Bilateral acute iris transillumination (BAIT) and Bilateral acute iris depigmentation (BADI)

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First described in the mid-2000s,[1] the vast majority of cases have been identified in Middle Eastern and European populations[1][2] [3][4][5] [6][7] although cases among Hispanics have been reported.[8][9][10] The vast majority of patients are young females in their 30s-40s after an upper respiratory illness[1][2][3] or use of systemic antimicrobials, particularly moxifloxacin.[11][12]

Bilateral acute depigmentation of the iris (BADI) and bilateral acute iris transillumination (BAIT) are likely on the same spectrum with the former describing acute onset depigmentation of the iris without transillumination or pupillary sphincter defects[1][13] and the latter entailing the presence of pupillary defects. The released pigment deposits into and occludes the trabecular meshwork often resulting in intraocular pressure (IOP) increases, although with a lower rate in BADI.[2] The pigment dispersion is from the iris pigment epithelium and stroma in BAIT and BADI, respectively.[14]


Systemic antimicrobials, particularly moxifloxacin but also clarithromycin and fumagilin therapy, have been implicated,[2][11][12][15][16][17][18][19] Of the fluoroquinolones, moxifloxacin had the highest risk for uveitis followed by ciprofloxacin.[20] Interestingly sensitivity to fluoroquinolone toxicity has been associated with HLA-B51 and HLA-B27 positivity in 40% and 20% of affected patients, respectively, in one study suggesting an underlying autoimmune aspect.[17][21] Fluoroquinolone toxicity may also be exacerbated by light in a similar fashion to fluoroquinolone-induced dermatitis.[8] Topical fluoroquinolone reaches asymmetric concentrations in the aqueous and vitreous compared to a more equal distribution when given systemically.[8] It has been suggested that the increased vitreous concentration of fluoroquinolone, particularly in phakic patients where posterior to anterior clearance can be impeded, presents greater toxicity to the iris pigment.[22] Interestingly, intravitreal fluoroquinolone may be cleared more rapidly than when given systemically.[22]

Antecedent viral infections have also been noted in about two thirds of patients.[13][23] Serologic studies for viral etiologies are often negative for acute infections.[7] Iris ischemia has also been suggested as causing iris depigmentation with one case of BAIT presenting with a cotton wool spot on fundus examination.[15][21]



Patients often present with photophobia, ocular pain and red eyes. Symptoms often began within 2-3 weeks of starting systemic antibiotics.[14] Visual acuity can be reduced but often recovers to baseline.[14]


Depigmentation of the iris often occurs at the iris root.[2][7] While pigmentary cells are evident in the anterior chamber, inflammatory cells are not. Ocular hypertension can result as well.[13][14] Gonioscopy reveals heavily pigmented trabecular meshwork (especially inferiorly) with an open angle.[14] Diffuse fine pigment on the corneal endothelium is often noted but keratic precipitates are absent.[14] In BAIT, diffuse patchy bilateral iris transillumination defects with pupillary mydriasis from sphincter paralysis are often seen.[14] It is often symmetric although asymmetric cases have also been reported.[2][7]  Posterior synechiae was found in 25%-50% of affected eyes, particularly in those with elevated intraocular pressures in the first week.[2][14][24] Anterior segment OCT in BAIT shows thinned iris[25] with normal configuration[25][26][27] although segmental posterior bowing is occasionally noted.[15][16][22] In BADI, anterior segment OCT shows iris root damage and iris stormed thinning without affect to the pigmentary epithelium.[28] 

Differential diagnosis

Herpetic and Fuch’s iridocyclitis often present unilaterally and with keratic precipitates. The former often has full thickness iris atrophy and the later with heterochromia.[29][30][31] Pigment dispersion often presents with pigment deposition on other ocular structures including the zonules, corneal endothelium and lens with concave iris morphology and characteristic spoke-like iris transillumination defects.[32][33]



Topical corticosteroids have been used[2] and discontinuation prior to complete resolution of depigmentation results in recurrent symptoms.[2][7] In cases of elevated IOP, almost half of affected eyes are refractory to anti glaucoma medications, some requiring filtration surgery.[14] Laser iridoplasty in cases of segmental posterior iris bowing may prove helpful in controlling IOP.[16] Filtration surgery with mitomycin-C has been shown to be effective in long term control of ocular hypertension secondary to BAIT/BADI with minimal lasting complication.[34][35] Trabectome has also been used in cases refractory to medical management.[36]

Disease Course

Follow-up exams reveal decreases in pigmentary release although the duration of time for resolution varies between 2 weeks to 14 months in some cases.[13][35] Some cases of BADI have shown some, but not complete, repigmentation of the iris after 3-4 years.[2][5][27]


Ocular hypertension in BAIT can progress to glaucoma. There has also been one case report of bilateral cystoid macular edema occurring 10 months after resolution of BAIT, believed to be secondary to persistent inflammation evidenced by the multiple BAIT recurrences prior to resolution.[37]


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