Bilateral Acute Iris Transillumination (BAIT) and Bilateral Acute Iris Depigmentation (BADI)

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Article initiated by:
Marez Megalla, MD
All contributors:
Liliya Benchetrit, Marez Megalla, MD, Ohoud A Owaidhah, MD
Assigned editor:
Ohoud A Owaidhah, MD
Review:
Assigned status Update Pending
 by Ohoud A Owaidhah, MD on August 25, 2023.


Background

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]

Etiology

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]

Diagnosis

Symptoms

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]

Examination

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]

Management

Treatment

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]

Complications

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]

References

  1. ↑ 1.0 1.1 1.2 1.3 Tugal-Tutkun I, Urgancioglu M. Bilateral acute depigmentation of the iris. Graefe’s Arch Clin Exp Ophthalmol. 2005;244(6):742–746.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Tugal-Tutkun I, Araz B, Taskapili M, et al. Bilateral acute depigmentation of the Iris: report of 26 new cases and four-year follow-up of two patients. Ophthalmology. 2009;116(8):1552–1557.
  3. ↑ 3.0 3.1 Portmann A, Gueudry J, Siahmed K, Muraine M. Le syndrome de dépigmentation bilatérale aiguë de l’iris. J French Ophthalomol. 2011;34(5):309–312.
  4. ↑ Heloisa Andrade Maestrini, et al. Bilateral acute depigmentation of the Iris (BADI): first reported case in Brazil. Arq Bras Oftalmol. 2013;76(1):42–44.
  5. ↑ 5.0 5.1 Ersöz M, Doğan B, Aşık Nacaroğlu Ş, Ayıntap E, Karaca Adıyeke S, Türe G. Bilateral acute depigmentation of iris: a report of two cases. J Tepecik Educ Res Hospit. 2016.
  6. ↑ Barraquer F, Mejía L. Bilateral acute depigmentation of the iris. First report on the american continent and 5 years follow-up of two patients. J Emmetropia. 2012;3:118–122.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 Amin, R., Nabih, A., Khater, N. Bilateral acute depigmentation of the iris in two siblings simultaneously. AJO. 2018; 10: 257-260.
  8. ↑ 8.0 8.1 8.2 Siefert HM, Domdey-Bette A, Henninger K, Hucke F, Kohlsdorfer C, Stass HH. Pharmacokinetics of the 8-methoxyquinolone, moxifloxa- cin: a comparison in humans and other mammalian species. J Antimicrob Chemother. 1999;43(Suppl):B:69–76.
  9. ↑ Bringas Calvo R, Iglesias Cortiñas D. Acute and bilateral uveitis secondary to moxifloxacin [in Spanish]. Arch Soc Esp Oftalmol. 2004;79:357-9.
  10. ↑ Plaza-Ramos, P., Heras-Mulero, H., Fanlo, P., Zubicoa, A. Bilateral acute iris transillumination syndrome. A case report. Arch Soc Esp Ophthalmol. 2018; 93(9): 447-450.
  11. ↑ 11.0 11.1 Knape R, Sayyad F, Davis J. Moxifloxacin and bilateral acute iris transillumination. J Ophthalmic Inflamm Infect. 2013;3(1):10.
  12. ↑ 12.0 12.1 Nascimento H, Sousa J, Campos M, Belfort Jr R. Acute iris depigmentation following systemic moxifloxacin. Clinics. 2013;68(7):899–900.
  13. ↑ 13.0 13.1 13.2 13.3 Tugal-Tutkun I. Bilateral acute Iris transillumination. Arch Ophthalmol. 2011;129(10):1312.
  14. ↑ 14.0 14.1 14.2 14.3 14.4 14.5 14.6 14.7 14.8 12 Tranos, P., Lokovitis, E., Masselos, S., et al. Bilateral acute iris transillumination following systemic administration of antibiotics. Eye. 2018; 32: 1190-1196.
  15. ↑ 15.0 15.1 15.2 Morshedi RG, Bettis DI, Moshirfar M, Vitale AT. Bilateral acute iris transillumination following systemic moxifloxacin for respiratory ill- ness: report of two cases and review of the literature. Ocul Immunol Inflamm. 2012;20(4):266–272.
  16. ↑ 16.0 16.1 16.2 Willermain, F., Deflorenne, C., Bouffioux, C., et al. Uveitis-like syndrome and iris transillumination after the use of oral moxifloxacin. Eye. 2010; 24: 1419.
  17. ↑ 17.0 17.1 Wefers Bettink-Remeijer M, Brouwers K, van Langenhove L, et al. Uveitis-like syndrome and iris transillumination after the use of oral moxifloxacin. Eye (Lond). 2009;23(12):2260–2262.
  18. ↑ 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(1):80–83.
  19. ↑ Tranos, P., Nasr, M., Asteriades, S., et al. Bilateral diffuse iris atrophy after the use of oral clarithromycin. Cutan Ocul Toxicol. 2014; 33(1): 79-81.
  20. ↑ Eadie, B., Etminan, M., Mikelberg, F., et al. Risk for uveitis with oral moxifloxacin: a comparative safety study. JAMA Ophthalmol. 2015;133(1):81-84.
  21. ↑ 21.0 21.1 Hinkle DM, Dacey MS, Mandelcorn E, et al. Bilateral uveitis asso- ciated with fluoroquinolone therapy. Cutan Ocul Toxicol. 2012;31 (2):111–116
  22. ↑ 22.0 22.1 22.2 Knape RM, Sayyad FE, Davis JL. Moxifloxacin and bilateral acute iris transillumination. J Ophthalmic Inflamm Infect. 2013;3(1):10.
  23. ↑ Perone, J., Chaussard, D., Hayek, G. Bilaterala cute iris transillumination (BAIT) syndrome: literature review. Clinical Ophthalmology; 2019:13 935–943.
  24. ↑ Maestrini, H., Maestrini, A., Machado, D., et al. Bilateral acute depigmentation of the iris (BADI): first reported case in Brazil. Are Bras Oftalmol. 2013; 76(1): 42-44.
  25. ↑ 25.0 25.1 Kawali, A., Mahendradas, P., Shetty, R., Acute depigmentation of the iris: a retrospective analysis of 22 cases. Can J Ophthalmol. 2019; 54(1): 33-39.
  26. ↑ Degirmenci C, Guven Yilmaz S, Palamar M, Ates H. Bilateral acute iris transillumination: case report. Saudi J Ophthalmol. 2016;30 (2):122–124.
  27. ↑ 27.0 27.1 Atilgan C., Kosekahya, P., Caglayan, M., et al. Bilateral acute depigmentation of iris: 3-year follow-up of a case. Therapeutic Advances in Ophthalmology. 2018; 10: 1-4.
  28. ↑ Escribano, P., Gonzalez, J. Bilateral acute depigmentation of the Iris: Findings in Anterior Segment Optical Coherence Tomography. Ocul Immunol Inflamm. 2019; 15: 1-5.
  29. ↑ Goktas A, Goktas S. Bilateral acute depigmentation of the iris first misdiagnosed as acute iridocyclitis. Int Ophthalmol. 2011;31(4):337–339. 
  30. ↑ Nalçacıoğlu P, Çakar Özdal P, Şimşek M. Clinical characteristics of fuchs' uveitis syndrome. Türk Oftalmoloji Dergisi. 2016;46(2):52–57.
  31. ↑ Jones N. Fuchs' heterochromic uveitis: a reappraisal of the clinical spectrum. Eye. 1991;5(6):649–661.
  32. ↑ Turgut B, Türkçüoğlu P, Deniz N, Çatak O. Annular and central heavy pigment deposition on the posterior lens capsule in the Pigment dispersion syndrome. Int Ophthalmol. 2007;28(6):441–445.
  33. ↑ Niyadurupola N, Broadway D. Pigment dispersion syndrome and pigmentary glaucoma - a major review. Clin Exp Ophthalmol. 2008;36(9):868–882.
  34. ↑ Bayraktar, S., Oray, M., Altan, C., et al. Long-term results of trabeulectomy with mitomycin C in patients with bilateral acute iris transillumination. J Glaucoma. 2019; 28(9): 797-802.
  35. ↑ 35.0 35.1 Gonul S, Bozkurt B. Bilateral acute iris transillumination (BAIT) initially misdiagnosed as acute iridocyclitis. Arq Bras Oftalmol. 2015;78(2):115–117.
  36. ↑ Den Beste KA, Okeke C. Trabeculotomy ab interno with Trabectome as surgical management for systemic fluoroquinolone-induced pig- mentary glaucoma: a case report. Medicine (Baltimore). 2017;96(43): e7936.
  37. ↑ Altan C, Basarir B, Kesim C. An unexpected complication in bilateral acute iris transillumination: cystoid macular edema. Indian J Ophthalmol. 2018;66(6):869–871.
  1. Fachin, D., Prestes, M., Cariello, A., et al. Bilateral acute depigmentation of the iris: a case report. Arq Bras Ofthalmol. 2016; 79 (2): 119-120.
  2. Jang L, Borruat F-X, Guex-Crosier Y. Bilateral acute iris transillu- mination: a rare cause of iris atrophy. report of 2 cases. Klin Monbl Augenheilkd. 2015;232(4):593–594.
  3. Rangel, C., Parra, M., Frederick, G., et al. An unusual case of bilateral anterior uveitis related to moxifloxacin: the first report in Latin America. GMS Ophthalmology Cases. 2017; 7: Doc18.
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