Commentary: Bilateral acute depigmentation of iris.

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!