Incubator escapee wiki

Uveitis

Article Discussion
(Redirected from Iritis)

Template:Short description Template:Infobox medical condition (new) Uveitis (Template:IPAc-en) is inflammation of the uvea, the pigmented layer of the eye between the inner retina and the outer fibrous layer composed of the sclera and cornea.<ref name="nei">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> The uvea consists of the middle layer of pigmented vascular structures of the eye and includes the iris, ciliary body, and choroid. Uveitis is described anatomically, by the part of the eye affected, as anterior, intermediate or posterior, or panuveitic if all parts are involved. Anterior uveitis (iridocyclitis) is the most common, with the incidence of uveitis overall affecting approximately 1:4500, most commonly those between the ages of 20–60. Symptoms include eye pain, eye redness, floaters and blurred vision, and ophthalmic examination may show dilated ciliary blood vessels and the presence of cells in the anterior chamber. Uveitis may arise spontaneously, have a genetic component, or be associated with an autoimmune disease or infection. While the eye is a relatively protected environment, its immune mechanisms may be activated resulting in inflammation and tissue destruction associated with T-cell activation.

Uveitis is an ophthalmic emergency that requires urgent control of the inflammation to prevent vision loss. Treatment typically involves the use of topical eye drop steroids, intravitreal injection, newer biologics, and treating any underlying disease. While initial treatment is usually successful, complications include other ocular disorders, such as uveitic glaucoma, retinal detachment, optic nerve damage, cataracts, and in some cases, a permanent loss of vision. In the United States uveitis accounts for about 10–20% of cases of blindness.

File:Blausen 0390 EyeAnatomy Sectional.png
Anterior eye showing uveal structures (iris, ciliary body, with adjacent choroid which connects them)

ClassificationEdit

Uveitis is classified anatomically into anterior, intermediate, posterior, and panuveitis forms—based on the part of the eye primarily affected.<ref>Jabs DA, Nussenblatt RB, Rosenbaum JT. Standardization of Uveitis Nomenclature (SUN) Working Group. Standardization of uveitis nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol 2005;140:509-516.</ref> Before the twentieth century, uveitis was typically referred to in English as "ophthalmia."<ref name="JAMA Ophthalmol">Template:Cite journal</ref>

  • Anterior uveitis includes iridocyclitis and iritis. Iritis is the inflammation of the anterior chamber and iris. Iridocyclitis is inflammation of the iris and ciliary body with inflammation predominantly confined to the ciliary body. Between 66% and 90% of uveitis cases are anterior in location (iritis).<ref>Template:Cite journal</ref> This condition can occur as a single episode and subside with proper treatment or may take on a recurrent or chronic nature.
  • Intermediate uveitis, also known as pars planitis, consists of vitritis—which is inflammation of cells in the vitreous cavity, sometimes with snowbanking, or deposition of inflammatory material on the pars plana. There are also "snowballs," which are inflammatory cells in the vitreous.
  • Posterior uveitis or chorioretinitis is the inflammation of the retina and choroid.
  • Panuveitis is the inflammation of all layers of the uvea.

CausesEdit

Uveitis is usually an isolated illness, but can be associated with many other medical conditions.<ref name=nei/> In anterior uveitis, no associated condition or syndrome is found in approximately one-half of cases. However, anterior uveitis is often one of the syndromes associated with HLA-B27. Presence of this type of HLA allele has a relative risk of evolving this disease by approximately 15%.<ref name="Kumar5-7">Table 5-7 in: Template:Cite book</ref>

The most common form of uveitis is acute anterior uveitis (AAU). It is most commonly associated with HLA-B27, which has important features: HLA-B27 AAU can be associated with ocular inflammation alone or in association with systemic disease. HLA-B27 AAU has characteristic clinical features including male preponderance, unilateral alternating acute onset, a non-granulomatous appearance, and frequent recurrences, whereas HLA-B27 negative AAU has an equivalent male to female onset, bilateral chronic course, and more frequent granulomatous appearance.<ref name="larson" /> Rheumatoid arthritis is not uncommon in Asian countries as a significant association of uveitis.<ref>Template:Cite journal</ref>

Noninfectious or autoimmune causesEdit

Template:More medical citations needed

Associated with systemic diseasesEdit

Systemic disorders that can be associated with uveitis include:<ref>White G. "Uveitis." Template:Webarchive AllAboutVision.com. Retrieved August 20, 2006.</ref><ref>Template:Cite journal</ref>

Infectious causesEdit

Uveitis may be an immune response to fight an infection caused by an organism in the eye. They are less common than non-infectious causes and require antimicrobial/ viral/ parasitic treatment in addition to inflammatory control. Infectious causes in order of global burden include:

File:PMID20029144 04 tubercular posterior uveitis.png
Subretinal abscess in tubercular posterior uveitis

|CitationClass=web }}</ref>


Drug-related side effectsEdit

  • Rifabutin, a derivative of Rifampin, has been shown to cause uveitis.<ref name="cdc">{{#invoke:citation/CS1|citation

|CitationClass=web }}</ref>

White dot syndromesEdit

Occasionally, uveitis is not associated with a systemic condition: the inflammation is confined to the eye and has unknown cause. In some of these cases, the presentation in the eye is characteristic of a described syndrome, which are called white dot syndromes, and include the following diagnoses:

Masquerade syndromesEdit

Masquerade syndromes are those conditions that include the presence of intraocular cells but are not due to immune-mediated uveitis entities. These may be divided into neoplastic and non-neoplastic conditions.

  • Non-neoplastic:
  • Neoplastic:

Signs and symptomsEdit

File:Ciliary-flush.jpg
Ciliary flush
File:Keratic-precipitates.jpg
Keratic precipitates
File:Hypopyon.jpg
Hypopyon in anterior uveitis, seen as yellowish exudation in lower part of anterior chamber of eye
File:Vascularised posterior synechia.jpg
Vascularised posterior synechia

The disease course, anatomy, and laterality can vary widely and are important to consider in diagnosis and treatment. Cases may be acute (sudden onset with < 3 month duration) and monophonic, acute and recurrent, or chronic.<ref>Template:Cite journal</ref> The signs and symptoms of uveitis may include the following:<ref name=nei/>

Anterior uveitis (iritis)Edit

Intermediate uveitisEdit

Most common:

  • Floaters, which are dark spots that float in the visual field
  • Blurred vision

Intermediate uveitis usually affects one eye. Less common is the presence of pain and photophobia.<ref>Template:Cite journal</ref>

Posterior uveitisEdit

Inflammation in the back of the eye is commonly characterized by:

  • Floaters
  • Blurred vision

PathophysiologyEdit

Immunological factorsEdit

Onset of uveitis can broadly be described as a failure of the ocular immune system and the disease results from inflammation and tissue destruction. Uveitis is driven by the Th17 T cell sub-population that bear T-cell receptors specific for proteins found in the eye.<ref name="nian" /> These are often not deleted centrally whether due to ocular antigen not being presented in the thymus (therefore not negatively selected) or a state of anergy is induced to prevent self targeting.<ref name="lamb" /><ref name="avi" />

Autoreactive T cells must normally be held in check by the suppressive environment produced by microglia and dendritic cells in the eye.<ref name="forr" /> These cells produce large amounts of TGF beta and other suppressive cytokines, including IL-10, to prevent damage to the eye by reducing inflammation and causing T cells to differentiate to inducible T reg cells. Innate immune stimulation by bacteria and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal expansion of the autoreactive Th1 and Th17 cells that possess potential to cause damage to the eye.

Whether through infection or other causes, this balance can be upset and autoreactive T cells allowed to proliferate and migrate to the eye. Upon entry to the eye, these cells may be returned to an inducible Treg state by the presence of IL-10 and TGF-beta from microglia. Failure of this mechanism leads to neutrophil and other leukocyte recruitment from the peripheral blood through IL-17 secretion. Tissue destruction is mediated by non-specific macrophage activation and the resulting cytokine cascades.<ref>Template:Cite journal</ref> Serum TNF-α is significantly elevated in cases while IL-6 and IL-8 are present in significantly higher quantities in the aqueous humour in patients with both quiescent and active uveitis.<ref>Template:Cite journal</ref> These are inflammatory markers that non-specifically activate local macrophages causing tissue damage.

Genetic factorsEdit

The cause of non-infectious uveitis is unknown but there are some strong genetic factors that predispose disease onset including HLA-B27<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> and the PTPN22 genotype.<ref>Template:Cite journal</ref>

Infectious agentsEdit

Recent evidence has pointed to reactivation of herpes simplex, varicella zoster and other viruses as important causes of developing what was previously described as idiopathic anterior uveitis.<ref>Template:Cite journal</ref> Bacterial infection is another significant contributing factor in developing uveitis.<ref>Template:Cite journal</ref>

DiagnosisEdit

Uveitis is assessed as part of a dilated eye exam.<ref name=nei/> Diagnosis includes dilated fundus examination to rule out posterior uveitis, which presents with white spots across the retina along with retinitis and vasculitis.<ref name=nei/>

Laboratory testing is usually used to diagnose specific underlying diseases, including rheumatologic tests (e.g. antinuclear antibody, rheumatoid factor) and serology for infectious diseases (Syphilis, Toxoplasmosis, Tuberculosis).

Major histocompatibility antigen testing may be performed to investigate genetic susceptibility to uveitis. The most common antigens include HLA-B27, HLA-A29 (in birdshot chorioretinopathy) and HLA-B51 (in Behçet disease).Template:Citation needed

Radiology X-ray may be used to show coexisting arthritis and chest X-ray may be helpful in sarcoidosis.

TreatmentEdit

Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or as oral therapy.<ref>Template:Cite journal</ref> Prior to the administration of corticosteroids, corneal ulcers must be ruled out. This is typically done using a fluorescence dye test.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. Successful treatment of active uveitis increases T-regulatory cells in the eye, which likely contributes to disease regression.<ref>Template:Cite journal</ref> In severe cases an injection of posterior subtenon triamcinolone acetate may also be given to reduce the swelling of the eye. <ref>BNF 45 March 2003</ref>

Intravitreal injection of steroid has proven to be a newer useful way to control inflammation for longer without the need for daily eyedrops. Dexamethasone and fluocinolone acetonide are two more commonly used options for noninfectious uveitis.<ref>Template:Cite journal</ref>

Non-biologic, steroid sparing therapies for noninfectious uveitis in adults are now more available. These include the disease-modifying antirheumatic drugs (DMARDs) methotrexate, mycophenolate, cyclosporine, azathioprine, and tacrolimus.<ref name=":1">Template:Cite journal</ref> In comparing various studies, methotrexate is more efficacious than mycophenolate in inflammatory control for most forms of panuveitis. Methotrexate also had little to no differences in safety outcomes compared to mycophenolate.<ref name=":1" />

In the case of herpetic uveitis, anti-viral medications, such as valaciclovir or aciclovir, may be administered to treat the causative viral infection.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>

EpidemiologyEdit

Uveitis affects approximately 38 to 714 per 100,000 people worldwide. <ref>{{cite journal |last1=Maghsoudlou |first1=P |last2=Epps |first2=SJ |last3=Guly |first3=CM |last4=Dick |first4=AD |date=2025-28-05 |title=Uveitis in Adults: A Review |journal=JAMA |doi=10.1001/jama.2025.4358 |url=https://jamanetwork.com/journals/jama/article-abstract/2834628 </ref> Uveitis is most common between the ages 20 to 60. In western countries, anterior uveitis accounts for between 50% and 90% of uveitis cases. In Asian countries the proportion is between 28% and 50%.<ref>Template:Cite journal</ref> Uveitis is estimated to be responsible for approximately 10%-20% of the blindness in the United States.<ref>Template:Cite journal</ref>

For non-infectious uveitis, women are more likely (57%) to be affected than men, possibly due to their higher prevalence of related autoimmune diseases.<ref name=":0">Template:Cite journal</ref> Vitamin D deficiency and smoking are risk factors for non-infectious uveitis.<ref name=:0/>

PrognosisEdit

The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication including cataracts, uveitic glaucoma, band keratopathy, macular edema and permanent vision loss may result if left untreated. The type of uveitis, as well as its severity, duration, and responsiveness to treatment or any associated illnesses, all factor into the outlook.<ref name=nei/>

See alsoEdit

ReferencesEdit

Template:Reflist

Further readingEdit

Template:Medical resources

Template:Eye pathology

Template:Authority control

Retrieved from "https://zalansite.site/mediawiki/index.php?title=Uveitis&oldid=612725"