Acute retinal necrosis pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The pathogenesis of acute [[retinal]] [[necrosis]] is characterized by [[retinal]] [[inflammation]] due to ocular [[viral]] infection. Particles from [[Herpes simplex virus]] 1 (HSV-1), [[Herpes simplex virus]] 2 (HSV-2), and [[Varicella zoster]] virus (VZV) infiltrate the [[retina]] through various locations of [[epithelial]] penetration, including the skin, [[conjunctiva]], [[cornea]], and [[nasal cavity]]. Acute [[retinal]] [[necrosis]] develops from HSV-1, HSV-2, and VZV due to the viruses' | The pathogenesis of acute [[retinal]] [[necrosis]] is characterized by [[retinal]] [[inflammation]] due to ocular [[viral]] infection. Particles from [[Herpes simplex virus]] 1 (HSV-1), [[Herpes simplex virus]] 2 (HSV-2), and [[Varicella zoster]] virus (VZV) infiltrate the [[retina]] through various locations of [[epithelial]] penetration, including the skin, [[conjunctiva]], [[cornea]], and [[nasal cavity]]. Acute [[retinal]] [[necrosis]] develops from HSV-1, HSV-2, and VZV due to the viruses' ability to transmit and replicate in the [[central nervous system]] (CNS), as well as their ability to transport anterograde through the [[optic nerve]], establish [[virus latency|latency]], reactivate, and cause [[retinal]] [[inflammation]]. For Caucasian populations, possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 [[antigens]] is correlated to genetic predisposition to ARN. For Japanese populations, possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 [[antigens]] is correlated to genetic predisposition to ARN. Acute [[retinal]] [[necrosis]] is associated with the following ocular conditions: [[progressive outer retinal necrosis]], [[uveitis]], [[cytomegalovirus retinitis]], toxoplasmic [[chorioretinitis]], and [[endophthalmitis]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
The pathogenesis of acute [[retinal]] [[necrosis]] is characterized by [[retinal]] [[inflammation]] due to ocular [[viral]] infection.<ref name="pmid10682968">{{cite journal |vauthors=Ganatra JB, Chandler D, Santos C, Kuppermann B, Margolis TP |title=Viral causes of the acute retinal necrosis syndrome |journal=Am. J. Ophthalmol. |volume=129 |issue=2 |pages=166–72 |year=2000 |pmid=10682968 |doi= |url=}}</ref> Particles from [[Herpes simplex virus]] 1 (HSV-1), [[Herpes simplex virus]] 2 (HSV-2), and [[Varicella zoster]] virus (VZV) infiltrate the [[retina]] via various modes of transmission:<ref name="pmid22889540">{{cite journal |vauthors=Grose C |title=Acute retinal necrosis caused by herpes simplex virus type 2 in children: reactivation of an undiagnosed latent neonatal herpes infection |journal=Semin Pediatr Neurol |volume=19 |issue=3 |pages=115–8 |year=2012 |pmid=22889540 |pmc=3419358 |doi=10.1016/j.spen.2012.02.005 |url=}}</ref> | |||
*[[Epithelial]] penetration of the skin: transmitted through the [[Ophthalmic nerve|ophthalmic]] branch of the [[trigeminal nerve]]. | |||
*[[Epithelial]] penetration of the [[conjunctiva]]: transmitted directly through the [[optic nerve]]. | |||
*[[Epithelial]] penetration of the [[cornea]]: transmitted through the [[Maxillary|maxillary]] branch of the [[trigeminal nerve]]. | |||
*[[Epithelial]] penetration of the [[nasal cavity]]: transmitted through the [[olfactory nerve]] in the [[subarachnoid space]]. | |||
*Acute [[retinal]] [[necrosis]] develops from HSV-1 and HSV-2 due to the viruses' ability to transmit and replicate in the [[central nervous system]] (CNS), as well as their ability to transport [[anterograde]] through the [[optic nerve]], establish [[virus latency|latency]], reactivate, and cause [[retinal]] [[inflammation]].<ref name ="HumanHerpes">{{cite book |last1=Whitley |first1=Richard |last2=Kimberlin |first2=David W. |last3=Prober |first3=Charles G. |date=2007 |title=Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis |url=http://www.ncbi.nlm.nih.gov/books/NBK47449/ |location=Cambridge, UK |publisher=Cambridge University Press |isbn=978-0511545313}}</ref> | |||
*[[Retinal]] [[inflammation]] is caused by the up-regulated production of [[cytokines]]. | |||
===Genetics=== | ===Genetics=== | ||
There is evidence of genetic predisposition to acute retinal necrosis: | |||
*For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 [[antigens]] is correlated with genetic predisposition to ARN.<ref name="pmid2801857">{{cite journal |vauthors=Holland GN, Cornell PJ, Park MS, Barbetti A, Yuge J, Kreiger AE, Kaplan HJ, Pepose JS, Heckenlively JR, Culbertson WW |title=An association between acute retinal necrosis syndrome and HLA-DQw7 and phenotype Bw62, DR4 |journal=Am. J. Ophthalmol. |volume=108 |issue=4 |pages=370–4 |year=1989 |pmid=2801857 |doi= |url=}}</ref> | |||
*For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 [[antigens]] is correlated to genetic predisposition to ARN.<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref> | |||
Possession of the above [[antigens]] in their respective demographics are correlated to impaired immunity and increased predisposition to infection. | |||
===Associated Conditions=== | ===Associated Conditions=== | ||
Acute retinal necrosis is associated with the following ocular conditions: | |||
*[[Progressive outer retinal necrosis]]<ref name="pmid24926266">{{cite journal |vauthors=Coisy S, Ebran JM, Milea D |title=Progressive outer retinal necrosis and immunosuppressive therapy in myasthenia gravis |journal=Case Rep Ophthalmol |volume=5 |issue=1 |pages=132–7 |year=2014 |pmid=24926266 |pmc=4036147 |doi=10.1159/000362662 |url=}}</ref> | |||
*[[Uveitis]]<ref name="urlFacts About Uveitis | National Eye Institute">{{cite web |url=https://nei.nih.gov/health/uveitis/uveitis |title=Facts About Uveitis | National Eye Institute |format= |work= |accessdate=}}</ref> | |||
*[[Cytomegalovirus retinitis]]<ref name="urlCMV retinitis: MedlinePlus Medical Encyclopedia">{{cite web |url=https://medlineplus.gov/ency/article/000665.htm |title=CMV retinitis: MedlinePlus Medical Encyclopedia |format= |work= |accessdate=}}</ref> | |||
* | *Toxoplasmic chorioretinitis<ref name="pmid22116459">{{cite journal |vauthors=Davis JL |title=Diagnostic dilemmas in retinitis and endophthalmitis |journal=Eye (Lond) |volume=26 |issue=2 |pages=194–201 |year=2012 |pmid=22116459 |pmc=3272204 |doi=10.1038/eye.2011.299 |url=}}</ref> | ||
*[[Endophthalmitis]] | |||
==References== | ==References== | ||
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[[Category:Disease]] | |||
[[Category:Ophthalmology]] | [[Category:Ophthalmology]] | ||
[[Category:Up-To-Date]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Infectious disease]] | |||
Latest revision as of 20:17, 29 July 2020
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Acute retinal necrosis pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
The pathogenesis of acute retinal necrosis is characterized by retinal inflammation due to ocular viral infection. Particles from Herpes simplex virus 1 (HSV-1), Herpes simplex virus 2 (HSV-2), and Varicella zoster virus (VZV) infiltrate the retina through various locations of epithelial penetration, including the skin, conjunctiva, cornea, and nasal cavity. Acute retinal necrosis develops from HSV-1, HSV-2, and VZV due to the viruses' ability to transmit and replicate in the central nervous system (CNS), as well as their ability to transport anterograde through the optic nerve, establish latency, reactivate, and cause retinal inflammation. For Caucasian populations, possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens is correlated to genetic predisposition to ARN. For Japanese populations, possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens is correlated to genetic predisposition to ARN. Acute retinal necrosis is associated with the following ocular conditions: progressive outer retinal necrosis, uveitis, cytomegalovirus retinitis, toxoplasmic chorioretinitis, and endophthalmitis.
Pathophysiology
Pathogenesis
The pathogenesis of acute retinal necrosis is characterized by retinal inflammation due to ocular viral infection.[1] Particles from Herpes simplex virus 1 (HSV-1), Herpes simplex virus 2 (HSV-2), and Varicella zoster virus (VZV) infiltrate the retina via various modes of transmission:[2]
- Epithelial penetration of the skin: transmitted through the ophthalmic branch of the trigeminal nerve.
- Epithelial penetration of the conjunctiva: transmitted directly through the optic nerve.
- Epithelial penetration of the cornea: transmitted through the maxillary branch of the trigeminal nerve.
- Epithelial penetration of the nasal cavity: transmitted through the olfactory nerve in the subarachnoid space.
- Acute retinal necrosis develops from HSV-1 and HSV-2 due to the viruses' ability to transmit and replicate in the central nervous system (CNS), as well as their ability to transport anterograde through the optic nerve, establish latency, reactivate, and cause retinal inflammation.[3]
- Retinal inflammation is caused by the up-regulated production of cytokines.
Genetics
There is evidence of genetic predisposition to acute retinal necrosis:
- For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens is correlated with genetic predisposition to ARN.[4]
- For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens is correlated to genetic predisposition to ARN.[5]
Possession of the above antigens in their respective demographics are correlated to impaired immunity and increased predisposition to infection.
Associated Conditions
Acute retinal necrosis is associated with the following ocular conditions:
- Progressive outer retinal necrosis[6]
- Uveitis[7]
- Cytomegalovirus retinitis[8]
- Toxoplasmic chorioretinitis[9]
- Endophthalmitis
References
- ↑ Ganatra JB, Chandler D, Santos C, Kuppermann B, Margolis TP (2000). "Viral causes of the acute retinal necrosis syndrome". Am. J. Ophthalmol. 129 (2): 166–72. PMID 10682968.
- ↑ Grose C (2012). "Acute retinal necrosis caused by herpes simplex virus type 2 in children: reactivation of an undiagnosed latent neonatal herpes infection". Semin Pediatr Neurol. 19 (3): 115–8. doi:10.1016/j.spen.2012.02.005. PMC 3419358. PMID 22889540.
- ↑ Whitley, Richard; Kimberlin, David W.; Prober, Charles G. (2007). Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge, UK: Cambridge University Press. ISBN 978-0511545313.
- ↑ Holland GN, Cornell PJ, Park MS, Barbetti A, Yuge J, Kreiger AE, Kaplan HJ, Pepose JS, Heckenlively JR, Culbertson WW (1989). "An association between acute retinal necrosis syndrome and HLA-DQw7 and phenotype Bw62, DR4". Am. J. Ophthalmol. 108 (4): 370–4. PMID 2801857.
- ↑ Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D (2014). "Clinical manifestation of self-limiting acute retinal necrosis". Med. Sci. Monit. 20: 2088–96. doi:10.12659/MSM.890469. PMC 4226315. PMID 25356955.
- ↑ Coisy S, Ebran JM, Milea D (2014). "Progressive outer retinal necrosis and immunosuppressive therapy in myasthenia gravis". Case Rep Ophthalmol. 5 (1): 132–7. doi:10.1159/000362662. PMC 4036147. PMID 24926266.
- ↑ "Facts About Uveitis | National Eye Institute".
- ↑ "CMV retinitis: MedlinePlus Medical Encyclopedia".
- ↑ Davis JL (2012). "Diagnostic dilemmas in retinitis and endophthalmitis". Eye (Lond). 26 (2): 194–201. doi:10.1038/eye.2011.299. PMC 3272204. PMID 22116459.