Ayoub KOURIMA

Mr. Ayoub KOURIMA

Faculty of Medicine and Pharmacy, Cadi Ayyad University, Marrakesh, Morocco
orcid

Research Focus & Metrics

Academic Career Length

1Year (2026-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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12 October 2026 in Antioxidants
Verified
Journal Article
Open access
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BKBeata Krasinska
Beata Krasinska
Tomasz UrbanowiczTomasz Urbanowicz
Tomasz Urbanowicz
MKMinseung Kang
Minseung Kang
SBSiwon Baek
Siwon Baek
AKAyoub KOURIMA
Ayoub KOURIMA
ATAndrzej Tykarski
Andrzej Tykarski
Background: ELAFIN (peptidase inhibitor 3, PI3) is an endogenous inhibitor of neutrophil elastase and proteinase 3, but its circulating profile in type 2 diabetes mellitus (T2DM) and cardiovascular disease remains poorly characterized. We investigated circulating ELAFIN in patients undergoing elective coronary angiography and explored its associations with metabolic, inflammatory, renal, cardiac, and angiographic phenotypes. Methods: Forty-three consecutive clinically stable patients undergoing elective coronary angiography, including nine with T2DM, were prospectively enrolled. Plasma ELAFIN was quantified by ELISA. Associations with clinical and laboratory variables were assessed using non-parametric comparisons, correlation analyses, and parsimonious multivariable regression. Discrimination analyses were considered exploratory. Results: Median ELAFIN was 5.03-fold higher in patients with T2DM than in those without T2DM (31.2 [28.3–36.2] vs. 6.2 [5.5–7.0] ng/mL; p < 0.001; Cliff’s δ = 0.85). The association remained pronounced after adjustment for age, sex, and renal function. ELAFIN was positively correlated with REG3A and creatinine, and inversely correlated with eGFR, whereas no significant associations were observed with angiographic coronary stenosis, LVEF, or NT-proBNP. Conclusions: Circulating ELAFIN was markedly elevated in T2DM and associated predominantly with renal and inflammatory characteristics rather than anatomical coronary disease or left ventricular dysfunction. Because oxidative stress and protease activity were not directly measured, their relationship with ELAFIN remains hypothesis-generating. These findings require validation in larger prospective cohorts.