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a)
(NPD) ophthalmic solution three to four times daily. The elevated lesions were resolved by the recheck 4 weeks later (Fig 4), consistent with granulation tissue and not regrowth of neoplasia, and the NPD ophthalmic solution was discontinued. No obvious side effects were noted during the four cycles
of MMC treatment. A few days after treatment was completed, the horse began developing depigmentation of the medial upper and lower left eyelids, intermittent epiphora and periocular crusting. The epiphora and periocular crusting resolved quickly with short courses of topical NPD, but recurred several times over the course of 1 month. Depigmentation of the eyelids was progressive during this time.
At the last recheck evaluation, 4 months following surgery, b)
there was no recurrence of corneal neoplasia. Mild fibrosis was present on the dorsal corneal surface, yet no raised lesions were present. The medial periocular skin was depigmented, but no erythema, swelling, or discharge was present. The operated eye was comfortable and visual. Due to distance and travel logistics, the owner elected not to return to ISU-LVMC for additional rechecks. Follow-up phone calls and photographs from the owner 10 months after surgery revealed significant improvement of periocular depigmentation and no evidence of corneal neoplasia recurrence.
Discussion
Fig 2: Photomicrographs of the affected cornea. Haematoxylin and eosin staining; 400 3 magnification. a) There are neoplastic cells within the epithelium containing occasional brown granules. b) There are clusters of neoplastic cells within the stroma, as well as neovascularisation and infiltrates of plasma cells, lymphocytes and eosinophils.
Follow-up Initial recheck 5 days post-operatively showed partially epithelialised keratectomy sites with grafts in place. At evaluation 19 days post-operatively, the left cornea was completely epithelialised with negative fluorescein staining; corneal sutures were still present and there were fine blood vessels and mild fibrosis present throughout the keratectomy sites. Treatment with topical mitomycin C 0.04% solution4 was started on the left eye 25 days following surgery as an adjunctive therapy to help prevent recurrence of neoplasia. The mitomycin C (MMC) was administered four times daily for 7 days, and discontinued for the following 7 days. This 2-week course was repeated for four cycles. Three weeks after starting MMC therapy, two slightly elevated, 2–3 mm diameter, white lesions were noted on the
dorsal left cornea at the keratectomy site. Nonelevated fibrotic tissue with fine blood vessels was also present. The elevated white lesions were thought to be granulation tissue during the healing process, or possibly regrowth of neoplasia. Biopsy was considered, but it was elected to first try treatment with topical neomycin/polymixin B/dexamethasone
The corneal masses in our case were originally suspected to be SCC based on appearance, location and initial cytology. However, histopathology of the corneal biopsies did not identify any characteristic features of SCC, such as intercellular bridges, individual cell keratinisation or keratin pearl formation (Grahn et al. 2013). Biopsies revealed oval-to-round neoplastic cells with rare cytoplasmic brown granules, and consideration was given to a poorly melanised malignant melanoma. However, a poorly differentiated SCC could not be ruled out based solely on histopathology. Variable histological and cytological patterns of
melanocytic neoplasms can make definitive diagnosis difficult. In veterinary and human medicine, IHC is commonly used to support a diagnosis of melanocytic neoplasia (Ramos-Vara et al. 2014). Normal melanocytes are dendritic cells derived from neuroectodermal melanoblasts, so markers of neuroectodermal tissues can assist in diagnosis and differentiation from other types of tumours, such as carcinomas (Koenig et al. 2001). Several IHC markers were used in our case, including vimentin, S100, melan-A and cytokeratin. Neoplastic cells within the cornea had strong
immunoreactivity to both vimentin and S100 antibodies. Vimentin is an intermediate filament expressed by mesenchymal and neuroectodermal cells, which has shown high sensitivity but low specificity as a marker for melanocytic neoplasia (Ramos-Vara et al. 2000; Ohsie et al. 2008). Vimentin consistently stains human melanocytic neoplasms (Nakhleh et al. 1990), and expression has been reported in 100% of canine oral melanocytic neoplasms (Ramos-Vara et al. 2000). The S100 marker is a calcium-binding protein that is another sensitive but nonspecific marker used for detection of human and animal melanocytic neoplasia (de Wit et al.
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