Ayoub Kourima
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Ayoub Kourima has a total of 16 co-authors. Here are the top co-authors by number of shared publications:
- Andrzej Tykarski
Department of Hypertensiology, Angiology, and Internal Medicine, Poznan University of Medical Sciences, ½ Dluga Street, 61-848 Poznan, Poland
1 shared publication - Beata Krasińska
Department of Hypertensiology, Angiology, and Internal Medicine, Poznan University of Medical Sciences, ½ Dluga Street, 61-848 Poznan, Poland
1 shared publication - Calogera Pisano
Department of Precision Medicine in Medical Surgical and Critical Area (Me.Pre.C.C.), University of Palermo, 90134 Palermo, Italy
1 shared publication - Ewelina Wojtasińska
Department of Hematology, Transplantation and Cellular Therapy, Poznan University of Medical Sciences, 84 Szamarzewskiego Street, 60-569 Poznan, Poland
1 shared publication - Giuseppe Maria Raffa
Department of Precision Medicine in Medical Surgical and Critical Area (Me.Pre.C.C.), University of Palermo, 90134 Palermo, Italy
1 shared publication - Joanna Kujawska
Department of Hematology, Transplantation and Cellular Therapy, Poznan University of Medical Sciences, 84 Szamarzewskiego Street, 60-569 Poznan, Poland
1 shared publication
Latest Publications
- Open Access
- 12 October 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (10) , 1315
Circulating ELAFIN Is Associated with a Distinct Renal–Inflammatory Phenotype in Type 2 Diabetes Mellitus
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.
- 12 October 2026
- Published by MDPI AG in Antioxidants
- Vol. 15 (10) , 1315
Open AccessCirculating ELAFIN Is Associated with a Distinct Renal–Inflammatory Phenotype in Type 2 Diabetes Mellitus
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.