
- 213 KB
- Volume
- 29
- Category
- Article
- ISSN
- 0009-9120
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Liver transplantation (LT) is the only curative option for patients with familial amyloid polyneuropathy (FAP) at present. Twenty patients with FAP underwent LT between May 1998 and June 2007. Transthyretin mutations included predominantly the Val30Met mutation but also 10 other mutations. Seven pat
Familial amyloidotic polyneuropathy is an inherited form of amyloidosis associated with a mutant form of a protein called transthyretin. The Methionine-30 variant is the most frequent mutation observed. This disorder is caused by deposition of this protein as amyloid in several organs, such as the h
To elucidate whether the amount of tissue-deposited amyloid in familial amyloid polyneuropathy (FAP) patients decreases or increases over the long-term course after liver transplantation (LT), we examined changes in histopathological and biochemical characteristics of abdominal fat amyloid in the tr
In patients with familial amyloidotic polyneuropathy (FAP), heart complications are prognostic factors for mortality and morbidity after liver transplantation (LT). However, only a few studies have analyzed the development of arrhythmia in transplant patients with FAP. We investigated the developmen
Familial amyloidotic polyneuropathy (FAP) patients present adrenergic cardiac input blockade secondary to amyloid deposits and sympathetic neuropathy. Consequently, their capacity to compensate for hemodynamic changes is limited. To avoid hemodynamic disturbances in sequential liver transplants, a s