In this online, self-learning activity:
Transthyretin amyloidosis (ATTR) is a progressive, multisystem, life-threatening disorder characterized by the extracellular deposition of misfolded, insoluble amyloid fibrils. As TTR is a protein present in human serum, and its role is to transport thyroxine and retinol-binding proteins, it is vital for behavior, cognition, nerve regeneration, and axonal growth. TTR itself is innately amyloidogenic even without the presence of genetic mutations. The familial variant of the disease (hATTR) is ATTR that is passed to offspring through autosomal dominant inheritance, whereas the wild type variant (wtATTR) refers to ATTR that occurs independently of genetic mutations. hATTR may present as late as mid-adulthood, but its symptoms usually start between the ages of 2 and 10 years. Left untreated, the average life expectancy of ATTR is 3 to 15 years from symptom onset.
The following HCPs: neurologists, cardiologists, and hematologists; physician assistants, nurse practitioners, nurses, and pharmacists in the aforementioned areas of specialty; and any other HCPs with an interest in or who may clinically encounter patients with ATTR.
Commercial Support Disclosure: This program is supported by an educational grant from Akcea Therapeutics.
This activity is free of charge.
Release Date: July 02, 2021 -- Expiration Date: July 01, 2023
Faculty: Michelle Kaku, MD -- Deepa Gopal, MD, MS
Introduction content: Cursory refresher and review of hATRR, including contrast wtATTR
Treatment in patients with TRR amyloidosis
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Faculty Disclosure: Michelle Kaku, MD, Assistant Professor of Neurology, Boston University, has no relevant financial disclosures.
Deepa Gopal, MD, MS, Assistant Professor of Cardiovascular Medicine, Boston University, has no relevant financial disclosures.
Disclosures of Educational Planners: Charles Turck, PharmD, BCPS, BCCCP has no relevant financial disclosures.
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Commercial Support Disclosure: This program is supported by an educational grant from Akcea Therapeutics
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