Amniotic membrane transplantation for wound dehiscence after deep lamellar keratoplasty: a case report

<p>Abstract</p> <p>Purpose</p> <p>To report amniotic membrane (AM) transplantation in a patient with wound dehiscence 5 months after deep lamellar keratoplasty (DLKP)</p> <p>Methods</p> <p>The patient was an 84-year-old Japanese man who had undergone right DLKP 5 months earlier for central corneal scarring due to recurrent stromal herpetic keratitis. He developed wound dehiscence with corneal stromal melting due to recurrence of stromal herpes in both the donor and recipient sites. "AM roll-in filling technique" and AM patching were performed.</p> <p>Results</p> <p>Following AM transplantation, stromal inflammation subsided and complete epithelization occurred within 10 days of surgery.</p> <p>At 8 months postoperatively, biomicroscopy revealed stable wound apposition or stromal gain. Following AM transplantation, stromal inflammation subsided and complete epithelialization was achieved within 10 days after surgery.</p> <p>Conclusion</p> <p>AM transplantation may offer an effective treatment modality for herpetic corneal wound dehiscence after DLKP.</p

Oral voclosporin: novel calcineurin inhibitor for treatment of noninfectious uveitis

Voclosporin, a novel immunomodulatory drug inhibiting the calcineurin enzyme, was developed to prevent organ graft rejection and to treat autoimmune diseases. The chemical structure of voclosporin is similar to that of cyclosporine A, with a difference in one amino acid, leading to superior calcineurin inhibition and less variability in plasma concentration. Compared with placebo, voclosporin may significantly reduce inflammation and prevent recurrences of inflammation in patients with noninfectious uveitis. Future studies have to show if these advantages are accompanied by greater clinical efficacy and fewer side effects compared with the classic calcineurin inhibitors

Identification of Ocular Autoantigens Associated With Juvenile Idiopathic Arthritis-Associated Uveitis

The purpose of the current study was to analyze the binding patterns of serum autoantibodies from juvenile idiopathic arthritis (JIA) and JIA-associated uveitis (JIAU) patients to proteomes from different ocular tissues and to identify potential ocular autoantigens in JIAU. Proteomes from porcine iris, ciliary body, or retina tissue were isolated, separated using 2D-gel electrophoresis, and transferred to a blotting membrane. The binding pattern of serum antibodies from JIA or JIAU patients or healthy controls to ocular proteins was visualized by using anti-human IgG secondary antibodies and chemiluminescence reaction. Selected protein spots were excised from silver-stained 2D gels and subjected to mass spectrometry. Serum antibodies binding to ocular proteins were detected in all patient groups and healthy controls. Irrespective of the patient groups, serum antibodies bound to 49 different protein spots of the retina proteome, to 53 of the ciliary body proteome, and to 44 of the iris proteome. The relative binding frequency of sera to these iris protein spots was significantly higher in JIAU than in JIA patients or healthy controls. Particularly in JIAU patients, cluster analyses indicated a broad range of serum antibodies directed against ocular antigens, mostly in the iris proteome. Iris proteins frequently bound by serum antibodies in all groups were identified as tubulin beta chain, vimentin, ATP synthase subunit beta, actin, and L-lactate dehydrogenase B chain. Iris proteins exclusively bound by JIAU serum antibodies were heat shock cognate 71 kDa protein and keratin. Although serum autoantibody binding to ocular antigens was not disease-specific, a significant diversity of autoantibodies against a broad range of antigens, particularly from the iris tissue, was detected in JIAU patients. As the iris is a major site of inflammation in JIAU, the present data give further evidence that autoantibodies may be involved in JIAU immunopathology

Adalimumab in Patients with Active Noninfectious Uveitis

BACKGROUND: Patients with noninfectious uveitis are at risk for long-term complications of uncontrolled inflammation, as well as for the adverse effects of long-term glucocorticoid therapy. We conducted a trial to assess the efficacy and safety of adalimumab as a glucocorticoid-sparing agent for the treatment of noninfectious uveitis. METHODS: This multinational phase 3 trial involved adults who had active noninfectious intermediate uveitis, posterior uveitis, or panuveitis despite having received prednisone treatment for 2 or more weeks. Investigators and patients were unaware of the study-group assignments. Patients were randomly assigned in a 1:1 ratio to receive adalimumab (a loading dose of 80 mg followed by a dose of 40 mg every 2 weeks) or matched placebo. All patients received a mandatory prednisone burst followed by tapering of prednisone over the course of 15 weeks. The primary efficacy end point was the time to treatment failure occurring at or after week 6. Treatment failure was a multicomponent outcome that was based on assessment of new inflammatory lesions, best corrected visual acuity, anterior chamber cell grade, and vitreous haze grade. Nine ranked secondary efficacy end points were assessed, and adverse events were reported. RESULTS: The median time to treatment failure was 24 weeks in the adalimumab group and 13 weeks in the placebo group. Among the 217 patients in the intention-to-treat population, those receiving adalimumab were less likely than those in the placebo group to have treatment failure (hazard ratio, 0.50; 95% confidence interval, 0.36 to 0.70; P<0.001). Outcomes with regard to three secondary end points (change in anterior chamber cell grade, change in vitreous haze grade, and change in best corrected visual acuity) were significantly better in the adalimumab group than in the placebo group. Adverse events and serious adverse events were reported more frequently among patients who received adalimumab (1052.4 vs. 971.7 adverse events and 28.8 vs. 13.6 serious adverse events per 100 person-years). CONCLUSIONS: In our trial, adalimumab was found to be associated with a lower risk of uveitic flare or visual impairment and with more adverse events and serious adverse events than was placebo

Fluocinolone acetonide intravitreal implant (Retisert((R))) in the treatment of sight threatening macular oedema of juvenile idiopathic arthritis-related uveitis

Purpose We describe eight patients with juvenile idiopathic arthritis-related chronic uveitis, who received a fluocinolone acetonide implant (FAI, Retisert (R), Bausch&Lomb) in one eye. All patients had poor visual acuity (VA) due to persistent macular oedema in one or both eyes despite treatment with antirheumatic medication. MethodsResultsMedian age of the patients was 22.9years (range, 14.1-39.7) and duration of uveitis 13.0years (range, 6.8-28.4) at FAI implantation. Median preoperative best-corrected visual acuity (BCVA) was 0.1 (range, 0.05-0.4) and Standardization of Uveitis Nomenclature, SUN-grade was SUN 2+ (range, 0.5-4.0). All patients had been treated extensively with systemic corticosteroids and antirheumatic drugs by the time of FAI implantation. The median follow-up time was 5.3years (range, 4.4-6.3). Macular edema resolved in a median time of 0.2years (range, 0.04-0.39) after the FAI implantation. The median BCVA was 0.5-0.63 (range, 0.1-1.0) from 1 to 5years of follow-up. Macular edema did not recur in 5 eyes after the implantation. In three eyes, the macular oedema relapsed at 2.7, 2.9 and 5.5 years of follow-up. All our patients needed antirheumatic drugs in addition to the FAI to treat their macular edema. During the follow-up, 7 eyes required further intraocular operations: 4 cataract operations, 4 intraocular pressure -lowering operations and 1 retinal detachment surgery were performed. ConclusionFluocinolone acetonide implant is a valuable option in the treatment of persistent macular edema associated with JIA-related uveitis refractory to systemic treatments.Peer reviewe