Objective. Arterial and venous thrombosis are among the clinical features o
f Behcet's disease (BD), the pathogenesis of which is not completely unders
tood. In this study, we investigated whether hyperhomocysteinaemia, being a
well known risk factor for thrombosis, is also a contributive risk factor
for the arterial and venous thrombosis of ED.
Method's. Eighty-four patients fulfilling the criteria of the International
Study Group for Behcet's Disease (54 males, 30 females, mean age 36 +/- 9
yr) were enrolled. All the patients were carefully screened for a history o
f venous thrombosis and were separated into two groups with respect to thro
mbosis history. Thirty-six healthy individuals (23 males, 13 females), matc
hed for age and sex with the ED group, were included as a negative control
group. Patients were excluded if they had any condition that might affect p
lasma homocysteine concentration. As methotrexate (MTX) causes hyperhomocys
teinaemia, we also included 29 rheumatoid arthritis patients (five males, 2
4 females) receiving MTX weekly. Fasting plasma homocysteine concentrations
were measured by high-performance liquid chromatography. The data were ana
lysed with the chi (2) test and Student's T-test.
Results. The highest homocysteine concentrations were found in the MTX grou
p (17.5 +/- 5.3 mu mol/l). Mean plasma homocysteine concentrations in ED pa
tients were significantly higher than in the healthy controls (11.5 +/- 5.3
vs 8.8 +/- 3.1 mu mol/l, P < 0.001). Among ED patients with a history of t
hrombosis, 20 of 31 (64%) had hyperhomocysteinaemia, and this was significa
ntly higher than in those without thrombosis (9%). On the other hand, there
was no significant difference between patients with non-thrombotic ED and
healthy controls (P > 0.05). In patients with thrombosis, we found no corre
lation between the duration of the postthrombotic period and homocysteine c
oncentration. Among all the variables investigated, only hyperhomocysteinae
mia was found to be related to thrombosis.
Conclusion. Hyperhomocysteinaemia may be assumed to be an independent risk
factor for venous thrombosis in ED. Unlike the factor V Leiden mutation, hy
perhomocysteinaemia is a correctable risk factor. This finding might lead t
o new avenues in the prophylaxis of thrombosis in ED.