ASSESSMENT OF SERUM HOMOCYSTEINE, ENDOTHELIN-1, AND NITRIC OXIDE LEVELS IN BEHÇET’S DISEASE

Abstract

Background:

Some prominent features of Behçet’s disease (BD) are arterial and venous thromboses as a result of endothelial dysfunction. Hyperhomocysteinemia is responsible for vascular endothelial injury due to an increased frequency of thrombogenesis. Endothelin-1 (ET-1) is a vasoconstrictor whereas nitric oxide (NO) is an endothelial vasorelaxing peptide that is responsible for the inhibition of platelet adhesion.

Aim:

To evaluate serum levels of homocysteine (Hcy) and determine whether hyperhomocysteinemia is considered as a contributing risk factor for venous and arterial thromboses of BD, and to correlate serum levels of ET-1 and NO with disease activity.

Materials and Methods:

We measured serum levels of Hcy, ET-1, and nitrite (NO ₂ ⁻) in 25 patients who fulfilled the criteria of the International Study Group for BD, and compared them to those of 15 healthy control subjects. Levels of Hcy and ET-1 were measured by using enzyme-linked immunosorbent assay (ELISA), whereas serum nitrite (NO ₂ ⁻) levels were measured by using Griess reaction as an indicator for NO production. All the patients were screened for a history of venous thrombosis and subdivided into thrombotic and nonthrombotic subgroups according to their thrombotic history. Patients with BD were divided into two subgroups, active and inactive, according to their clinical and laboratory findings.

Results:

There were significant increases in serum levels of Hcy, ET-1, and nitrite in BD patients compared to those in controls. There was a significant increase in serum Hcy levels in thrombotic compared to nonthrombotic subgroups. Positive correlations were detected between the serum ET-1 and nitrite levels with disease activity in BD patients.

Conclusion:

Hyperhomocysteinemia may play some role in the development of venous and arterial thromboses in BD. Increased NO production might ave critical biological activities that are relevant to pathological events in the active period of the disease.