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.