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Browsing Articles by Subject "AA amyloidosis"

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    ANTI-INFLAMMATORY, ANTIOXIDANT, AND ANTI-ATHEROSCLEROTIC EFFECTS OF NATURAL SUPPLEMENTS ON PATIENTS WITH FMF-RELATED AA AMYLOIDOSIS: A NON-RANDOMIZED 24-WEEK OPEN-LABEL INTERVENTIONAL STUDY
    (life, 2022) Romano, Micol; Garcia-Bournissen, Facundo; Piskin, David; Rodoplu, Ulkumen; Piskin, Lizzy; Elzagallaai, Abdelbaset A.; Tuncer, Tunc; Sezer, Siren; Ucuncuoglu, Didar; Honca, Tevfik; Poddighe, Dimitri; Yavuz, Izzet; Stenvinkel, Peter; Yilmaz, Mahmut Ilker; Demirkaya, Erkan
    We aimed to evaluate the effect of a combination of natural products on parameters related to inflammation, endothelial dysfunction, and oxidative stress in a cohort of familial Mediterranean fever (FMF) patients with Serum Amyloid A amyloidosis, in a non-randomized, 24-week open-label interventional study. Morinda citrifolia (anti-atherosclerotic-AAL), omega-3 (anti-inflammatory-AIC), and extract with Alaskan blueberry (antioxidant-AOL) were given to patients with FMF-related biopsy-proven AA amyloidosis. Patients were >18 years and had proteinuria (>3500 mg/day) but a normal estimated glomerular filtration rate (eGFR). Arterial flow-mediated dilatation (FMD), carotid intima media thickness (CIMT), and serum biomarkers asymmetric dimethylarginine (ADMA), high sensitivity C-reactive protein (hs-CRP), pentraxin (PTX3), malondialdehyde (MDA), Cu/Znsuperoxide dismutase (Cu/Zn-SOD), and glutathione peroxidase (GSH-Px) were studied at baseline and after 24 weeks of treatment. A total of 67 FMF-related amyloidosis patients (52 male (77.6%); median age 36 years (range 21–66)) were enrolled. At the end of a 24-week treatment period with AAL, AIC, and AOL combination therapy, ADMA, MDA, PTX3, hsCRP, cholesterol, and proteinuria were significantly decreased compared to baseline, while CuZn-SOD, GSH-Px, and FMD levels were significantly increased. Changes in inflammatory markers PTX3, and hsCRP were negatively correlated with FMD change, and positively correlated with decreases in proteinuria, ADMA, MDA, cholesterol, and CIMT. Treatment with AAL, AIC and AOL combination for 24 weeks were significantly associated with reduction in inflammatory markers, improved endothelial functions, and oxidative state. Efficient control of these three mechanisms can have long term cardiovascular and renal benefits for patients with AA amyloidosis.
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    ItemOpen Access
    ASSESSMENT OF SURROGATE MARKERS FOR CARDIOVASCULAR DISEASE IN FAMILIAL MEDITERRANEAN FEVER-RELATED AMYLOIDOSIS PATIENTS HOMOZYGOUS FOR M694V MUTATION IN MEFV GENE
    (Life, 2022) Sahin, Sezgin; Romano, Micol; Guzel, Ferhat; Piskin, David; Poddighe, Dimitri; Sezer, Siren; Kasapcopur, Ozgur; Appleton, C. Thomas; Yilmaz, Ilker; Demirkaya, Erkan
    Cardiovascular disease (CVD) remains underestimated in familial Mediterranean feverassociated 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 flowmediated 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.