Ocular Inflammatory Disease: aggressive therapy needed

Learn more about iritis and uveitis by reading related articles.

Moderators: Mike Bartolatz, kwork

Post Reply
Mike Bartolatz
Posts: 6595
Joined: Fri Feb 06, 2004 9:58 pm

Ocular Inflammatory Disease: aggressive therapy needed

Post by Mike Bartolatz » Sun Mar 07, 2004 1:32 pm

Return to Medscape coverage of: American Academy of Ophthalmology 2003 Annual Meeting | Highlights of the American Academy of Ophthalmology 2003 Annual Meeting


You must read all articles in this activity to prepare for the post test.


Ocular Inflammatory Disease: The Importance of Aggressive Therapy
Disclosures

C. Stephen Foster, MD, FACS


Introduction
The 2003 Annual Meeting of the American Academy of Ophthalmology in Anaheim, California, featured the first ever subspecialty day devoted to ocular inflammatory diseases in general, and to uveitis in particular.[1] The day provided the most up-to-date information on the state of the art for diagnosis and treatment of ocular inflammatory diseases, particularly from information harvested from evidence-based medicine reviews of the literature. Three major themes emerged by the end of the day:

Uveitis is extremely important epidemiologically in underdeveloped, developing, and developed societies alike, accounting for a very large medical and economic burden on populations.


Despite the progress made since the introduction of steroid therapy in 1950, large numbers of patients eventually are blinded by the consequences of recurrent or chronic uveitis; this problem is consistently agreed to be the third leading cause of preventable blindness in all developed societies.


If we ever hope to reduce the prevalence of blindness that is secondary to uveitis, ophthalmologists in large numbers must embrace a philosophy of earlier, more aggressive therapy with a limit to the total amount of steroid ultimately used. In other words, this means they must embrace the idea of collaboration with physicians who are experienced in the use of steroid-sparing immunomodulatory therapy.
Epidemiology and Diagnosis
Dr. Emmett T. Cunningham Jr.,[2] Professor of Ophthalmology at New York University School of Medicine, reported on the epidemiology of uveitis. Uveitis accounts for 5% to 20% of cases of legal blindness in North America and Europe, depending upon the reporting center, and up to 25% in the developing world. The incidence of uveitis in the developed world is 20 cases per 100,000 population per year, with a prevalence of 200 cases per 100,000 individuals, or 1 in 500. Dr. Cunningham pointed out that the prevalence in the developing world may be 5- to 10-fold higher than in developed countries, and that the incidence in children and in the elderly is about 5- to 10-fold lower than in adults. However, the blinding prevalence in children is actually higher than in adults, primarily because of delayed detection and an increased prevalence of posterior uveitis in the pediatric age group.

Dr. Russell Van Gelder,[3] Assistant Professor of Ophthalmology at Washington University School of Medicine, addressed the matter of recent advances in the diagnosis of uveitis. Patients with recurrent disease clearly need aggressive evaluation, as do patients with particularly severe inflammation and patients with any suggestions on review of systems of an associated systemic disorder. A thorough medical history and review of systems is in order. Dr. Van Gelder emphasized that the FTA-ABS test is the appropriate test for uveitis suspected to be associated with latent syphilis, since 30% of patients with latent syphilis are VDRL-negative. He also spoke to the matter of polymerase chain reaction (PCR) technology, which has revolutionized our ability to diagnose infectious causes of uveitis much earlier now than in the past, through the detection of microbial DNA in fluids (aqueous humor or vitreous) harvested during diagnostic evaluations.

Treatment
Basic therapeutic principles involve a certain aggressiveness to therapy. Dr. C. Stephen Foster, Professor of Ophthalmology at Harvard Medical School and Director of the Immunology and Uveitis Service at the Massachusetts Eye and Ear Infirmary, discussed practice patterns during his opening remarks and later in his presentation.[4] Initially, he reviewed published recommendations from the International Uveitis Study Group and the American Uveitis Society that emphasize that certain diseases categorically require the employment, from the very first moment, of immunomodulatory agents, given the poor outcomes that eventually attend such disorders when steroids represent the only mode of treatment. Such diseases include sympathetic ophthalmia, Vogt-Koyanagi-Harada's disease, multifocal choroiditis with pan uveitis, birdshot retinochoroidopathy, Behçet's disease with retinal vasculitis, rheumatoid sclerouveitis, polyarteritis nodosa, Wegener's granulomatosis, and juvenile idiopathic arthritis-associated uveitis, which is chronic or recurrent.

In instances in which immunomodulatory therapy is not mandatory, Dr. Foster advocated a graded, stepladder approach, beginning with steroids, adding oral nonsteroidal anti-inflammatory agents, when not contraindicated, to those patients in whom uveitis continues to recur when steroids are tapered or discontinued, and then advancing to steroid-sparing immunomodulatory therapy in the event that the aforementioned, lesser aggressive strategies do not induce a durable remission. There are concerns about malignancies and sterility through the use of steroid sparing immunomodulatory therapy, but it should be noted that the nonalkylating agents do not carry such risks, provided the treating physician selects patients who do not already have an underlying problem that places them at heightened risk for malignancy later in life (eg, chronic Epstein Barr virus infection). One Harvard study of 160 patients treated with methotrexate for recurrent uveitis between 1985 and 1999 saw 8 patients discontinue medication because of elevated liver enzymes, and 3 discontinue the medication because of progressive leukopenia.[5] Another prior publication from the Harvard group[6] on the matter of malignancy development studied 554 patients for a total of 1261 person-years of follow up and detected 5 malignancies. Two were in patients with systemic disease risk factors for a heightened likelihood of malignancy at some point in life, and 1 occurred in a patient in whom only prednisone had been used. This left, then, 2 patients, one on cyclosporin and the other on azathioprine, who had developed malignancy out of this 1261 person-year follow-up cohort -- a prevalence actually lower than the expected prevalence of malignancy in a randomly selected population.

The immunomodulatory agent groups of drugs currently employed by uveitis specialists in the care of patients with chronic or recurrent uveitis include the antimetabolites (azathioprine, methotrexate, and mycophenolate mofetil), the T-cell inhibitors (cyclosporin and tacrolimus), and the alkylating agents (chlorambucil and cyclophosphamide).[7] Therapy with biologics (etanercept, infliximab, daclizumab, IVIG, and others) is currently experimental, and evidence-based medicine exercises through peer-reviewed literature are not possible on this subject.

Herpes Uveitis
Herpes uveitis is an underrecognized cause of recurrent uveitis, occurring in somewhere between 1.5 and 15 persons per 100,000 population.[8] It is often associated with elevated intraocular pressure, and that, coupled with 2 other diagnostic signs, iris atrophy and diminished corneal sensation, basically establishes the diagnosis. Definitively establishing the diagnosis, through culture or other technique from anterior chamber tapping, is rarely necessary, although it is eminently possible now, particularly through the employment of PCR technology. Long-term therapy with antiviral agents (acyclovir or valacyclovir) prevents reactivation of the virus from ganglionic latency and hence prevents additional episodes of infectious uveitis. However, additional episodes of uveitis may occur as a consequence of an autoimmune component, caused by the iris damage from the infectious episodes of the disease.

Pediatric Uveitis
Dr. Albert T. Vitale,[9] Associate Professor of Ophthalmology at the University of Utah, addressed the major problems associated with managing pediatric uveitis: delayed diagnosis due to the "silent" nature of the disease in so many children, and amblyopia, which may occur in children under 10, resulting in poor vision even once the uveitis problem and/or the cataract that has developed are treated. Chronic, undetected or chronic, undertreated uveitis frequently results in glaucoma and in retinal complications in children with uveitis; approximately a third of children with a history of uveitis experience severe loss of vision. Moreover, 2 of the most common causes of pediatric uveitis, juvenile idiopathic arthritis and sarcoidosis, are also 2 of the most devastating, with some of the poorest outcomes resulting from undertreatment. Dr. Vitale emphasized that improving the outcomes for children with uveitis is going to require early and aggressive anti-inflammatory therapy, earlier case detection, and better coordination of care among ophthalmologists, pediatricians, and rheumatologists experienced in the use of immunomodulatory agents.

Intermediate Uveitis
How should we treat intermediate uveitis? Dr. Janet Davis,[10] Professor of Ophthalmology at the University of Miami, advocated a stepladder approach, beginning with periocular steroid injections, progressing to peripheral retinal cryopexy in locations with pars planitis with exudates on the pars plana or neovascularization of this region, and then advancing, in most cases in which recurrence of uveitis continues despite these approaches, to systemic immunomodulatory therapy or to pars plana vitrectomy, or to both. Each of these latter approaches has its advantages and disadvantages, and the exact selection of which method to pursue is patient-dependent. Dr. Scott Whitcup,[11] Assistant Clinic Professor of Ophthalmology at UCLA School of Medicine, noted that corticosteroids remain the mainstay of therapy for sarcoidosis and uveitis, but methotrexate and cyclosporin are now well-recognized steroid-sparing strategies to be employed in patients who have become steroid-dependent.

Retinal Vasculitis
According to Dr. Quan Nguyen,[12] Assistant Professor of Ophthalmology at the Wilmer Eye Institute, Johns Hopkins University School of Medicine, retinal vasculitis:

Is a potentially blinding inflammatory ocular disease


Is frequently associated with an occult, sometimes potentially lethal systemic disease


Effective treatment of retinal vasculitis, whether it is associated with a systemic disorder, typically requires the use of systemic medication, since steroid drops and injections rarely effectively treat this problem.
Dr. Nguyen pointed out that with arteriole involvement, the discovery of an underlying systemic disease is especially common. Both infectious and noninfectious as well as focal and systemic causes for retinal vasculitis exist, with the differential diagnosis, therefore, being exceptionally broad, and the diagnostic evaluation of the patient often being especially complex. The medical review of systems is one of the most valuable steps in the diagnostic evaluation. Infectious etiologies, such as syphilis and herpes simplex, varicella zoster virus, Bartonella, tuberculosis, leptospirosis, and Brucellosis, require specific antibiotic therapy. Noninfectious causes typically require systemic steroid therapy, and in particular when there is an associated systemic autoimmune disease, systemic immunomodulatory therapy will also be required. Not to offer such therapy, for example, to a person with Behçet's disease or polyarteritis nodosa or Wegener's granulomatosis, regardless of whether there is some extraocular manifestation of that disease, would basically be tantamount to negligence.

Surgery
The surgical aspects of caring for the patient with uveitis, both diagnostically and therapeutically, were addressed in several sessions. Dr. E. Mitchel Opremcak,[13] Clinical Associate Professor at the Ohio State University School of Medicine, discussed the increasing usefulness of PCR analysis of intraocular fluids harvested in the course of the diagnostic efforts in the patient with uveitis. He also demonstrated the technique and utility of both chorioretinal biopsies and endoretinal biopsies, processed for electromicroscopy, immunopathology studies, and PCR analysis. His advice was to biopsy, when possible, superiorly and nasally -- performing chorioretinal biopsies for anterior lesions and endoretinal biopsies for posterior lesions. The area that is biopsied should be an active pathology rather than old, organized scarred material. When possible, material at the border of an area of active disease should also be harvested. Since the amount of material being harvested is so small, the details of tissue handling and processing are complex, and Dr. Opremcak advised having an ophthalmic pathologist in the operating room at the time of the surgery, so that the material can be processed immediately by the pathologist.

Cataract and glaucoma remain risks for the uveitis patient. While the prevention of cataract development by more aggressive, earlier therapy and limited steroid use is preferred, Dr. James P. Dunn, Jr., at the Johns Hopkins University School of Medicine,[14] noted that once the cataract has developed, there are good outcomes. It is important that patients are carefully selected, uveitis is placed into remission for at least 3 months prior to the surgery, supplemental perioperative steroids are used, glaucoma is controlled, meticulous surgical technique is employed, and wisdom is employed in the decision of whether to include a lens implant in the surgical plan. Poor candidates for inclusion of a lens implant include children with juvenile idiopathic-associated chronic uveitis, patients with particularly severe, chronic intermediate uveitis, and patients with uveitis associated with systemic disease that has been impossible to place into durable remission. When a lens implant is used, acrylic lenses may be preferable to silicone lenses. In cases of glaucoma, Dr. Peter A. Netland, Professor of Ophthalmology at the University of Tennessee School of Medicine,[15] emphasized that the unequivocal key to successful surgery in a patient with uveitic glaucoma is induction of remission of the uveitis, since postoperative inflammation and/or recurrence of uveitis postoperatively are the features most responsible for failure, either of a mitomycin C trabeculectomy or of a valve procedure.

Finally, Dr. Glen J. Jaffe, Professor of Ophthalmology at Duke University School of Medicine,[16] addressing the matter of therapeutic vitreoretinal surgery in patients with uveitis, also emphasized:

The importance of aggressively treating the underlying inflammation and/or infection


The critical importance of attention to detail in performing vitrectomy to relieve traction on the retina


The importance of attending to all treatable areas of choroidal neovascularization.
Dr. Jaffe reported on the preliminary data of an investigational intravitreal drug delivery device currently under investigation for the sustained release of fluocinolone over a 3-year period into the vitreous cavity. The results are encouraging, but the device obviously is not a cure-all, since it is, after all, a locally administered steroid that will not address underlying systemic disease; patients with bilateral disease would require bilateral implants; and the device is not without some complications (cataract, retinal detachment, and glaucoma).

Other Conditions
A number of conditions were discussed at the annual clinical meeting of the American Uveitis Society, which was held in conjunction with the International Uveitis Study Group at the AAO. Dr. Carlos Pavesio[17] presented his group's experience with serial electroretinography studies on 17 patients with birdshot retinochoroidopathy, confirming earlier observations from our group at the Massachusetts Eye and Ear Infirmary[18] that ERG data (voltages and 30-hz implicit time latency) are exquisitely sensitive monitors of disease activity in patients with birdshot. He concluded that "objective electrophysiological assessment of retinal function demonstrated improvement following treatment and provides a reliable method of monitoring treatment efficacy." We are strong advocates of this monitoring technique for birdshot retinochoroidopathy, believing that ERG testing on such patients should be done at least twice yearly and any time the patient complains of diminished visual function yet clinical assessment fails to objectively confirm such degradation.

Dr. George Marak[19] addressed the matter of Gram-negative sepsis, wondering why, since Gram-negative bacterial endotoxin induces experimental uveitis in animals, and there are 200,000 hospital admissions for Gram-negative sepsis in the United States each year, we never see uveitis in such patients. Dr. Marak's experiments disclosed that mice employed in the creation of the experimental endotoxin uveitis model receive approximately 3.75 million times the dose of endotoxin that produces clinical symptoms in humans, and that the intravitreal injections in mice that are performed are 10,000 times the fatal systemic concentration of endotoxin. Hence, it would appear that in the clinical circumstance in humans, the amount of endotoxin available to produce inflammation in the eye is vastly less than that employed in the experimental model.

Dr. Russell Read,[20] Assistant Professor of Ophthalmology at the University of Alabama, speaking for the Vogt-Koyanagi-Harada (VKH) therapy group, an international consortium engaged in a retrospective survey of current treatment patterns in acute and subacute VKH, reported on 76 patients who met the study criteria. The patients on average had been followed elsewhere for 39 days following the onset of symptoms before presentation to a uveitis specialist. Steroids were always employed in the care of the patients, but immunomodulatory therapy was typically required as well, with alkylating therapy clearly having the best outcome. Azathioprine plus methotrexate appeared to offer good results as well; 60% of patients on combination cyclosporine and prednisone failed therapy, and 15% of patients on cyclosporine developed clinically important central nervous system (CNS) lesions. All told, 14% of patients had profound loss of vision from the ocular manifestations of VKH.

Dr. Ronald Buggage and colleagues,[21] of the National Eye Institute, at the National Institutes of Health in Bethesda Maryland, reported on CNS lesion development, this time in a 13-year-old patient with Behçet's disease who was being treated with intravenous daclizumab for the ocular complications of Behçet's disease. The medication was eventually withdrawn, and 3 weeks after the last daclizumab infusion, the patient developed severe headache with nausea and vomiting. Neuroimaging studies revealed diffused leptomeningeal and cerebellar enhancement, and despite aggressive intravenous steroid therapy, an emergent neurosurgical procedure was required, during which the cerebellar tonsils were excised. Immunopathologic studies of the excised tissue revealed activated T cells and macrophages in the tissue. Daclizumab therapy was reinstituted. Dr. M. Accortini[22] reported on the long-term follow-up of patients with Behçet's disease who had been treated with immunosuppressive chemotherapeutic agents. He found that cyclosporin A was effective in 42% of the patients, and combining it either with methotrexate or azathioprine resulted in 6% more of the cases being effectively controlled. Other immunosuppressive agents were required, without the use of cyclosporin, to control the disease in the remaining 52% of the patients.

Long-Term Follow-Up
During a free paper session at the main meeting, Dr. Krista Rosenberg[23] reported on the analysis that she and her colleagues performed at the Bascom Palmer Eye Institute, University of Miami, Florida. A total of 149 patients who had had uveitis beginning in childhood were reviewed retrospectively to examine the prevalence and type of ocular complications from pediatric uveitis. Eighty-nine percent developed at least 1 complication; 619 complications were documented; worse eye median visual acuity at 10 years was 20/250 (range: 20/15 -- NLP); and the median time to reduction of vision to less than 20/200 was 15.7 months. Sixty-eight patients (35.6%) had ocular surgery, 38 of them in both eyes. The authors concluded that most children with uveitis develop complications, and these complications increase with the duration of disease. Median age at diagnosis had been 8.4 years, and the patients had been followed for prolonged periods, with a median follow-up of 33.5 months. The authors found that pediatric uveitis frequently produces ocular complications, with a 74% risk of severe vision loss in at least 1 eye by 3 years of follow-up. Cataract (52%), posterior synechiae (48%), glaucoma (42%), optic nerve edema (42%), and cystoid macular edema (20%) were the predominant complications encountered.

Their findings supported and confirmed those of Edelsten and associates,[24] in which moderate to severe loss was found in approximately 10% of their population. In those children being followed by rheumatologists, the complication rate was considerably less (12%) compared with those patients being followed by ophthalmologists prior to referral (47%) -- emphasizing the fact that ophthalmologists caring for patients with pediatric uveitis should strongly consider early referral to a uveitis specialist. Zak and associates,[25] in a 25-year follow-up study of 65 adults with a history of juvenile idiopathic uveitis, came to the same conclusion. The average follow-up in this study group was nearly 27 years after the onset of juvenile idiopathic arthritis; ocular complications occurred in 20% of cases. Twenty-three percent of these patients were blind, and half the complications that were seen were seen late -- that is, they evolved very slowly through time. Finally, Özdal and associates,[26] from McGill University in Canada, followed 18 patients, all with ocular complications at the time of their referral to McGill, who had juvenile idiopathic arthritis-associated uveitis. The mean duration of uveitis at the time that they entered into the McGill system was 20.5 years. Thirty percent had visual acuity of less than 20/150, and 70% had vision less than 20/50.

The conclusion from these groups has been the same: outcomes will be improved only with earlier disease detection and increased vigor of therapy by physicians skilled in the use of immunomodulatory agents. Legislation requiring vision screening referral of very young children is also critical.

References
Nguyen QD, Foster CS, Program directors. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Cunningham ET. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Introduction to uveitis and principles of diagnosis: epidemiology and classification of uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Van Gelder R. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Introduction to uveitis and principles of diagnosis: principles and diagnosis and recent advances. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Foster CS. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Principles of management: basic principles. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Samson CM, Waheed NK, Baltatzis S, Foster CS. Methotrexate treatment of uveitis. Ophthalmology. 2001;108:1134-1139. Abstract
Lane L, Tamesis R, Rodriguez A, et al. Systemic immunosuppressive therapy and the occurrence of malignancy in patients with ocular inflammatory disease. Ophthalmology. 1995;102:1530-1535. Abstract
Jabs DA. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Principles of management: oral corticosteroids and immunomodulatory therapy. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Margolis TP. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Infectious and pediatric uveitis and the spondyloarthropathies: herpes eye disease. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Vitale AT. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Infectious and pediatric uveitis and the spondyloarthropathies: pediatric uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Davis JL. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: The uveitic syndromes -- autoimmune and posterior uveitis: intermediate uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Whitcup S. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: The uveitic syndromes -- autoimmune and posterior uveitis: sarcoidosis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Nguyen QD. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: The uveitic syndromes -- autoimmune and posterior uveitis: retinal vasculitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Opremcak EM. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Surgery in uveitis and ocular inflammatory diseases: diagnostic surgery in uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Dunn JP Jr. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Surgery in uveitis and ocular inflammatory diseases: cataract surgery in uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Netland PA. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Surgery in uveitis and ocular inflammatory diseases: glaucoma surgery in uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Jaffe GJ. Uveitis 2003: Diagnosis and Management of Ocular Inflammation in the 21st Century: Surgery in uveitis and ocular inflammatory diseases: vitreoretinal surgery in uveitis. Uveitis Subspecialty Day. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15, 2003; Anaheim, California.
Pavesio CE, Robson AG, Koh AC, Graham EC, Holder GE. Electrophysiological characteristics and monitoring in the management of birdshot chorioretinopathy (BSRC). Program and abstracts of the American Uveitis Society Meeting held at the American Academy of Ophthalmology 2003 Annual Meeting; November 15-18, 2003; Anaheim, California.
Zacks DM, Samson CM, Loewenstein J, Foster CS. Electroretinograms as an indicator of disease activity in birdshot retinochoroidopathy. Graefes Arch Clin Exp Ophthalmol. 2002;240:601-607. Abstract
Marak GF. Of mice and men -- endotoxic uveitis. Program and abstracts of the American Uveitis Society Meeting held at the American Academy of Ophthalmology 2003 Annual Meeting; November 15-18, 2003; Anaheim, California.
Read RW, for the VKH Therapy Group (Accortini M, Bodaghi B, Chee SP, Kawashima H, LeHoang P, Okada A, Pivett-Pezzi P, Rao N, Secchi A, Tabbara K, Usui M). A retrospective multinational survey of current treatment patterns in acute and subacute Vogt-Koyanagi-Harada disease. Program and abstracts of the American Uveitis Society Meeting held at the American Academy of Ophthalmology 2003 Annual Meeting; November 15-18, 2003; Anaheim, California.
Buggage R, Li Z, Chan CC, Nussenblatt R. Acute Neuro-Beh?et's following the discontinuation of daclizumab for the treatment of ocular Beh?et's disease. Program and abstracts of the American Uveitis Society Meeting held at the American Academy of Ophthalmology 2003 Annual Meeting; November 15-18, 2003; Anaheim, California.
Accortini M. Long-term follow-up of patients with Beh?et's disease treated with immunosuppressive agents. Program and abstracts of the American Uveitis Society Meeting held at the American Academy of Ophthalmology 2003 Annual Meeting; November 15-18, 2003; Anaheim, California.
Rosenberg K, Feuer WJ, Davis JL. Ocular complications of pediatric uveitis. Program and abstracts of the American Academy of Ophthalmology 2003 Annual Meeting; November 15-18, 2003; Anaheim, California. PA002.
Edelsten C, Lee V, Bentley CR, Kanski JJ, Graham EM. An evaluation of baseline risk factors predicting severity in juvenile idiopathic arthritis associated uveitis and other chronic anterior uveitis in early childhood. Br J Ophthalmol. 2002;86:51-56. Abstract
Zak M, Fledelius H, Petersen FK. Ocular complications and visual outcomes in juvenile chronic arthritis: a 25 year follow-up study. Acta Ophthalmol Scand. 2003;81:211-215. Abstract
Özdal PC, Vianna RNG, Deschenes J. Visual outcome of juvenile rheumatoid arthritis associated uveitis in adults. Ocul Immunol Inflamm. In Press.




You must read all articles in this activity to prepare for the post test.

Copyright © 2003 Medscape.










Target Audience

Learning Objectives

Faculty and Disclosures

Accreditation Statements

Instructions for Participation and Credit

Hardware/Software Requirements

Privacy and Confidentiality

Post Test and Evaluation
CME in this activity indicates continuing education for medical professionals.




SEARCH



Medscape DrugInfo

MEDLINE

Advanced Search



• About Medscape • Privacy & Ethics • Terms of Use • Help • WebMD Health



All material on this website is protected by copyright, Copyright © 1994-2004 by Medscape. This website also contains material copyrighted by 3rd parties. Medscape requires Netscape or Microsoft browsers in versions 5 or higher.
Mike Bartolatz
Moderator

Post Reply