TY - JOUR
T1 - Genetic analysis and natural history of Charcot-Marie-Tooth disease CMTX1 due to GJB1 variants
AU - Inherited Neuropathies Consortium-Rare Disease Clinical Research Network
AU - Record, Christopher J.
AU - Skorupinska, Mariola
AU - Laura, Matilde
AU - Rossor, Alexander M.
AU - Pareyson, Davide
AU - Pisciotta, Chiara
AU - Feely, Shawna M.E.
AU - Lloyd, Thomas E.
AU - Horvath, Rita
AU - Sadjadi, Reza
AU - Herrmann, David N.
AU - Li, Jun
AU - Walk, David
AU - Yum, Sabrina W.
AU - Lewis, Richard A.
AU - Day, John
AU - Burns, Joshua
AU - Finkel, Richard S.
AU - Saporta, Mario A.
AU - Ramchandren, Sindhu
AU - Weiss, Michael D.
AU - Acsadi, Gyula
AU - Fridman, Vera
AU - Muntoni, Francesco
AU - Poh, Roy
AU - Polke, James M.
AU - Zuchner, Stephan
AU - Shy, Michael E.
AU - Scherer, Steven S.
AU - Reilly, Mary M.
AU - Abreu, Lisa
AU - Anderson, Kimberly A.
AU - Baratta, Silvia
AU - Berry, Debbie
AU - Blake, Julian
AU - Cavalca, Eleonora
AU - Cornett, Kayla
AU - Cortese, Andrea
AU - Donlevy, Gabrielle
AU - Dragon, Amanda
AU - Dudziec, Magdalena
AU - Estilow, Katy Eichinger Tim
AU - Ferment, Valerie
AU - Grant, Natalie
AU - Grider, Tiffany
AU - Hyslop, Emily
AU - Jones, Tara
AU - Kressin, Nicole
AU - Leon, Wendy
AU - Magri, Stefania
N1 - Publisher Copyright:
© The Author(s) 2023.
PY - 2023/10/1
Y1 - 2023/10/1
N2 - Charcot-Marie-Tooth disease (CMT) due to GJB1 variants (CMTX1) is the second most common form of CMT. It is an X-linked disorder characterized by progressive sensory and motor neuropathy with males affected more severely than females. Many reported GJB1 variants remain classified as variants of uncertain significance (VUS). In this large, international, multicentre study we prospectively collected demographic, clinical and genetic data on patients with CMT associated with GJB1 variants. Pathogenicity for each variant was defined using adapted American College of Medical Genetics criteria. Baseline and longitudinal analyses were conducted to study genotype-phenotype correlations, to calculate longitudinal change using the CMT Examination Score (CMTES), to compare males versus females, and pathogenic/likely pathogenic (P/LP) variants versus VUS. We present 387 patients from 295 families harbouring 154 variants in GJB1. Of these, 319 patients (82.4%) were deemed to have P/LP variants, 65 had VUS (16.8%) and three benign variants (0.8%; excluded from analysis); an increased proportion of patients with P/LP variants compared with using ClinVar's classification (74.6%). Male patients (166/319, 52.0%, P/LP only) were more severely affected at baseline. Baseline measures in patients with P/LP variants and VUS showed no significant differences, and regression analysis suggested the disease groups were near identical at baseline. Genotype-phenotype analysis suggested c.-17G>A produces the most severe phenotype of the five most common variants, and missense variants in the intracellular domain are less severe than other domains. Progression of disease was seen with increasing CMTES over time up to 8 years follow-up. Standard response mean (SRM), a measure of outcome responsiveness, peaked at 3 years with moderate responsiveness [change in CMTES (ΔCMTES) = 1.3 ± 2.6, P = 0.00016, SRM = 0.50]. Males and females progressed similarly up to 8 years, but baseline regression analysis suggested that over a longer period, females progress more slowly. Progression was most pronounced for mild phenotypes (CMTES = 0-7; 3-year ΔCMTES = 2.3 ± 2.5, P = 0.001, SRM = 0.90). Enhanced variant interpretation has yielded an increased proportion of GJB1 variants classified as P/LP and will aid future variant interpretation in this gene. Baseline and longitudinal analysis of this large cohort of CMTX1 patients describes the natural history of the disease including the rate of progression; CMTES showed moderate responsiveness for the whole group at 3 years and higher responsiveness for the mild group at 3, 4 and 5 years. These results have implications for patient selection for upcoming clinical trials.
AB - Charcot-Marie-Tooth disease (CMT) due to GJB1 variants (CMTX1) is the second most common form of CMT. It is an X-linked disorder characterized by progressive sensory and motor neuropathy with males affected more severely than females. Many reported GJB1 variants remain classified as variants of uncertain significance (VUS). In this large, international, multicentre study we prospectively collected demographic, clinical and genetic data on patients with CMT associated with GJB1 variants. Pathogenicity for each variant was defined using adapted American College of Medical Genetics criteria. Baseline and longitudinal analyses were conducted to study genotype-phenotype correlations, to calculate longitudinal change using the CMT Examination Score (CMTES), to compare males versus females, and pathogenic/likely pathogenic (P/LP) variants versus VUS. We present 387 patients from 295 families harbouring 154 variants in GJB1. Of these, 319 patients (82.4%) were deemed to have P/LP variants, 65 had VUS (16.8%) and three benign variants (0.8%; excluded from analysis); an increased proportion of patients with P/LP variants compared with using ClinVar's classification (74.6%). Male patients (166/319, 52.0%, P/LP only) were more severely affected at baseline. Baseline measures in patients with P/LP variants and VUS showed no significant differences, and regression analysis suggested the disease groups were near identical at baseline. Genotype-phenotype analysis suggested c.-17G>A produces the most severe phenotype of the five most common variants, and missense variants in the intracellular domain are less severe than other domains. Progression of disease was seen with increasing CMTES over time up to 8 years follow-up. Standard response mean (SRM), a measure of outcome responsiveness, peaked at 3 years with moderate responsiveness [change in CMTES (ΔCMTES) = 1.3 ± 2.6, P = 0.00016, SRM = 0.50]. Males and females progressed similarly up to 8 years, but baseline regression analysis suggested that over a longer period, females progress more slowly. Progression was most pronounced for mild phenotypes (CMTES = 0-7; 3-year ΔCMTES = 2.3 ± 2.5, P = 0.001, SRM = 0.90). Enhanced variant interpretation has yielded an increased proportion of GJB1 variants classified as P/LP and will aid future variant interpretation in this gene. Baseline and longitudinal analysis of this large cohort of CMTX1 patients describes the natural history of the disease including the rate of progression; CMTES showed moderate responsiveness for the whole group at 3 years and higher responsiveness for the mild group at 3, 4 and 5 years. These results have implications for patient selection for upcoming clinical trials.
KW - ACGS
KW - ACMG
KW - CMT1X
KW - Cx32
KW - connexin 32
UR - http://www.scopus.com/inward/record.url?scp=85168384640&partnerID=8YFLogxK
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U2 - 10.1093/brain/awad187
DO - 10.1093/brain/awad187
M3 - Article
C2 - 37284795
AN - SCOPUS:85168384640
SN - 0006-8950
VL - 146
SP - 4336
EP - 4349
JO - Brain
JF - Brain
IS - 10
ER -