Discussion
Frontal bone hemangiomas are very rare tumors for which the origin is
not yet clear. Some studies suggested a congenital origin – which
remains doubtful since the mean age in most case reports was about 30
years – while other studies reported a post-traumatic
development4. However, no link between sever
thyrotoxicosis and bone hemangiomas have been reported yet.
Firstly, changes in the systemic circulation – as may occur in venous
obstruction and in heart failure – may result in changes in arterial
and/or venous pressures which might explain the development of a
vascular malformation. These changes might be the result of her sever
thyrotoxicosis which has persisted for more than a year.
Secondly, the possible link between the lesion and high-dose IV GC
administration in a short period (7.5 grams in 10 weeks). To our
knowledge, no cases of hemangiomas resulting from high-dose of GC
therapy have been described5. We propose two
mechanisms: 1/ circulatory changes resulting from high-dose IV
GC, which could be explained by the expression of both type 1 and type 2
11β-hydroxysteroid dehydrogenase isozymes in the arterial wall; which
might have a direct impact on vascular physiology, 2/ the
increased risk of bone loss associated with the IV GC therapy; as a
result of (i) a decrease in bone formation, by directly
inhibiting osteoblastic proliferation and differentiation, and by
increasing the apoptosis of mature osteoblasts, (ii) an increase
in bone resorption by stimulating osteoclastogenesis. According to the
literature, this bone loss caused by high-dose GC therapy is most
pronounced in the first months following a high-dose GC therapy, and the
fact that the lesion appeared four months after the IV GC might suggest
a physiopathological link.
In conclusion, frontal bone hemangiomas are rare lesions, for which the
etiology is not clear. To our knowledge, there are no studies which have
described the occurrence of bone hemangiomas in patients having severe
GO, or in patients treated with high-dose IV GC. We suggest a possible
link between IV GC which might have resulted in endothelial alterations,
and/or bone loss. Severe thyrotoxicosis might have contributed due to
possible circulatory alterations. Finally, the role of carbimazole
cannot be excluded despite the lack of evidence.