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uveitis (n.)
1.inflammation of the uvea of the eye
Uveitis (n.)
1.(MeSH)Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)
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⇨ definição - Wikipedia
⇨ Anterior uveitis acute, recurrent or subacute • Herpesviral uveitis, anterior • Sympathetic uveitis • Uveitis, Anterior • Uveitis, Intermediate • Uveitis, Posterior • Uveitis, Suppurative • Uveitis, Sympathetic • sympathetic uveitis
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Wikipedia
Uveitis | |
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Classification and external resources | |
Hypopyon in anterior uveitis, seen as yellowish exudate in lower part of anterior chamber of eye |
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ICD-10 | H20 |
ICD-9 | 364 |
DiseasesDB | 13676 |
eMedicine | oph/580 emerg/284 |
MeSH | D014605 |
Uveitis specifically refers to inflammation of the middle layer of the eye, termed the "uvea" but in common usage may refer to any inflammatory process involving the interior of the eye.
Uveitis is estimated to be responsible for approximately 10% of the blindness in the United States.[1] Uveitis requires an urgent referral and thorough examination by an ophthalmologist or optometrist along with urgent treatment to control the inflammation.
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Uveitis may be classified anatomically into anterior, intermediate, posterior and panuveitic forms, based on which part of the eye is primarily affected by the inflammation.
In 2004, a group of international uveitis specialists convened in Baltimore, MD, to standardize the method of reporting data in uveitis clinical trials, including anatomical classification. The results of this meeting were published in the American Journal of Ophthalmology in 2005.[2]
Medical signs of Anterior Uveitis include dilated ciliary vessels, presence of cells and flare in the anterior chamber, and keratic precipitates ("KP") on the posterior surface of the cornea.
Most common:
Intermediate uveitis normally only affects one eye. Less common is the presence of pain and photophobia.[3]
Inflammation in the back of the eye is commonly characterised by:
This section requires expansion. (May 2012) |
The cause of non-infectious uveitis is unknown but there are some strong genetic factors that predispose disease onset including HLA-B27[4][5] and the PTPN22 genotype.[6]
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.[7] Bacterial infection is another significant contributing factor in developing uveitis.[8]
Uveitis may be a (normal) immune response to fight an infection inside the eye[citation needed]. While representing the minority of patients with uveitis, such possible infections include:
This article needs additional citations for verification. (May 2012) |
Onset of Uveitis can broadly be described as a failure of the Ocular immune system and 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.[9] These are often not deleted centrally whether due to ocular antigen not being presented in the thymus and are therefore not negatively selected or a state of anergy is induced to prevent self targeting.[10][11] Autoreactive T cells, therefore, must normally be held in check by the suppressive environment wrought by Microglia and dendritic cells in the eye.[12] 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 will lead 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[13] 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.[14] These are inflammtory markers that non-specifically activate local macrophages causing tissue damage.
Myriad conditions can be associated with uveitis, including diseases with major extra-ocular involvement, as well as syndromes confined to the eye. 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 this type of HLA allele has a relative risk of evolving this disease by approximately 15%.[15]
Systemic disorders that can be associated with uveitis include:[16]
In many cases, uveitis is not associated with a systemic (i.e. extraocular) condition: the inflammation is confined to the eye. In some of these cases, the presentation in the eye is characteristic of a described syndrome, and include the following diagnoses:
It has been suggested that this section be split into a new article. (Discuss) Proposed since May 2012. |
Masquerade syndromes are ophthalmic disorders that clinically present as either an anterior or posterior uveitis, but are not primarily inflammatory. The following are some of the most common:
Diagnosis is performed using a dilated fundus examination for Posterior Uveitis which presents with white spots across the retina along with retinitis and vasculitis.
Uveitis is typically treated with glucocorticoid steroids, either as topical eye drops (prednisolone acetate) or oral therapy with corticosteroids.[18] Prior to the administration of corticosteroids, corneal ulcers must be ruled out. This is typically done using a fluoresence dye test.[19] In addition to corticosteroids, topical cycloplegics, such as atropine or homatropine, may be used. Successful treatment of active uveitis will see an increase in T-regulatory cells in the eye which is likely to contribute to disease regression.[20] In some cases an injection of PSTTA (posterior subtenon triamcinolone acetate) may also be given to reduce the swelling of the eye. [21]
Antimetabolite medications, such as methotrexate are often used for recalcitrant or more aggressive cases of uveitis. Experimental treatments with Infliximab or other anti-TNFs' infusions may prove helpful.
On May 7, 2012 the journal investigative Ophthalmology & Visual Science stated that "Metformin inhibits the process that causes that inflammation". The scientists believe that it has a good chance of being rapidly adopted as an anti-uveitis drug, since Metformin is already used so widely as a therapy for diabetes.[22]
The prognosis is generally good for those who receive prompt diagnosis and treatment, but serious complication (including cataracts, glaucoma, band keratopathy, retinal 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 in to the outlook.[1]
Uveitis affects roughly 1 in 4500 people and is most common between the ages 20 to 60 most affected, with men and women affected equally. In the west, Anterior Uveitis accounts for between 50% and 90% of Uveitis cases while in Asian countries the proportion drops to be between 28% and 50%.[23]
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