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AbstractBacteria are suspected contributors to several forms of immune-mediated, noninfectious forms of uveitis including that associated with ankylosing spondylitis, sarcoidosis, Behçet’s disease and inflammatory bowel disease. Endotoxin (lipopolysaccharide)-induced uveitis has been a widely used model for more than 2 decades. Both rats and mice develop a transient, bilateral anterior uveitis after a systemic injection of endotoxin. Inflammation posterior to the lens is generally milder than anterior segment inflammation. The uveitis is severer if the lipopolysaccharides are injected intraocularly. The model has been invaluable in helping to identify mediators induced in the inflamed eye and in testing pharmacologic approaches to reduce eye inflammation. Muramyl dipeptide is another bacterial cell component that can induce uveitis in laboratory animals. Muramyl dipeptide is especially intriguing as a cause of uveitis because it activates the intracellular protein, Nod2, and mutations in the NOD2 gene are the cause of the autosomal dominant form of uveitis that is characteristic of Blau syndrome. Since a mutation in a gene that codes for a protein which senses a bacterial product consistently results in uveitis, it is critical to understand more fully the mechanisms by which bacterial products cause uveitis in laboratory animals.Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

AbstractExperimental melanin-protein-induced uveitis (EMIU), which is also known as experimental autoimmune anterior uveitis, was first described in 1993 by Broekhuyse et al. This experimental uveitis may be induced in certain inbred and outbred rat strains by immunization with bovine ocular melanin. The inflammation shares clinical features with human acute anterior uveitis. The duration of the first episode is approximately 1 month. Spontaneous recovery to a near normal clinical state is the rule, but multiple recurrences are common. Slit-lamp biomicroscopic examination reveals a florid anterior-chamber reaction, with formation of a retro-iridal empyema, fibrin clots and posterior synechiae. At a microscopic level, leukocytic infiltration is first observed in the anterior uvea. Although this tissue remains the site of maximum inflammation throughout an attack, in severe cases, limbitis, vitritis and choroiditis are also observed. Abrogation of EMIU occurs after treatment with anti-CD4 antibody, indicating that the uveitis is controlled by CD4-positive T cells. Several research groups have used EMIU to investigate various aspects of the pathogenesis of acute anterior uveal inflammation, including the participation of different leukocyte subsets, the expression of cell adhesion molecules, cytokines, chemokines and nitric oxide, the role of complement and the impact of apoptosis. In addition, EMIU has also been used to evaluate various biologic interventions with potential implications for the treatment of human disease.Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Uveitis or intraocular inflammation is a major cause of visual loss. Acute anterior uveitis (AAU) affects ∼40% of patients with ankylosing spondylitis (AS) but also affects patients with no evidence of spondylarthritis. We sought to determine whether a unique genetic region could be implicated in a specific manifestation—AAU—of a multisystem, inflammatory, genetically complex disease, AS.Individuals from families multiplex for AAU were genotyped at 400 markers representing the ABI PRISM linkage map MD‐10, and at the HLA–B, DRB1, DQA1, DQB1, and DPB1 alleles. Among the family members with AAU, 76 affected sibpairs were analyzed (6 without concomitant AS, 12 discordant for AS, and 58 concordant for AS). Two‐point and multipoint nonparametric linkage analyses were performed, and 1‐parameter allele‐sharing model logarithm of odds (LOD) scores were determined.As previously reported for AS, linkage at the major histocompatibility complex region (chromosome 6p21) was evident, exhibiting the highest multipoint LOD score (4.96 at marker HLA–B). Strong linkage was seen at a region on chromosome 9p21–9p24, with a LOD score of 3.72 at marker D9S157. When compared with a companion cohort of AS families, the linkage at this region was found in association with AAU but not with AS. A third region on chromosome 1q23–1q31 was observed to have suggestive linkage (LOD 2.05 at marker D1S238), which overlaps with a region associated with AS.This is the first study in which a genetic region for AAU has been identified by genome‐wide scan. Even though AS was highly prevalent in this cohort of families, a locus at chromosome 9p21–9p24 was identified that uniquely associates with AAU. Identifying the genetic perturbation at this region may advance our understanding of the mechanisms involved in tissue‐specific pathology of complex inflammatory diseases. [ABSTRACT FROM AUTHOR]

Purpose: A case of linear IgA disease is reported to alert ophthalmologists and physicians to this unusual cause of chronic cicatrizing conjunctivitis. Methods: Clinical records of a patient suffering from linear IgA disease were reviewed. Results: A 65-year-old woman with a complicated medical history experienced rapidly progressive chronic cicatrizing conjunctivitis leading to corneal perforation. Undiagnosed gingivitis and palatal ulceration had been present for 5 years prior to the onset of ocular symptoms and vitamin C deficiency had followed the consequent dietary restrictions. A diagnosis of linear IgA disease was made on conjunctival biopsy, which demonstrated linear deposits of IgA along the epithelial basement membrane. The perforation was managed successfully with a conjunctival pediculate flap. Control of the inflammation was achieved with systemic prednisolone and cyclophosphamide but at the expense of serious systemic side-effects. Conclusions: Linear IgA disease causes progressive conjunctival cicatrization in many affected individuals. Although dapsone generally controls the inflammation, heavier systemic immunosuppression was required in this case. Involvement of skin or other mucosal surfaces may become symptomatic before the conjunctivitis, and physicians must be educated to refer patients for ophthalmological review on diagnosis. Conversely, ophthalmologists encountering ocular linear IgA disease should be aware of the possibility of other mucosal involvement requiring physician intervention. [ABSTRACT FROM AUTHOR]

Purpose: A case of trichotillomania, or compulsive hair-pulling, involving the eyelids is presented to alert ophthalmologists to this common, but frequently overlooked cause of eyelash and eyebrow alopecia. Methods and results: Clinical records of a 33-year-old woman suffering from trichotillomania were reviewed. Compulsive hair-pulling began in childhood and had become chronic. Psychiatric intervention was unsuccessful. Conclusions: The diagnosis of trichotillomania is made on history and slit-lamp examination findings. A skin biopsy may be necessary to exclude alopecia areata. Adults should be referred to a psychiatrist. Although childhood disease is usually benign, often reflecting a disturbed parent-child relationship, in adults hair-pulling is generally chronic and associated with psychiatric illness. [ABSTRACT FROM AUTHOR]