Soluble P-selectin levels in diabetes mellitus patients with coronary artery disease.

UNLABELLED: Type 2 (non-insulin-dependent) diabetes is associated with a marked increase in the risk of coronary heart disease. Platelets play a significant role in coronary artery disease. Soluble P-selectin is an index of platelets activation. In this study, Soluble P-selectin levels were measured by ELISA in the peripheral blood of 55 diabetic patients with coronary artery disease [21 acute myocardial infarction (AMI), 20 with unstable angina (UA), 14 with stable angina (SA)], 20 patients with diabetes mellitus without coronary artery disease (DM without), and 10 healthy controls. Soluble P-selectin level was significantly higher in patients with AMI (M+/-SD; 239.3+/-13.0 ng/ml), than those with UA (141.5+/-15.2 ng/ml), SA (92.1+/-7.7 ng/ml), DM without (89.8+/-7.1 ng/ml), and healthy control (86.1+/-4.5 ng/ml) (P < 0.001). In patients with US, sP-selectin was found to be significantly elevated as compared to the SA, DM without and control group. sP-selectin was not significantly different in DM without as compared to healthy controls. The sP-selectin levels was correlated to the duration of diabetes mellitus(R=0.33, P=0.03 ). Moreover, sP-selectin level was significantly higher in AMI patients with recurrent anginal attack as compared to that in those with single attack Multivariate analysis revealed that sP-selectin level at presentation had high adverse influence on coronary artery insult compared to healthy LDL cholesterol level, and the degree of hypertension. IN CONCLUSION: Plasma levels of soluble P-selectin were increased in patients with AMI, and UA compared to patients with SA and normal controls. Measurement of soluble P-selectin may be helpful marker of impending coronary artery insult in diabetic patients.

Accelerated neutrophil apoptosis in neutropenic patients with hepatosplenic schistosomiasis is induced by serum Fas ligand.

Neutropenia in patients with hepatosplenic (HS) schistosomiasis may stem from enhanced neutrophil apoptosis. However, the molecular mechanism of neutrophil apoptosis has not been clearly defined. Neutrophils harvested from neutropenic patients with HS schistosomiasis (n = 25), non-neutropenic patients with hepatointestinal (HI) schistosomiasis (n = 10), and age- and sex-matched healthy control subjects (n = 10) were examined for the degree of apoptosis after incubation with autologous sera. Neutrophil apoptosis was quantified by flow cytometry through determination of propidium iodide nuclear staining and confirmed by DNA gel electrophoresis at 0 time (fresh neutrophil), 4 and 24 h culture. Neutrophils from healthy subjects were also incubated with either 10% heterologous normal or neutropenic serum, with and without anti-Fas ligand antibody. Serum Fas ligand levels were assessed in sera of patient groups and healthy controls by ELISA. Compared with normal controls and HI, HS group demonstrated greater neutrophil apoptosis in the presence of autologous serum (P < 0.01, < 0.05, respectively). Furthermore, compared with normal neutrophils exposed to heterologous normal serum, those exposed to heterologous neutropenic serum exhibited higher apoptosis rates (P < 0.01). The apoptotic effect of neutropenic sera is attenuated by anti-Fas ligand. Fas expression was significantly higher in HS group as compared to both HI and normal healthy controls (P < 0.05). Serum Fas ligand levels were significantly higher among HS group as compared to both HI and control groups (P < 0.01 for both). Neutrophil apoptosis was not correlated to the size of spleen in HS group. In conclusion, the rate of neutrophil apoptosis is accelerated in neutropenic HS schistosomiasis. These findings suggest that enhanced neutrophil apoptosis demonstrated in HS patients is triggered by soluble Fas ligand, which is mostly derived from spleen.