Literature DB >> 32796279

Hereditary transthyretin amyloidosis: current treatment.

David Adams1, Michel Slama2.   

Abstract

PURPOSE OF REVIEW: Hereditary transthyretin amyloidosis (ATTRv) is a rare autosomal dominant, life-threatening disease. Until recently only early stages of ATTRv-PN (polyneuropathy) had access to disease-modifying therapy (DMT), whereas there was no specific treatment for ATTRv-CM (cardiomyopathy). This review updates our knowledge about results of three phase 3 clinical trials, expert's consensus for early diagnosis and emerging biomarkers. RECENT
FINDINGS: Two phase 3 studies using RNAi and antisense oligonucleotides (ASO) were successful. Primary endpoints were progression of neuropathic score mNIS +7 and quality of Life (QOL) in a population of ATTRv-PN at different levels of severity. They knock downed circulating amyloidogenic mutant and wild-type TTR. Safety concerned ASO with a risk of thrombocytopenia. RNAi showed possible reversibility of the disease. Phase 3 ATTRACT trial-tested tafamidis versus placebo in patients with ATTRv-CM and ATTRwt-CM and showed a significant reduction of all-cause mortality and rates of cardiovascular-related hospitalizations. All three drugs obtained marketing authorization by European Medicines Agency (EMA) and Food and drug administration (FDA). Early diagnosis criteria for ATTRv-PN and ATTRv-CM are available. Ongoing clinical trials for ATTRv are presented. New biomarkers are plasma neurofilament light chain, intraepidermal nerve fiber density.
SUMMARY: The majority of patients with ATTRv may have now access to a DMT. Criteria for early diagnosis are available.

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Year:  2020        PMID: 32796279     DOI: 10.1097/WCO.0000000000000852

Source DB:  PubMed          Journal:  Curr Opin Neurol        ISSN: 1350-7540            Impact factor:   5.710


  4 in total

1.  The integration of genetically-regulated transcriptomics and electronic health records highlights a pattern of medical outcomes related to increased hepatic transthyretin expression.

Authors:  Gita A Pathak; Antonella De Lillo; Frank R Wendt; Flavio De Angelis; Dora Koller; Brenda Cabrera Mendoza; Daniel Jacoby; Edward J Miller; Joel N Buxbaum; Renato Polimanti
Journal:  Amyloid       Date:  2021-12-22       Impact factor: 6.571

2.  ATF6 Activation Reduces Amyloidogenic Transthyretin Secretion through Increased Interactions with Endoplasmic Reticulum Proteostasis Factors.

Authors:  Jaleh S Mesgarzadeh; Isabelle C Romine; Ethan M Smith-Cohen; Julia M D Grandjean; Jeffery W Kelly; Joseph C Genereux; R Luke Wiseman
Journal:  Cells       Date:  2022-05-17       Impact factor: 7.666

3.  Muscle MRI as a Useful Biomarker in Hereditary Transthyretin Amyloidosis: A Pilot Study.

Authors:  Guido Primiano; Tommaso Verdolotti; Gabriella D'Apolito; Andrea Di Paolantonio; Valeria Guglielmino; Angela Romano; Gabriele Lucioli; Marco Luigetti; Serenella Servidei
Journal:  Genes (Basel)       Date:  2021-11-11       Impact factor: 4.096

4.  TTR Gly83Arg Mutation: Beyond Familial Vitreous Amyloidosis.

Authors:  Zhenxian Li; Kang Du; Xujun Chu; He Lv; Wei Zhang; Zhaoxia Wang; Yun Yuan; Lingchao Meng
Journal:  Front Neurol       Date:  2022-02-03       Impact factor: 4.003

  4 in total

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