Early-onset Marfan syndrome (eoMFS) is a severe and rare form of Marfan syndrome characterized by severe atrioventricular valve insufficiency developing before or shortly after birth. It is unclear which factors (interventions and/or genotype) influence survival. Forty-one individuals with eoMFS with a fibrillin-1 gene (FBN1) variant in exon 24-32 (CRCh37) were included. At the last follow-up, 14/41 (34%) were alive (8 months-18 years) and 27/41 (66%) were deceased. Median age of death was 1 month and 88% of the deaths occurred before 5 months of age. More individuals alive past the age of 16 months versus those who were deceased before that age had undergone cardiovascular surgery at an older age (13 months, range 3-72, vs. 2 months, range 2-2, p = 0.03). Survival was better in those with single amino acid substitutions/small in-frame deletions than in those with large in-frame deletions (p = 0.007), but variants involving a cysteine substitution in an EGF-like domain versus those involving other amino acids did not significantly influence survival. EoMFS ranges from a (pre-)neonatal life-threatening disorder to a disorder with enhanced survival, creating a window for cardiovascular surgery. Individuals with single amino acid substitutions/small in-frame deletions had better survival compared to those with variants significantly impacting exon 24-32 length.

Download full-text PDF

Source
http://dx.doi.org/10.1111/cge.14722DOI Listing

Publication Analysis

Top Keywords

marfan syndrome
12
in-frame deletions
12
influence survival
8
exon 24-32
8
cardiovascular surgery
8
single amino
8
amino acid
8
acid substitutions/small
8
substitutions/small in-frame
8
survival
5

Similar Publications

Early-onset Marfan syndrome (eoMFS) is a severe and rare form of Marfan syndrome characterized by severe atrioventricular valve insufficiency developing before or shortly after birth. It is unclear which factors (interventions and/or genotype) influence survival. Forty-one individuals with eoMFS with a fibrillin-1 gene (FBN1) variant in exon 24-32 (CRCh37) were included.

View Article and Find Full Text PDF

Marfan syndrome (MFS) is an autosomal dominant disease caused by mutations in the gene (FBN1) of fibrillin-1, a major determinant of the extracellular matrix (ECM). Functional impairment in the cardiac left ventricle (LV) of these patients is usually a consequence of aortic valve disease. However, LV passive stiffness may also be affected by chronic changes in mechanical load and ECM dysfunction.

View Article and Find Full Text PDF

Corneal Biomechanics Are Associated With FBN1 Mutations in Patients With Marfan Syndrome and Ectopia Lentis.

Invest Ophthalmol Vis Sci

March 2025

Eye Institute and Department of Ophthalmology, Eye & ENT Hospital, Fudan University, Shanghai, China.

Background: We investigated the corneal biomechanical properties and their genotype-phenotype correlation correlations in patients with Marfan syndrome (MFS) and ectopia lentis (EL).

Methods: Patients with MFS with EL underwent panel-based next-generation sequencing in this retrospective cohort study. The FBN1 genotypes were categorized into the dominant-negative (DN) group and the haploinsufficiency (HI) group.

View Article and Find Full Text PDF

Purpose Phenotype-based ascertainment of probands in studies of Mendelian disorders may exclude individuals with mild phenotypes or that lack health care access. We explore this premise in All of Us Research Program participants with pathogenic variation causal for three Mendelian conditions: autosomal dominant polycystic kidney disease (ADPKD), Marfan syndrome, and neurofibromatosis type 1 (NF1). Methods We identified All of Us Research Program participants with putatively pathogenic variation in NF1, FBN1, PKD1, and PKD2.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!