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Definição e significado de Uveitis

Definição

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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Uveitis (n.) [MeSH]


uveitis (n.)


Wikipedia

Uveitis

                   
Uveitis
Classification and external resources

Hypopyon in anterior uveitis, seen as yellowish exudate in lower part of anterior chamber of eye
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.

Contents

  Anatomical classification

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.

  • "Anterior uveitis" (or iridocyclitis) is the inflammation of the iris and anterior chamber. Anywhere from two-thirds to 90% of uveitis cases are anterior in location. This condition can occur as a single episode and subside with proper treatment or may take on a recurrent or chronic nature.
  • "Intermediate uveitis" (pars planitis) consists of vitritis - inflammatory cells in the vitreous cavity, sometimes with snowbanking, or deposition of inflammatory material on the pars plana.
  • "Posterior uveitis" (or chorioretinitis) is the inflammation of the retina and choroid.
  • "Pan-uveitis" is the inflammation of all the layers of the uvea.

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]

  Symptoms

  Anterior Uveitis

  Signs

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.

  Intermediate Uveitis

Most common:

Intermediate uveitis normally only affects one eye. Less common is the presence of pain and photophobia.[3]

  Posterior Uveitis

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

  Causes

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]

  Other Infectious causes

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:

  Pathophysiology

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.

  Conditions associated with uveitis and uveitis syndromes

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 associated with uveitis

Systemic disorders that can be associated with uveitis include:[16]

  Uveitis Syndromes

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:

  Masquerade syndromes

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:

  • Anterior segment
  • Posterior segment

  Diagnosis

Diagnosis is performed using a dilated fundus examination for Posterior Uveitis which presents with white spots across the retina along with retinitis and vasculitis.

  Treatment

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]

  Prognosis

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]

  Epidemiology

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]

  See also

  Footnotes

  1. ^ Gritz, D (1 March 2004). "Incidence and prevalence of uveitis in Northern California The Northern California Epidemiology of Uveitis Study". Ophthalmology 111 (3): 491–500. DOI:10.1016/j.ophtha.2003.06.014. 
  2. ^ 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.
  3. ^ Babu, BM; Rathinam, SR (2010 Jan-Feb). "Intermediate uveitis.". Indian journal of ophthalmology 58 (1): 21–7. DOI:10.4103/0301-4738.58469. PMC 2841370. PMID 20029143. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2841370. 
  4. ^ Wakefield, D; Chang, JH; Amjadi, S; Maconochie, Z; Abu El-Asrar, A; McCluskey, P (2011 Apr). "What is new HLA-B27 acute anterior uveitis?". Ocular immunology and inflammation 19 (2): 139–44. DOI:10.3109/09273948.2010.542269. PMID 21428757. 
  5. ^ Caspi, Rachel R. (NaN undefined NaN). "A look at autoimmunity and inflammation in the eye". Journal of Clinical Investigation 120 (9): 3073–3083. DOI:10.1172/JCI42440. 
  6. ^ Burn, Garth L.; Svensson, Lena; Sanchez-Blanco, Cristina; Saini, Manoj; Cope, Andrew P. (1 December 2011). "Why is PTPN22 a good candidate susceptibility gene for autoimmune disease?". FEBS Letters 585 (23): 3689–3698. DOI:10.1016/j.febslet.2011.04.032. 
  7. ^ Jap, A; Chee, SP (2011 Nov). "Viral anterior uveitis.". Current opinion in ophthalmology 22 (6): 483–8. DOI:10.1097/ICU.0b013e32834be021. PMID 21918442. 
  8. ^ Dick, Andrew D. (1 January 2012). "Road to Fulfilment: Taming the Immune Response to Restore Vision". Ophthalmic Research 48 (1): 43–49. DOI:10.1159/000335982. 
  9. ^ Nian, H.; Liang, D.; Zuo, A.; Wei, R.; Shao, H.; Born, W. K.; Kaplan, H. J.; Sun, D. (12 January 2012). "Characterization of Autoreactive and Bystander IL-17+ T Cells Induced in Immunized C57BL/6 Mice". Investigative Ophthalmology & Visual Science 53 (2): 897–905. DOI:10.1167/iovs.11-8297. 
  10. ^ Lambe T, Leung JC, Ferry H, et al. (April 2007). "Limited peripheral T cell anergy predisposes to retinal autoimmunity". J. Immunol. 178 (7): 4276–83. PMID 17371984. 
  11. ^ Avichezer D, Grajewski RS, Chan CC, et al. (December 2003). "An immunologically privileged retinal antigen elicits tolerance: major role for central selection mechanisms". J. Exp. Med. 198 (11): 1665–76. DOI:10.1084/jem.20030413. PMC 2194140. PMID 14657219. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2194140. 
  12. ^ Forrester, JV; Xu, H; Kuffová, L; Dick, AD; McMenamin, PG (2010 Mar). "Dendritic cell physiology and function in the eye.". Immunological reviews 234 (1): 282–304. DOI:10.1111/j.0105-2896.2009.00873.x. PMID 20193026. 
  13. ^ Khera, TK; Copland, DA; Boldison, J; Lait, PJ; Szymkowski, DE; Dick, AD; Nicholson, LB (2012 May). "Tumour necrosis factor-mediated macrophage activation in the target organ is critical for clinical manifestation of uveitis.". Clinical and experimental immunology 168 (2): 165–77. DOI:10.1111/j.1365-2249.2012.04567.x. PMID 22471277. 
  14. ^ Valentincic, NV; de Groot-Mijnes, JD; Kraut, A; Korosec, P; Hawlina, M; Rothova, A (2011). "Intraocular and serum cytokine profiles in patients with intermediate uveitis.". Molecular vision 17: 2003–10. PMC 3154134. PMID 21850175. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3154134. 
  15. ^ Table 5-7 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.  8th edition.
  16. ^ White G. "Uveitis." AllAboutVision.com. Retrieved August 20, 2006.
  17. ^ McGonagle D, McDermott MF (2006) A proposed classifi cation of the immunological diseases. PLoS Med 3(8): e297. doi:10.1371/journal.pmed.0030297
  18. ^ Pato, E; Muñoz-Fernández, S; Francisco, F; Abad, MA; Maese, J; Ortiz, A; Carmona, L; Uveitis Working Group from Spanish Society of, Rheumatology (2011 Feb). "Systematic review on the effectiveness of immunosuppressants and biological therapies in the treatment of autoimmune posterior uveitis.". Seminars in arthritis and rheumatism 40 (4): 314–23. DOI:10.1016/j.semarthrit.2010.05.008. PMID 20656330. 
  19. ^ "Fluorescein eye stain". NIH. http://www.nlm.nih.gov/medlineplus/ency/article/003845.htm. Retrieved 15 May 2012. 
  20. ^ Ruggieri, S; Frassanito, MA; Dammacco, R; Guerriero, S (2012-05-07). "Treg Lymphocytes in Autoimmune Uveitis.". Ocular immunology and inflammation. DOI:10.3109/09273948.2012.681830. PMID 22564107. 
  21. ^ BNF 45 March 2003
  22. ^ "Diabetes drug could treat leading cause of blindness". May 8, 2012. http://www.antaranews.com/en/news/81923/diabetes-drug-could-treat-leading-cause-of-blindness. 
  23. ^ Chang, JH; Wakefield, D (2002 Dec). "Uveitis: a global perspective.". Ocular immunology and inflammation 10 (4): 263–79. PMID 12854035. 

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