Background: Although calcitriol (1,25-dihydroxycholecalciferol) and vitamin D 2 inhibit retinoblastoma growth in the athymic (nude) mouse xenograft (Y-79 cell line) model of retinoblastoma, they can cause severe toxicity. Objective: To examine the toxicity of and dosedependent response for the inhibition of tumor growth for 1␣-hydroxyvitamin D 2 (1␣-OH-D 2), an analogue with reduced systemic toxicity, in the athymic Y-79 mouse model. Methods: Mice were randomized into treatment and control groups for 5-week toxicity and dose-response studies. Treatment was via oral gavage 5 times per week. Doseresponse studies measured tumor inhibition and drug serum levels. Tumor size and body weight were measured weekly together with various criteria for toxicity. Animals were euthanized at the end of the treatment period. Tumors and kidneys were harvested, and serum was analyzed for calcium and drug levels. Results: Doses of 0.1 to 1.2 µg/d were selected on the basis of toxicity studies for the dose-response trial. Tumor weight and volume in the 0.2-µg and 0.3-µg doses were significantly lower than in controls. Mortality rates and kidney calcification in mice treated with doses of 0.1 to 0.3 µg were lower than those observed in studies of calcitriol and vitamin D 2. Conclusion: A vitamin D analogue, 1␣-OH-D 2 , inhibits tumor growth in this xenograft model of retinoblastoma with less toxicity than calcitriol and vitamin D 2 .
An 89-year-old female patient with a history of a left orbital floor fracture repair with synthetic implant 12 years prior, presented with a three-week history of blurry vision, inferior conjunctival chemosis and proptosis of the left eye. CT scan revealed a well-circumscribed subperiosteal lesion with superior elevation of the orbital floor implant. The patient underwent transconjunctival orbital surgery with removal of the implant and drainage of the subperiosteal hemorrhagic cyst. The patient had an uncomplicated postoperative course, with resolution of the proptosis, chemosis, and return of normal vision. This case represents an unusual late complication of orbital fracture repair with associated reduced visual acuity.
Introduction: Recently there has been an evolving paradigm shift toward the treatment of facial volume loss either alone or in conjunction with more traditional modalities. Although volume augmentation is commonly used in rejuvenation of the upper orbital sulcus and brow, the effect on the upper eyelid has not yet been documented. This article describes one clinician's experience (A.N.K.) with autologous fat grafting to the upper orbital sulcus and the effect on upper eyelid position. Materials and Methods: After a detailed clinical evaluation of the periorbital region including overall facial aging, brow position, and eyelid laxity, 7 patients underwent autologous fat transfer to the periorbital region. Comparison of photos taken before and after the procedure showed a clear increase in the upper eyelid height. Results: All 7 patients described in this study demonstrated objective increase in upper lid height after periorbital autologous fat transfer, ranging from 0.41 mm to 2.08 mm, with a mean of 1.00 mm. Discussion: Periocular volume augmentation and its effect on lower eyelid position have been described previously. An attempt to alter upper eyelid height with volume augmentation directly to the upper eyelid has also been described recently. However, to the authors' knowledge, this is the first report of volume augmentation to the periorbital region affecting upper eyelid position in this manner. The clinical application of this observational data is not yet clear. However, the potential exists for extension of this modality to upper eyelid malposition such as ptosis.
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