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COMMENTARY
Year : 2019  |  Volume : 67  |  Issue : 1  |  Page : 134

Commentary: Bilateral acute depigmentation of iris


Uveitis Services, Aravind Eye Hospital, Thavalakuppam, Pondicherry, India

Date of Web Publication21-Dec-2018

Correspondence Address:
Dr. S Bala Murugan
Uveitis Services, Aravind Eye Hospital, Thavalakuppam, Pondicherry
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijo.IJO_1512_18

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How to cite this article:
Murugan S B. Commentary: Bilateral acute depigmentation of iris. Indian J Ophthalmol 2019;67:134

How to cite this URL:
Murugan S B. Commentary: Bilateral acute depigmentation of iris. Indian J Ophthalmol [serial online] 2019 [cited 2019 Aug 20];67:134. Available from: http://www.ijo.in/text.asp?2019/67/1/134/248128



Bilateral acute depigmentation of iris[1] (BADI) is a rare, recently described entity of unknown etiology[2] first characterized in 2006 by Tukal-Tutkun et al. More common in middle-age females it presents asymptomatically with a unique bilateral symmetrical simultaneous depigmentation of iris and consequent focal/diffuse stromal atrophy and pigment dispersion in anterior segment, including the trabecular meshwork. What is unique is the iris pigment epithelia rarely goes in for atrophy with no transillumination defects,[3] nil pupillary abnormalities,[3] nil inflammatory parameters,[2] and repigmentation may occur spontaneously.[2]

With no confirmed causes, the speculated etiologies postulated includes[2] viral etiologies such as cytomegalovirus, herpes simplex, herpes zoster, toxic effects following fumigation therapy,[4] iris ischemia, and neurotrophic mechanisms. Preceded by flu-like illness, upper respiratory tract infections, oral moxifloxacin [sans topical moxifloxacin], increase in intraocular pressure (IOP) may occur with sparse inflammatory indices.

When faced with a real-time scenario, the clinician needs clear focus in delineating the differentials[3] such as Fuch's heterochromic iridocyclitis, herpetic iridocyclitis, pigment dispersion syndrome, and pseudoexfoliation syndrome. The diagnostic criteria for Fuch's uveitis with diffuse stellate keratic precipitates with predominant unilaterality, milder inflammation, cataract are useful features to differentiate. Viral uveitis causes have a pathognomic trabeculitis with its unique fibrinous keratic precipitates, IOP spikes, reduced corneal sensitivity, and characteristic patterns of iris pigment epithelial defects leading to transillumination defects. The pointers to delineate pigment dispersion syndrome[5] from BADI are the lack of pigment deposition on the lens and zonules and the chronicity.

The investigations to document BADI include gonioscopy, pupillometry, tonometry, and serum antibodies against the viruses, as well as polymerase chain reactions against the virus primers. What is fascinating is the lucid subtle differences of BADI with bilateral acute iris transillumination[6] (BAIT), wherein there is iris epithelial transillumination defect, atonic dilated pupil, and higher tendency of IOP spikes. Usually, BAIT is resistant to medical treatment and needs surgical glaucoma interventions,[7] which a clinician needs to decipher in the long term. Human leukocyte antigen (HLA) B-51 positive individuals have a genetic predisposition[8] to develop moxifloxacin-induced BAIT. This can be applied in real-time practice, if feasible.

The clinical variants of BADI include the asymmetrical presentation as proposed by Barraquer and Mejiaian (2005) and Tugal Tutkun (2009) and few fibrinoid aqueous closer to cornea. Treatment of BAIT includes appropriate anti-inflammatory medications (sans steroids usage per merit),[9] antiglaucoma medications, and empirical antiviral therapy, either topically or orally as per the severity. Sparse inflammatory signs should alert the clinician from mistreating with aggressive anti-inflammatory medications[9] as the condition is self-limiting if the differentials are carefully ruled out! Projecting BADI in future, we can anticipate future publications on BADI with anterior segment angiogram, iridography, anterior segment autoflourescence that is a true treat to an astute clinician, no wonder!



 
  References Top

1.
Yangzes S, Singh SR, Ram J. Bilateral acute depigmentation of iris. Indian J Ophthalmol 2019;67:133.  Back to cited text no. 1
  [Full text]  
2.
Fachin DR, Prestes MF, Cariello AJ, Nóbrega MJ. Bilateral acute depigmentation of the iris: A case report. Arq Bras Oftalmol 2016;79:119-20.  Back to cited text no. 2
    
3.
Amin R, Nabih A, Khater N. Bilateral acute depigmentation of the iris in two siblings simultaneously. Am J Ophthalmol Case Rep 2018;10:257-60.  Back to cited text no. 3
    
4.
Gonul S, Bozkurt B, Okudan S, Tugal-Tutkun I. Bilateral acute iris transillumination following a fumigation therapy: A village-based traditional method for the treatment of ophthalmomyiasis. Cutan Ocul Toxicol 2015;34:80-3.  Back to cited text no. 4
    
5.
Lascaratos G, Shah A, Garway Heath D. The genetics of pigment dispersion syndrome and pigmentary glaucoma. Surv Ophthalmol 2013;58:164-75.  Back to cited text no. 5
    
6.
Tugal-Tutkun I, Onal S, Garip A, Taskapili M, Kazokoglu H, Kadayifcilar S, et al. Bilateral acute iris transillumination. Arch Ophthalmol 2011;129:1312-9.  Back to cited text no. 6
    
7.
Gonul S, Bozkurt B. Bilateral acute depigmentation of the iris (BADI):First reported case in Brazil. Arq Bras Oftalmol. 2014;77:201. Comment on: Arq Bras Oftalmol 2013;76:42-4.  Back to cited text no. 7
    
8.
Atilgan CU, Kosekahya P, Caglayan M, Berker N. Bilateral acute depigmentation of iris: 3-year follow-up of a case. Ther Adv Ophthalmol2018;10:2515841418787988. doi: 10.1177/2515841418787988.  Back to cited text no. 8
    
9.
Goktas A, Goktas S. Bilateral acute depigmentation of the iris first misdiagnosed as acute iridocyclitis. Int Ophthalmol 2011;31:337-9.  Back to cited text no. 9
    




 

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