top of page

What is Uveitis?

Uveitis is an inflammation of one or all parts of the uvea, or the vascular area between the retina and sclera of the eye. The anterior uvea is composed of the iris and ciliary body; an irritation of this segment, or anterior uveitis, leads to acute painful symptoms and photophobia. Inflammation of the posterior uvea, including the choroid, retina, and retinal vasculature, carries a risk of painless visual loss. Uveitis of all types affects children and adults, and the etiology is most commonly idiopathic.

 

At the Connecticut Uveitis Foundation, we strive to help diagnose and treat patients with all types of uveitis and the eye and visual complications that arise from uveitic diseases. We are made up of a group highly trained, compassionate, and skilled physicians, assisted by the latest technology in diagnostic testing as well as the best in medical and surgical treatments. 

Epidemiology

Uveitis may affect individuals of any age, gender, or geographic location without preference. In the US, the incidence of uveitis is about 15 cases per 100,000, although a study carried out in Northern California found the incidence to be higher at 52.4 cases per 100,000 person-years. Incidences similar to those in the US have been reported in Denmark (14 per 100,000 person-years) and France (17 per 100,000 person-years). The prevalence in the US and other western countries is about 38 per 100,000. Acute anterior uveitis is particularly common in Finland, with an annual incidence of 22.6 per 100,000 person-years and a prevalence of 68.7 per 100,000. The peak age of presentation is between age 30 and 40 years. Anterior uveitis, specifically iritis, is the most common form, representing about 75% of cases. Posterior uveitis is less common, followed by intermediate uveitis.

Etiology can be divided into idiopathic, infectious, and noninfectious causes. Infecting organisms include herpes simplex virus (HSV), herpes zoster virus, CMV, HIV, Lyme disease, toxoplasmosis, TB, syphilis, and histoplasmosis. Noninfectious causes include seronegative arthropathies, inflammatory bowel disease, autoimmune disorders, sarcoidosis, multiple sclerosis, and eye trauma.

Acute anterior uveitis may be idiopathic, or associated with HLA-B27-related disease or viral eye disease. One study found that 49.4% of patients with anterior uveitis tested positive for the HLA-B27 antigen. [9] Posterior uveitis is associated with localized infections or systemic infection, or systemic inflammatory disease. Rarely, uveitis can be caused by a previous eye injury or underlying neoplasm.

 

Insults to ocular structures, such as trauma or infection, lead to an inflammatory response within the uvea. Traumatic eye injury results in ocular inflammation due to a breakdown of the blood-brain barrier. Release of potent inflammatory mediators (prostaglandins and leukotrienes) leads to vascular leakage and the influx of inflammatory cells. Uveitis may also result from infectious disease. Micro-organisms cause intraocular damage either by direct lysis of host cells or by producing endotoxins or exotoxins toxic to the ocular microenvironment. These breakdown products induce the recruitment of host inflammatory cells (neutrophils and macrophages) and associated production of free radicals and enzymes to eliminate the infectious organism. In the process, further tissue damage occurs. Ocular inflammation is also associated with immunologic disorders. An autoimmune attack begins with an antigen-specific immune response (T cells and B cells) to ocular antigens. Autoantibodies may bind specific antigens, as in peripheral ulcerative keratitis and ocular cicatricial pemphigoid, and complement is activated and macrophages are recruited to the site. This leads to direct tissue damage. In contrast, an autoimmune response may lead to immune complex formation and deposition in the blood vessels and activation of the immune response. Immune complexes appear to be involved in SLE, Wegener granulomatosis, and other vasculitides. Finally, an autoimmune uveitis can occur via a cell-mediated mechanism in which autoreactive T-cells recognize self-antigen and lead to tissue damage by direct infiltration and production of cytokines, amplifying the immune response.

Etiology and Pathophysiology

Connecticut Uveitis Foundation was just awarded the Allergan Foundation Community Grant to improve Uveitis education and awareness. 

Visit Us

 

Connecticut Uveitis Foundation

1043 Farmington Avenue

West Hartford, CT 06107

 

Tel:  860-561-8617

Fax: 860-561-8657

info@uveitisct.org

 

bottom of page