This study suggests that the confocal microscopy of the cornea is capable of supporting a clinical diagnosis in patients with uveitis.

BackgroundHerpetic anterior uveitis is a frequent cause of infectious uveitis. A definite diagnosis is obtained by anterior chamber puncture and polymerase chain reaction, an invasive procedure. We hypothesized that patients with herpetic anterior uveitis have a certain pattern of inflammatory cells in their cornea that distinguishes herpetic anterior uveitis from other uveitis types. This study is a prospective, controlled, observational study. Ten patients are with active herpetic anterior uveitis and 14 patients are with Fuchs uveitis syndrome. Patients were imaged with the Heidelberg Retina Tomograph with the Rostock Cornea Module attachment. Three images of the subepithelial area of the cornea were evaluated for dendritiform inflammatory cells. Means were calculated and used for analysis. The contralateral unaffected eyes and numbers published in the literature served as controls.ResultsThe number of dendritiform inflammatory cells in herpetic anterior uveitis was compared to that in the Fuchs uveitis syndrome. Of the eyes of patients with herpetic anterior uveitis, 80% had an average of 98.0±10.8 cells/mm2 (mean±standard error of the mean (SEM), n=10) in their affected eyes and 60.4±26.4 cells/mm2, (n=6) in 30% of their fellow eyes. Patients with Fuchs uveitis syndrome had moderately elevated dendritiform inflammatory cells (47.0±9.7 cells/mm2, n=14) in 96.4% of their affected eyes and normal numbers (23.0±7.3 cells/mm2, n=13) in 46.4% of their fellow eyes. The difference between the four groups was significant (p=0.0004).ConclusionsPatients with herpetic anterior uveitis had significantly higher levels of dendritiform inflammatory cells in their subepithelial cornea than patients with Fuchs uveitis syndrome, which can be detected by in vivo confocal microscopy. The clinically unaffected eyes of herpetic anterior uveitis patients showed a co-response regarding dendritiform inflammatory cell elevation. We conclude that high numbers of dendritiform inflammatory cells in the cornea of uveitis patients may support the clinical diagnosis of herpetic anterior uveitis.

Purpose We report a case of Juvenile Idiopathic Arthritis (JIA) and Anterior Uveitis (AU) responding well to Tocilizumab, a new humanized monoclonal antibody against the IL‐6 receptor, after having been refractory to classical immunosuppressive agents as well as to TNF‐α inhibitors. Methods The Patient was treated in our center from 2007‐2012. Collected data included: visual acuity (VA), anterior chamber cells and –flare, flaremeter measurements, intraocular pressure (IOP), presence of macular edema (ME) and cataract, topical and systemic medications, number and site of affected joints, laboratory inflammation parameters. Results Patient was born 1996, diagnosed with JIA 1998 and with AU 2005. Inflammation was initially controlled with methotrexate and corticosteroids, VA fluctuated between 20/40‐20/15(OD) and 20/20(OS). In 2007 VA decreased to 20/200(OD) as ME developed. Additional systemic therapy included between 2008 and 2009: Ciclosporin, Adalimumab, Mycophenolate, Leflunomide, and Infliximab. Control of ocular and/or joint inflammation was always insufficient or short lived. Between 2008 and 2010 ME required multiple periocular Triamcinolone injections. IOP first rose in 2008 to 34mmHg(OD), requiring combined topical and systemic therapy and finally trabeculectomy in 2010. Cataract developed on both eyes. Tocilizumab therapy was started in 02/2010. Since then AU and joints are free from inflammation. Cataract‐surgery and implantation of an artificial lens in OD was performed successfully in 2011. Systemic steroids could be reduced to 2 mg/d. IOP is <20mmHg; VA is stable at 20/32(OD) and 20/50(OS). Conclusion Tocilizumab may be another treatment option for JIA‐associated uveitis which is refractory to established immunosuppressants.

Purpose Herpetic uveitis (HU) is a frequent infectious cause of anterior uveitis. A definite diagnosis can be obtained by anterior chamber puncture and PCR, an invasive procedure not all patients consent to. We hypothesized that patients with HU typically have high amounts of dendritiform inflammatory cells (DCs) in their corneal subepithelial nerve plexus (SNP),which are detectable by in vivo confocal microscopy and distinguish HU from other uveitis types. Methods Patients with clinical suspicion of HU without keratitis and patients with Fuchs Uveitis Syndrome (FUS) were imaged with the Rostock Cornea Module attachment on the HRT III (HRT‐RCM)(Heidelberg Engineering) on both eyes. DCs in the SNP were counted by two observers using a cell counting software. Means of the cell counts were used for analysis. Diagnosis of HU was confirmed by anterior chamber puncture or by clinical improvement due to Acyclovir therapy. Statistical significance was assessed with a Kruskal‐Wallis or a Mann Whitney U test,when appropriate. Results Patients with HU showed significantly higher amounts of DCs in their affected eyes (93.3±10.6 cells/mm2, Mean±SEM, n=10) but also in their unaffected eyes (59±25 cells/mm2, n=7), than patients with FUS, who had an average DC‐density of 46.4±10.4 cells/mm2(n=15) in their affected and 21±6 cells/mm2(n=15) in their unaffected eyes. Conclusion High amounts of DCs in the corneal SNP were a typical finding in herpetic AU. Much lower numbers of DCs were present in FUS, a clinical similar uveitis type presumably also of viral origin. Imaging corneas of patients with clinical suspicion of HU with the HRT‐RCM is a non‐invasive, low risk technique which can be a useful addition in distinguishing HU from other anterior uveitis aetiologi