Oral cimetidine adjuvant therapy for recalcitrant, diffuse conjunctival papillomatosis
ABSTRACT To describe a case of recurrent, advanced conjunctival papillomatosis, treated by oral cimetidine (CIM) combined with secondary surgical intervention and an application of intraoperative mitomycin C.
Case report and literature review.
A 9-year-old boy suffered from recurrent, progressive, diffuse multifocal conjunctival papillomatosis over the left upper and lower palpebral and the fornical conjunctiva. He underwent 3 separate surgeries; however, they did not prevent tumor recurrence. The recurrent lesions were more severe and extensive than before the surgeries. To avoid postoperative symblepharon, ankyloblepharon, dry eye, and possible corneal neovascularization after extensive lesion excision, oral CIM at a dosage of 200 mg 4 times daily was administered for 4 months before surgery. A debulking excision of the residual tumor with an intraoperative application of mitomycin C was performed as a secondary therapy after the main mass decreased in size. Postoperative oral CIM was continued for 6 months. The papillomatosis cleared without recurrence or symblepharon, ankyloblepharon, conjunctival scarring, or corneal neovascularization after 4 years of follow-up examinations.
Oral CIM can be used as an initial, nonsurgical strategy for treating cases of massive, recalcitrant conjunctival papillomatosis. If there is tumor shrinkage, surgical debulking with applications of mitomycin C may be sufficient to eliminate any residual tumor tissue without inducing conjunctival scarring or corneal neovascularization.
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ABSTRACT: To report a case of a corneal papilloma-like lesion associated with human papilloma virus type 6. A 48-year-old woman presented with a 2-year history of ocular discomfort and gradual visual deterioration in her right eye. Ophthalmic examination revealed an elevated, semitranslucent, well-defined vascularized mass approximately 4 × 2.5 mm in size localized to the right cornea. The surface of the mass appeared smooth and many small, shallow, and irregular elevations were noted. An excisional biopsy was performed. The underlying cornea was markedly thinned, and fine ramifying vasculature was also noted on the exposed corneal stroma. Typical koilocytic change was observed on the histopathologic examination. Polymerase chain reaction revealed the existence of human papilloma virus type 6 DNA. Here we describe a case of an isolated corneal papilloma-like lesion. Although the corneal extension of the limbal or the conjunctival papillomas has been commonly observed, an isolated corneal papilloma-like lesion with underlying stromal destruction has only rarely been reported.Cornea 11/2010; 30(5):600-3. DOI:10.1097/ICO.0b013e3181fb51fb · 2.36 Impact Factor
Chapter: Ocular Surface Squamous NeoplasiaIntraepithelial Neoplasia, 02/2012; , ISBN: 978-953-307-987-5
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ABSTRACT: BACKGROUND AND PURPOSE: Fibroblast-to-myofibroblast differentiation is associated with scarring, an important issue in corneal surgery. Moxifloxacin (MOX), commonly applied to prevent post-operative infection, would benefit more if it modifies fibroblast-to-myofibroblast differentiation other than antimicrobial activity. Our purpose was to explore whether MOX has anti-fibrotic effect in human corneal fibroblasts (HCFs). EXPERIMENTAL APPROACH: HCFs were incubated in MOX-containing medium concurrently with transforming growth factor (TGF)-β1 (co-treatment), before (pre-treatment) or after (post-treatment) adding TGF-β1. HCF contractility was evaluated with a type I collagen gel contraction assay. Expression of α-smooth muscle actin (α-SMA), Smad2, phospho-Smad2-Ser467, Smad4, and Smad7 was determined by immunoblotting. Formation of α-SMA-positive filaments and distribution of active Smad2 were observed under confocal microscopy. Expression of TGF-β receptor types I (TGFBR1) and II (TGFBR2) was assessed with flow cytometry. KEY RESULTS: MOX did not affect gel contractility or α-SMA filament formation in HCFs without TGF-β1 stimulation. MOX did, however, retard HCF-containing gel contractility and α-SMA filament formation following TGF-β1 stimulation in the pre-treatment and co-treatment groups but not in the post-treatment group. MOX blocked expression of Smad2, phospho-Smad2-Ser467, and TGFBR1 under TGF-β1 incubation. Additionally, MOX enhanced Smad7 expression in TGF-β1-incubated HCFs, but did not interfere with TGF-β1-triggered Smad2 nuclear translocation or Smad4 expression. CONCLUSIONS AND IMPLICATIONS: MOX inhibited TGF-β1-induced fibroblast-to-myofibroblast differentiation via blocking TGFBR1 and enhancing Smad7 expression. MOX should be used before or during surgery to achieve these effects. These results suggest a de novo mechanism by which MOX participates in corneal wound healing.British Journal of Pharmacology 10/2012; 168(6). DOI:10.1111/bph.12015 · 4.99 Impact Factor