Send to

Choose Destination
See comment in PubMed Commons below
Ophthal Plast Reconstr Surg. 2012 Jan-Feb;28(1):27-9. doi: 10.1097/IOP.0b013e31822e9560.

Histopathology of brow fat in thyroid-associated orbitopathy.

Author information

Jules Stein Eye Institute, UCLA, Los Angeles, California, USA.



We propose that brow enlargement seen in patients with thyroid-associated orbitopathy (TAO) occurs secondary to the autoimmune process in Graves disease and that the changes in brow fat are histologically identical to those seen in orbital fat.


With informed consent, brow and orbital fat was obtained from patients with TAO and from patients with no significant past medical history undergoing orbital decompression, blepharoplasty, and/or brow fat removal. Histologic examination was performed on the orbital and brow fat.


Fat histologies obtained from patients with TAO and those without known systemic disease were compared. Specimens from patients with TAO showed an increase of fibrosis and fibrous septae. Furthermore, certain biologic markers, including insulin-like growth factor 1 receptor β (IGF-1Rβ) and thyroid-stimulating hormone receptor (TSHR), were increased in the fat obtained from patients with TAO. This was identical in both the brow and the orbital fat. Fat from patients with no significant past medical history showed normal fat histology, absence of fibrous septae, and decreased marker expression.


Graves disease is a systemic autoimmune disease that affects patients in a variety of ways. In addition to the orbital changes seen in these patients, we have observed an increase in the brow fat compartment. We are intrigued to find that the histologic changes are identical in both the orbital and the brow fat of patients with TAO. The increased IGF-1Rβ and TSHR expression in both the brow and the orbital fat further support their role as putative markers in patients with Graves disease.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer
    Loading ...
    Support Center