There were no safety findings associated with vitamin A deficiency following treatment with patisiran or vutrisiran in patients with transthyretin (TTR) amyloidosis (ATTR), according to a pooled analysis of clinical trials and post-marketing data presented at the Heart Failure 2026 meeting in Barcelona, Spain.
“Alternative pathways independent of TTR facilitate vitamin A transport,” the researchers concluded.
A Columbia University research team, led by Thomas H. Brannagan, MD, set out to determine if TTR-lowering treatments are associated with adverse events caused by vitamin A deficiency in patients with TTR-mediated amyloid cardiomyopathy (ATTR-CM) or TTR amyloid poluneuropathy (ATTR-PN). Looking at 5 clinical trials spanning patients with ATTR-CM and ATTR-PN, the investigators analyzed outcomes from 613 patients treated with patisiran, 709 with vutrisiran, and 583 who received a placebo.