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Treatment with iodine prior to thyroidectomy has been shown to reduce
intraoperative bleeding in patients with Graves Disease (GD). However, the
molecular interrelation between iodine treatment and reduced bleeding remains
unclear. The purpose of this study is to examine whether the described effect
results from a reduction of microvessel density.
We used immunohistochemical staining to determine the vascular surface
density (VSD) and the most important stimulator for angiogenesis, VEGF, in
thyroid tissue of patients with GD and non-toxic goiter.
Two groups of GD patients were compared: GD patients treated with antithyroid
drugs only and GD patients who underwent iodine treatment in addition to
antithyroid drugs. Non-toxic goiter patients were used as control group.
No significant differences of microvessel density were recorded among all
groups. VEGF was detected in all non-toxic goiters, only a small amount of GD
goiters with iodine treatment were positive for VEGF and hardly any GD goiters
in the group of antithyroid drugs. Within the group of iodine treated GD, the
duration of pharmacological therapy longer than 1 year seemed to cause lower
VEGF levels than shorter therapy.
Due to the fact that untreated GD goiters are more vascularized than non-toxic
goiters, we interpret the absence of difference among the groups as a reduction
of microvessel density induced by therapy with antithyroid drugs. Under
therapy with antithyroid drugs VEGF is reduced significantly. Thus we reason
that antithyroid treatment is accountable for lowered levels of vascularization.
To analyze the effect of iodine on vascularization separately, it is necessary to investigate GD patients without antithyroid therapy with and without iodine
In our study setting no reduction of microvessel density under iodine treatment
was detected. We assume other mechanisms to be responsible for the
reduction of intraoperative bleeding in GD goiters after iodine therapy.