CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 2, March/April 2014
64
AFRICA
Germany). High-density lipoprotein cholesterol (HDL-C) levels
were detected following sodium phosphotungustate–magnesium
chloride precipitation. LDL-C levels were calculated according
to the Friedwald formula. Leukocyte, platelet, erythrocyte, white
blood cell, haematocrit and haemoglobin counts were performed
by Sysmex 9000 (Roche Diagnostics) device.
Coagulation screening tests, coagulation factors, inhibitors
and fibrinolysis tests were performed using the Dade Behring
System (BCS, Dade Behring, Marburg, Germany) as follows:
•
Prothrombin time (PT) and active partial thromboplastin time
(aPTT) were measured using conventional methods and the
results were saved on a coagulometer (BCS, Dade Behring).
•
D-dimer levels were measured with the Plus D-dimer test
(Dade Behring) method. This is a turbidometric test enriched
with latex, which was developed for quantitative analysis of
cross-linked fibrin degradation products in human plasma. It
is done by a Dade Behring coagulation analyser device.
•
Coagulation factors (F VII, F VIII, F IX, F X, F XI and F
XII) were measured by coagulometric methods and
in vitro
diagnostic devices.
•
The activated protein:C resistance ratio (APCR) was meas-
ured using a modified APC kit and automatic coagulometer
(BCS, Dade Behring).
•
In order to identify the von Willebrand factor ristocetin
co-factor activity in human plasma, the thrombocyte agglu-
tination method and
in vitro
diagnostic devices were used.
•
Antithrombin activity was measured using a Berichom ATIII
using the synthetic chromogenic substrate method.
•
Protein C and S activities were measured with a coagulomet-
ric method.
•
Plasminogen and antiplasmin activities were measured using
a chromogenic substrate method.
•
Lupus anticoagulants were identified using modified dilute
Russell viper venom (LA scanning separator/LA2 conforma-
tion separator).
•
Fibrinogen levels were identified using Claus methods.
•
Plasminogen activator inhibitor levels were identified with
activity-based functional tests.
Results
The demographic variables and Behcet’s disease criteria are
shown in Table 1. In the venous system, three patients had lower
extremity deep-vein thrombosis (in one patient it was bilaterally).
These three patients had ocular involvement. One patient had
superior caval venous and bilaterally internal jugular venous
thrombosis. Three patients had thrombosis in the vena saphena
magna. Deep venous insufficiency was seen in 16 patients.
In the arterial system, iliac artery occlusion was seen in
one patient (this patient had in-stent stenosis and a history of
balloon angioplasty). Three patients had carotid artery–intimal
hyperplasia.
Echocardiography: left ventricular systolic/diastolic diameter
was 4.2–6/4.3–6 cm, the aortic annulus was 4 cm in two patients,
six patients had 2+ aortic valve insufficiency, and three patients
had 1+ mitral valve insufficiency. Aortic valve involvement was
16%; 24 patients (63%) had venous insufficiency, three had
deep-vein thrombosis (they all also had ocular involvement).
One patient had superior vena caval and bilaterally internal
jugular venous thrombosis and ocular involvement. One patient
had iliac arterial thrombosis and stent history. Three patients had
carotid artery intimal hyperplasia.
Table 2 shows laboratory results for coagulation and lipid
parameters.
Discussion
Behcet’s disease is a multi-systemic inflammatory disorder.
Autoimmune factors are involved in its aetiology. Immune
fluorescence studies revealed IgM, IgG and
β
1 globulin on the
vascular endothelial walls and the serum contained increased
amounts of IgD, IgG, IgM, C1, C2, C3, C4 and immune
complexes. The increased prevalence of the HLA-B5 tissue gene
group suggests a genetic role as aetiological factor.
13-15
Vascular Behcet’s disease occurs more frequently in patients
with ocular involvement. Behcet’s disease is a non-specific
vasculitis involving both veins and arteries. Infiltration of
lymphocytes, mononuclear cells and mast cells can be observed
around the blood vessels, causing endothelial swelling and
fibrinoid degeneration. Venous system involvement is mostly
seen as thrombosis and/or varicosis.
Table 1. Demographic variables and criteria
for Behcet’s disease.
Parameters
n
(%)
Age (years)
37.8 (33.8–41.7)
Gender (male/female)
24/14
Time since the diagnosis (years)
7.6 (6.1–9.1)
Recurrent oral ulcer (%)
38 (100)
Genital ulcer (%)
24 (63)
Arthralgia (%)
31 (84)
Leather findings (%)
23 (62)
Eye involvement (%)
4 (10.5)
Positive Paterji test (%)
12 (3.2)
Table 2. Laboratory findings for coagulation and lipid
parameters.
Parameter
s
Mean
value
Mini-
mum
value
Maxi-
mum
value
Normal
values
Total cholesterol (mg/dl)
167 149 227 0–200
Low-density lipoprotein cholesterol
(mg/dl)
148 69 185 0–130
High-density lipoprotein cholesterol
(mg/dl)
47 41 52 0–60
Very low-density lipoprotein
cholesterol (mg/dl)
22 18 25 5–40
Triglycerides (mg/dl)
104 87 121 0–150
Fibrinogen (mg/dl)
433 383 483 200–400
D-dimer (
µ
g/dl)
215 142 289 125–375
Protein-S (%)
108 81 134 70–150
Protein-C (%)
103 90 116 60–125
Antithrombin 3 (%)
45 36 56 75–125
PTT (sn)
12.2 11.5 12.9 10–14
APTT (sn)
32 29 35 31–40
Vitamin B
12
(pg/dl)
533 414 653 200–950
Folate (ng/dl)
7.8 4.8 10.7 3–17
Homocysteine (mmol/l)
12.4 9.5 15.2 5–15
Factor 5 (%)
89.6 78.5 100.7 79–121
