Background Galectin‑3 protein that is encoded by lectin galactoside-binding soluble-3 (LGALS-3) gene serves as an important genetic factor in type 2 diabetes mellitus (T2DM) and its cardiovascular obstacles in various populations. We aimed to elicit the pro-inflammatory effect of galectin-3 as determined by interleukin-6 (IL-6) serum levels and to explore the relationship between galectin-3 (LGALS-3 rs4652) gene variation and its expression levels with coronary artery disease (CAD) risk among T2DM Egyptian patients. Methods:  112 lean subjects were compared to 100 T2DM without CAD and 84 T2DM with CAD. A tetra-primer amplification refractory mutation system polymerase chain reaction was used to test LGALS-3 (rs4652) and galectin-3 expression was tested with a quantitative real-time polymerase chain reaction. Serum IL-6 was measured using an enzyme-linked immunosorbent assay. Results: We found that the prevalence of LGALS-3 (rs4652) AC genotype and galectin-3 gene expression levels in T2DM with CAD were significantly higher than the additional 2 groups and were correlated positively to IL-6 circulating levels also, the C allele carriers (AC+CC) had significantly higher relative Galectin-3 expression levels compared to the A allele carriers (AA). Conclusion:  We concluded that galectin-3 expression levels and LGALS-3 (rs4652) AC genotype were coronary artery disease risk factors in type two diabetics among an Egyptian sample.

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Background: Vascular calcification (VC) plays a major role in cardiovascular disease (CVD), which is one of the main causes of mortality in patients with chronic kidney disease (CKD). During the early stages of CKD, Fibroblast growth factor-23 (FGF-23) levels increase to keep serum phosphorus within the normal range. FGF23 may be associated with death and cardiovascular events in CKD patients. Aim: The study aimed at early detection of breast arterial calcification (BAC) and higher levels of FGF-23 as indicators of systemic VC in patients with different stages of CKD. Methodology: The patients were divided into 3 groups; representing stages 2, 3 & 4 of CKD women, and the 4 th group was considered as a control group. The selected participants were subjected to history taking, mammogram to detect BAC and biochemical assessment of lipid profile, Serum creatinine, Mg, P, Ca, PTH and FGF23. Results: the presence of BAC in about 81.8% of stage 4 CKD patients compared with 50% in stage 3 CKD, also in the majority of stage 4 CKD patients had high FGF-23. Receiver operator characteristic (ROC) curve analysis showed serum FGF-23 as a potential predictor of BAC (AUC=0.874) in CKD patients at the cut-off point of 77.5ng/ml (sensitivity 78%, specificity 76%). Conclusion: Although it is difficult to determine the definite stage at which the risk of VC begins but, in our study, it began late in stage 2 CKD, gradually increased prevalence through stage 3, and became significantly higher in stage 4. FGF-23 could be a good predictor of BAC in CKD