ABSTRACT
PURPOSE: To report novel optical coherence tomography findings in a case of anti-α-enolase cancer associated retinopathy. OBSERVATIONS: An elderly female presented with bilateral decreased vision and a recent diagnosis of ovarian carcinoma. Optical coherence tomography demonstrated bilateral loss of outer retinal structures and macular edema. Serum testing found antibodies against α-enolase and 82-84 kDa proteins. Outer retinal structures showed recovery, macular edema resolved and repeat anti-retinal antibody testing became negative following cancer therapy and topical difluprednate treatment. CONCLUSIONS AND IMPORTANCE: Cancer associated retinopathy is a paraneoplastic disease that results in damage to retinal structures through an autoimmune response. The damage is generally considered to be irreversible; however, in rare cases, such as observed here, retinal structures may demonstrate recovery after treatment.
ABSTRACT
OBJECTIVE: Thyroid eye disease (TED) is generally treated with oral corticosteroid therapy. A steroid sparing drug could be a useful adjunct. We reviewed our experience with methotrexate as a corticosteroid sparing agent to treat TED. METHODS: Retrospective chart review from two eye inflammation clinics. Patients with TED who were unable to discontinue prednisone therapy without disease recurrence were included. RESULTS: 14 patients who were receiving an average of 32 mg/day of prednisone were treated with methotrexate, usually 15 mg/week orally or 20 mg/week subcutaneously. Five patients discontinued therapy for a lack of benefit or intolerance. Of the 9 patients who remained on methotrexate, all were able to discontinue prednisone completely after an average duration of 7.5 months. Improved visual acuity by at least two lines on the Snellen chart was achieved by 7 of 12 patients with reduced acuity and partial improvement in ocular motility was achieved in 5 of 14 patients. CONCLUSIONS: Methotrexate provided an effective steroid sparing effect in a subset of patients with TED.
ABSTRACT
We investigated the expression of the functional endotoxin receptor proteins Toll-like receptor-4 and CD14 in human eyes. Toll-like receptor-4 and CD14 proteins were detected by immunohistochemical analysis of sections of whole human eyes embedded in paraffin with monoclonal antibodies against human toll-like receptor-4 (HTA-125), human CD14 (RPA-M1), or as a control, an irrelevant mouse IgG1k (MOPC-21). Incubation of explants with a neutralizing anti-toll-like receptor-4 monoclonal antibody was used to determine if lipopolysaccharide stimulation of tumor necrosis factor or interleukin-6 secretion was dependent on Toll-like receptor-4 activity. Reverse transcription-polymerase chain reaction was used to detect mRNAs for toll-like receptor-4, tumor necrosis factor-alpha, interleukin-1beta, interleukin-6 and interleukin-8, 3 hr after stimulation of cultured iris microvascular endothelial cells. By immunohistochemistry, human ciliary body non-pigmented epithelial cells showed strong expression of the endotoxin receptor proteins, toll-like receptor-4 and CD14. Toll-like receptor-4 antibodies significantly inhibited lipopolysaccharide-stimulated tumor necrosis factor secretion by the ciliary body. Toll-like receptor-4 mRNA was constitutively expressed in iris endothelial cells and slightly down-regulated by endotoxin. mRNA levels for tumor necrosis factor-alpha, interleukin-1beta, interleukin-6 and interleukin-8 were all increased by endotoxin treatment. This is the first report that shows intraocular (ciliary body and iris) expression of toll-like receptor-4, other than in cornea. Our results show that the ciliary body also expresses CD14, which is anatomically colocalized with toll-like receptor-4. This suggests a potential interaction between both molecules during endotoxin activation of ciliary body cells. The juxtaposition of toll-like receptor-4 and CD14 in the anterior uveal tract helps to explain the sensitivity of the iris/ciliary body to bacterial endotoxin as seen in the standard animal model of endotoxin-induced uveitis.