Introduction
Historically, uveitis is a term used to describe inflammatory processes of the portion of the eye
known as the uvea, which is composed of the iris, ciliary body, and the choroid; however, any area of
the eye can be inflammed. Uveitis can be further subdivided into anterior, intermediate, posterior,
and panuveitis based on the primary anatomical location of the inflammation in the eye. Symptoms
and consequences can range from pain and conjunctival injection to complete vision loss. Anterior
uveitis is epitomized by the anterior segment being the predominate site of inflammation.
Intermediate uveitis is defined by inflammation of the vitreous cavity and pars plana, while posterior
uveitis involves the retina and choroid. Inflammation in panuveitis includes all layers.[1]
Anatomic locations of uveitis:
Anterior
Intermediate
Posterior
Panuveitis
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Etiology
Uveitis is most often idiopathic but has been associated with traumatic, inflammatory, and infectious
processes. Patients may present with concurrent systemic symptoms or infectious diseases to
suggest an etiology affecting more than just the eye. Idiopathic cases of uveitis account for 48 to
70% of uveitis cases.[2] Systemic inflammatory disorders commonly associated with anterior uveitis
include: HLA-B27-associated entities, juvenile idiopathic arthritis, inflammatory bowel disease,
sarcoidosis, Behcet's disease (BD) or tubulo-interstitial nephritis (TINU). Multiple sclerosis,
sarcoidosis, and TINU are causes of intermediate uveitis with systemic manifestations, while Vogt-
Koyanagi-Harada syndrome, leukemia, lupus, BD, and multiple sclerosis can cause a posterior uveitis
with systemic manifestations. BD is a systemic vasculitis that can also present with pan-uveitis.[3]
Infectious processes are thought to account for approximately 20% of all uveitis cases but underlying
causes can vary geographically [4]. Infectious causes include viruses (HSV, VZV, CMV), bacteria
(endophthalmitis, syphilis, tuberculosis, etc), or parasites/worms (toxoplasmosis, Lyme Disease,
toxocara, Bartonella sp. or other atypical infections).[5][6]
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Epidemiology
Uveitis can affect people of all ages and can vary significantly by geographic location and age of the
patient [7]. In a study done from 2006 to 2007, the incidence of uveitis was 24.9 cases per 100,000
persons. Prevalence rates for 2006 and 2007 came in at 57.5 and 58 respectively per 100,000
persons [8]. There was no difference in the incidence rate between men and women, but women
had a higher prevalence [8]. Anterior uveitis is the most prevalent form, accounting for
approximately 50% of uveitis cases, while posterior uveitis is the least common. Ongoing
inflammation seen in untreated uveitis and complications related to this uncontrolled inflammation
are estimated to be responsible for approximately 10% of the blindness in the United States.
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Pathophysiology
The pathophysiology of uveitis in general is not well understood. Groups have hypothesized that
trauma to the eye can cause cell injury or death which leads to the release of inflammatory cytokines
leading to a post-traumatic uveitis. Uveitis caused by inflammatory diseases is thought to be due to
molecular mimicry, where an infectious agent cross-reacts with ocular-specific antigens. Vision-
threatening inflammation is mediated by CD4 Th1 cells. Normally, only activated lymphocytes are
allowed past the blood-retina barrier, thus decreasing sensitization of naïve T cells to ocular
proteins. Researchers have proposed there is molecular mimicry between retinal S-Ag peptides and
a peptide from disease associated HLA-B antigens, which leads to targeting of ocular proteins and
inflammatory response.[9]
