Assessment of Surrogate Markers for Cardiovascular Disease in Familial Mediterranean Fever-Related Amyloidosis Patients Homozygous for M694V Mutation in MEFV Gene
Tarih
2022Yazar
Sezer, Siren
Demirkaya, Erkan
Yilmaz, Ilker
Poddighe, Dimitri
KASAPÇOPUR, ÖZGÜR
Appleton, C. Thomas
ŞAHİN, SEZGİN
Romano, Micol
Guzel, Ferhat
Piskin, David
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Cardiovascular disease (CVD) remains underestimated in familial Mediterranean fever-associated AA amyloidosis (FMF-AA). We aimed to compare early markers of endothelial dysfunction and atherosclerosis in FMF-AA with a homozygous M694V mutation (Group 1 = 76 patients) in the Mediterranean fever (MEFV) gene and in patients with other genotypes (Group 2 = 93 patients). Measures of increased risk for future CVD events and endothelial dysfunction, including flow-mediated dilatation (FMD), pentraxin-3 (PTX3), and carotid intima-media thickness (cIMT), and fibroblast growth factor 23 (FGF23) as a marker of atherosclerotic vascular disease were compared between groups. The frequency of clinical FMF manifestations did not differ between the two groups apart from arthritis (76.3% in Group 1 and 59.1% in Group 2, p < 0.05). FMD was significantly lower in Group 1 when compared with Group 2 (MD [95% CI]: -0.6 [(-0.89)-(-0.31)]). cIMT, FGF23, and PTX3 levels were higher in Group 1 (cIMT MD [95% CI]: 0.12 [0.08-0.16]; FGF23 MD [95% CI]: 12.8 [5.9-19.6]; PTX3 MD [95% CI]: 13.3 [8.9-17.5]). In patients with FMF-AA, M694V homozygosity is associated with lower FMD values and higher cIMT, FGF23, and PTX3 levels, suggesting increased CVD risk profiles. These data suggest that a genotype-phenotype association exists in terms of endothelial dysfunction and atherosclerosis in patients with FMF-AA.
Bağlantı
http://hdl.handle.net/20.500.12627/184137https://avesis.istanbul.edu.tr/api/publication/a903f69e-3a4b-4bc5-a9b9-c6e13c7df9d2/file
https://doi.org/10.3390/life12050631
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