Osteopontin (OPN), a bone-related protein, is present within the atherosclerotic plaques, most strikingly in calcified plaques. Valvular calcifications are accepted as a part of the spectrum of atherosclerosis and are associated with atherosclerotic calcification in the coronary arteries. The study aimed to evaluate the association of plasma OPN with the presence and extent of coronary stenosis, mitral annular calcification (MAC), and aortic valve sclerosis in stable angina patients. We studied 120 subjects who underwent coronary angiography because of ischemic chest pain. Coronary artery disease (CAD) was defined as > or = 50% stenosis in > or = 1 coronary artery. MAC and aortic valve sclerosis were detected by echocardiography. Lipid profile, high sensitive C-reactive protein (hsCRP), and OPN were measured in all studied subjects. Patients with CAD had increased plasma OPN when compared with those without CAD (P < 0.001). Plasma OPN levels were significantly positively correlated with atherogenic lipid profile, hsCRP, MAC grading, aortic valve sclerosis grading, and the number of stenosed coronary vessels in CAD patients. In multivariate analysis, OPN was an independent predictor of CAD (P = 0.01), MAC (P = 0.01), and aortic valve sclerosis (P = 0.04). In conclusion, OPN is an independent predictor of MAC and aortic valve sclerosis. Plasma OPN levels reflect the extent of coronary stenosis and can be used as a biomarker to identify patients with coronary atherosclerosis.

Background and Aims: Inflammatory bowel diseases (IBD) have been reported to be caused by a complex interplay of immunological, infectious, and genetic factors. Previous studies have suggested that adipokines play a role in IBD by inducing proinflammatory cytokines. We aimed to evaluate the role of visfatin in the diagnosis algorithm of active IBD. Methods: 85 newly diagnosed IBD patients [56 diagnosed with ulcerative colitis (UC) and 29 with Crohn‘s disease (CD)] and 30 healthy controls were included. IBD phenotypes were described accordingly to Montreal classification. Hemoglobin, total leucocytic count (TLC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), albumin, fecal calprotectin and serum visfatin were measured. Results: The serum visfatin level was found to be significantly higher in patients with IBD than those in the control group (p<0.001). It was significantly positively correlated with CRP, ESR, and FC in both IBD groups. Receiver operating characteristic curve analysis of visfatin in diagnosis of UC revealed an area under curve of 0.911. At cutoff ≥1.4 ng/ml, the sensitivity was 92.9% and the specificity was 86.7%.. In CD group, at the same cutoff, AUC was 0.974, sensitivity was 96.6% and specificity was 86.7%. There was a statistically significant elevation of serum visfatin in extensive UC (E3) as compared to the other groups. A cutoff ≥3.25 ng/ml revealed 88.9% sensitivity, and 100% specificity in detection of E3 UC. Serum visfatin was significantly increased in CD stricturing phenotype (B2) as compared to non-stricturing non-penetrating CD (B1). A cutoff ≥3.5 ng/ml revealed 83.3% sensitivity, and 100% specificity in detection of B2. Conclusions: The serum visfatin level were significantly higher in patients with IBD than in controls. Serum visfatin might be a novel noninvasive marker to detect activity in IBD patients and can be used as predictor of disease extension in patients with UC.

Background: Fragile histidine triad (FHIT) gene is a tumor suppressor gene which involved in breast cancer pathogenesis. Epigenetics alterations in FHIT contributes to tumorigenesis of breast cancer. Objective: Our objective was to study FHIT promoter region hypermethylation in Egyptian breast cancer patients and its association with clinicopathological features. Materials and Methods: Methylation-specific polymerase chain reaction was performed to study the hypermethylation of FHIT promoter region in 20 benign breast tissues and 30 breast cancer tissues. Results: The frequency of hypermethylation of FHIT promoter region was significantly increased in breast cancer patients compared to bengin breast disease patients. The Odd´s ratio (95%CI) of development of breast cancer in individuals with FHIT promoter hypermethylation (MM) was 11.0 (1.22-250.8). There were also significant associations between FHIT promoter hypermethylation and estrogen, progesterone receptors negativity, tumor stage and nodal involvment in breast cancer pateints. Conclusions: Our results support an association between FHIT promotor hypermethylation and development of breast cancer in Egyptian breast cancer patients. FHIT promoter hypermethylation is associated with some poor prognostic features of breast cancer.

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