TY - JOUR
T1 - Hereditary Transthyretin Amyloidosis in Austria
T2 - Clinical, Genetic, and Demographic Insights from a Nationwide Cohort
AU - Ermolaev, Nikita
AU - Löscher, Wolfgang N
AU - Verheyen, Nicolas
AU - Pölzl, Gerhard
AU - Ablasser, Klemens
AU - Agis, Hermine
AU - Binder, Christina
AU - Bonderman, Diana
AU - Cetin, Hakan
AU - Duca, Franz
AU - Griedl, Theresa Antonia
AU - Hacker, Sandra
AU - Höller, Viktoria
AU - Kammerlander, Andreas
AU - Kellermair, Lukas
AU - Kleinveld, Vera E A
AU - Kronberger, Christina
AU - Mörtl, Deddo
AU - Poledniczek, Michael
AU - Reiter, Christian
AU - Rettl, Rene
AU - Schmid, Lena Marie
AU - Schwegel, Nora
AU - Schaumberger, Elisabeth
AU - Sunder-Plassmann, Raute
AU - Ungericht, Maria
AU - Windhager, Reinhard
AU - Zimprich, Fritz
AU - Badr Eslam, Roza
AU - Auer-Grumbach, Michaela
N1 - Publisher Copyright:
© 2026 by the authors.
PY - 2026/3/4
Y1 - 2026/3/4
N2 - Background/Objectives: Hereditary transthyretin amyloidosis (ATTRv) is a heterogeneous multisystem disease caused by pathogenic transthyretin gene (TTR) variants. Increased awareness and availability of disease-modifying therapies have resulted in increased diagnoses, even in previously nonendemic regions. The aim of this study was to update the nationwide Austrian ATTRv registry by characterizing the clinical, genetic, and regional distribution of TTR variants. Methods: This multicenter, observational analysis examined ATTRv cases diagnosed in Austria between 2014 and 2025. Individuals were included according to the presence of pathogenic or likely pathogenic variants or variants of uncertain significance (VUSs) in TTR. Results: In total, 100 individuals were identified, including symptomatic and asymptomatic carriers. Compared with our previously presented data, the number of genetically confirmed ATTRv cases has more than doubled. Twenty-three TTR variants were identified. The most frequent pathologic variants were p.His108Arg (26%), p.Ile127Phe (11%), and p.Thr69Ile (9%), while p.Val113Leu (9%) represented the most frequent VUS. Significant regional clustering of p.His108Arg was documented in Vienna and Lower Austria. Other findings included a rising number of p.Val142Ile carriers and phenotypically relevant VUSs in 20 patients. Conclusions: Our findings revealed an increasing detection rate of ATTRv in a nonendemic European region. These data underscore the importance of multidisciplinary evaluation, cascade testing, and long-term monitoring to improve early diagnosis and timely management in hereditary amyloidosis.
AB - Background/Objectives: Hereditary transthyretin amyloidosis (ATTRv) is a heterogeneous multisystem disease caused by pathogenic transthyretin gene (TTR) variants. Increased awareness and availability of disease-modifying therapies have resulted in increased diagnoses, even in previously nonendemic regions. The aim of this study was to update the nationwide Austrian ATTRv registry by characterizing the clinical, genetic, and regional distribution of TTR variants. Methods: This multicenter, observational analysis examined ATTRv cases diagnosed in Austria between 2014 and 2025. Individuals were included according to the presence of pathogenic or likely pathogenic variants or variants of uncertain significance (VUSs) in TTR. Results: In total, 100 individuals were identified, including symptomatic and asymptomatic carriers. Compared with our previously presented data, the number of genetically confirmed ATTRv cases has more than doubled. Twenty-three TTR variants were identified. The most frequent pathologic variants were p.His108Arg (26%), p.Ile127Phe (11%), and p.Thr69Ile (9%), while p.Val113Leu (9%) represented the most frequent VUS. Significant regional clustering of p.His108Arg was documented in Vienna and Lower Austria. Other findings included a rising number of p.Val142Ile carriers and phenotypically relevant VUSs in 20 patients. Conclusions: Our findings revealed an increasing detection rate of ATTRv in a nonendemic European region. These data underscore the importance of multidisciplinary evaluation, cascade testing, and long-term monitoring to improve early diagnosis and timely management in hereditary amyloidosis.
UR - https://www.scopus.com/pages/publications/105032772302
U2 - 10.3390/jcm15051958
DO - 10.3390/jcm15051958
M3 - Journal article
C2 - 41827375
SN - 2077-0383
VL - 15
JO - Journal of Clinical Medicine
JF - Journal of Clinical Medicine
IS - 5
M1 - 1958
ER -