Serum leptin and adiponectin in cerebrovascular disorders

الملخص EN

Background: cerebrovascular stroke is one of the major causes of morbidity and mortality worldwide.

Ischemic cerebrovascular disease is a common complication of atherosclerosis.

Also, atherosclerosis is considered the underlying cause of transient ischemic attack (TIA) which is an important determinant of ischemic stroke.

Adiponectin and leptin are two adipocytokines that were suggested to play a role in insulin resistance, and hence in endothelial dysfunction.

So, they may be involved in atherosclerotic diseases such as ischemic stroke. Objective: the aim of this study was to assess the role of both leptin and adiponectin as well as homeostasis model assessment for insulin resistance (HOMA-IR) in atherosclerotic cerebrovascular disease and to assess their clinical utility in differentiation between patients with TIA, and those with ischemic stroke.

Moreover, the influence of atherosclerotic risk factors namely, diabetes mellitus (DM), hypertension, dyslipidemia and smoking on serum leptin and adiponectin levels was also studied in both groups of patients.

Study design: this study was conducted on thirty-three patients with TIA (aged 39-51 years), thirty patients with ischemic stroke (aged 40-53 years) and 20 age and sex matched healthy controls.

All studied individuals were subjected to history taking with stress on the history of smoking, hypertension and diabetes mellitus.

Clinical and neurological examination.

Serum glucose, lipid profile including total cholesterol, HDL-C, LDL-C and triglycerides were assayed on the Synchron Cx7 auto-analyzer.

Serum leptin, adiponectin and insulin were assayed using sandwich enzyme immunoassay technique.

Lastly, HOMA-IR; index of insulin resistance, was calculated.

Results: serum adiponectin was significantly decreased in both patients groups as compared to the control group (P<0.001, respectively).

It was significantly lower in ischemic stroke patients than in TIA patients (P<0.05).

Serum fasting insulin (FI), HOMA-IR and leptin were significantly increased in both studied groups as compared to the control group (P<0.001, respectively).

Furthermore, serum fasting insulin and HOMA-IR were significantly higher in ischemic stroke patients than in TIA patients (P<0.001, respectively).

The correlation study revealed a significant negative correlation between adiponectin and each of fasting glucose, FI, HOMA-IR, total cholesterol, LDL-C and triglycerides, in addition to a significant positive correlation with HDL-C in both studied groups (P<0.05).

On the other hand, a significant positive correlation between serum leptin and each of FI, HOMA-IR, total cholesterol and triglycerides was revealed in both patients’ groups.

In addition, there was a significant positive correlation with LDL-C in ischemic stroke patients (P<0.05).

One way ANOVA revealed that increased number of atherosclerotic risk factors (DM hypertension, dyslipidemia and smoking) resulted in a significant difference in both serum leptin and adiponectin levels in both studied patients’ groups.

ROC curve analysis revealed that serum adiponectin at a cut-off (3.9 μg / mL) showed a superior performance over other parameters in discriminating ischemic stroke patients with a sensitivity (70%), specificity (100%) and diagnostic efficiency (75%).

Furthermore, the combined use of both adiponectin at cut-off (3.9 μg / mL) and HOMA-IR at cut-off (4) improved both the sensitivity and efficiency into 76% and 83% respectively.

In conclusion, hyperleptinemia and hypoadiponectinemia are associated with increased risk of ischemic stroke and transient ischemic attack.

Serum adiponectin in conjunction with HOMA-IR can help in differentiation between ischemic stroke patients from those with transient ischemic attack and may help in predicting patients at risk to develop ischemic stroke.

Finally, hyperleptinemia and hypoadiponectinemia may accelerate the vascular complications in diabetic, hypertensive, dyslipidemic and smoking patients.