TJ Sullivan et al.1 reported that 16% of cases with lid BDhad an initial diagnosis of blepharitis, possibly becauseof the tumour’s propensity to involve hair shaft folliclesand adnexal structures. Early biopsy from the most rep-resentative region of the lesion is necessary to establishdiagnosis before treatment and multiple biopsies areindicated if SCC is suspected.1,2 Our case highlights howthese tumours can masquerade as common conditionsand the importance of maintaining a high index ofsuspicion.

Although surgical excision is considered to be the goldstandard treatment for cutaneous tumours, complicationsinclude infection, graft/wound contraction, lagophthalmosand poor cosmesis.3 There are no randomized controlledtrials comparing treatments and data on efficacy arelimited. Newer therapies such as photodynamic therapy,5

topical 5-FU1,2 and more recently imiquimod4 may providea suitable alternative to the conventional approach inselected cases. The possibility of recurrence following non-surgical therapies may remain due to the tumour’s propen-sity to affect eyelash hair shaft follicles.

5-Fluorouracil induces inhibition of DNA synthesis,creating a thymine deficiency that promotes cell death,2,5

particularly targeting rapidly multiplying tumour cells.The 5% Cream is usually applied twice daily for4–8 weeks and low recurrence rates (8–12%) are associatedwith longer treatment duration.2 The delayed local inflam-matory reaction is usually well tolerated.2,5

Topical 5-FU is a well-established treatment for SCC insitu outside the ocular appendages. To our knowledge, thisis the first report of BD involving the eyelids successfullytreated with 5-FU. This topical preparation has the advan-tage of allowing patients to self-administer therapy. Oph-thalmologists should consider this alternative to eyelidsurgery.

Eamon Sharkawi MD FRCOphth,1,2

Mehrad Hamedani MD1 andMassoud Fouladi MD FRCOphth2

1Jules Gonin Eye Hospital, Lausanne, Switzerland; and2Department of Ophthalmology, William Harvey

Hospital, Ashford, Kent, UKReceived 10 January 2011; accepted 2 March 2011.

REFERENCES

1. Sullivan TJ, Boulton JE, Whitehead KJ. Intraepidermalcarcinoma of the eyelid. Clin Experiment Ophthalmol 2002;30: 23–7.

2. Moreno G, Chia AL, Lim A, Shumack S. Therapeuticoptions for Bowen’s disease. Australas J Dermatol 2007;48: 1–8.

3. Verity DH, Collin JR. Eyelid reconstruction: the state ofthe art. Curr Opin Otolaryngol Head Neck Surg 2004; 12:344–8.

4. Tsang HH, Huynh NT, Hollenbach E. Topical therapywith imiquimod for eyelid lesion. Clin Experiment Oph-thalmol 2006; 34: 179–81.

5. Salim A, Leman JA, McColl JH, Chapman R, MortonCA. Randomized comparison of photodynamic therapywith topical 5-fluorouracil in Bowen’s disease. Br J Der-matol 2003; 148: 539–43.

Intravitreal ranibizumab forchoroidal neovascularizationassociated with circumscribedchoroidal haemangioma

Circumscribed choroidal haemangioma (CCH) is a benignvascular tumour of the choroid. When symptomatic, itstreatment is generally reserved for decreased visual acuityor metamorphopsia from cystoid macular oedema or exu-dative foveal detachment.1 The therapeutic optionsinclude argon laser photocoagulation, transpupillarythermotherapy, episcleral radioactive plaque therapy,photodynamic therapy (PDT) and intravitreal injectionof anti-vascular endothelium growth factor (VEGF)bevacizumab.

A 66-year-old woman presented for visual reductionin right eye (RE). Best-corrected visual acuity (BCVA)was 6/120 in RE, and 6/6 in left eye (LE). Fundus exami-nation revealed overall normal findings in the LE, and in

a b

Figure 1. (a) Left upper lid Bowen’s Disease, prior to treatment. (b) Complete resolution of lesion following treatment with topical5-fluorouracil cream.

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© 2011 The AuthorsClinical and Experimental Ophthalmology © 2011 Royal Australian and New Zealand College of Ophthalmologists

the RE a large juxtafoveal well-circumscribed red-orangemass and subfoveal choroidal neovascularization (CNV)with intraretinal haemorrhage were present (Fig. 1).There were no typical signs of age-related macular degen-eration (AMD), such as drusen and pigment mottling ineither eye. On B-scan ultrasonography the mass in REshowed a high internal reflectivity, and was sized9.9 mm/8.4 mm in diameter, and 3.5 mm in thickness.Fluorescein angiography showed in the RE a subfovealpredominantly classic CNV and prearterial patchy fillingof the mass with late patchy staining. Indocyanine greenangiography confirmed the presence of the CNV, clearlydelineated the CCH vascularization and showed charac-teristic late wash out of the dye. Spectral-domain opticalcoherence tomography (SD-OCT, Cirrus HD-OCT, CarlZeiss-Meditec, Dublin, CA, USA) showed presence ofcystoid macular oedema and subretinal fluid within thefovea, and absence of any exudative changes overlyingthe juxtafoveal mass. The mass in the RE was diagnosedwith CCH.

Nine monthly intravitreal ranibizumab injections(0.5 mg per 0.05 mL) were administered to treat the activeCNV. At month 9 visit, BCVA had increased to 6/30. Fluo-rescein angiography, indocyanine green angiography andSD-OCT revealed the CNV closure and absence of

intraretinal and subretinal fluid, which lasted until12 months after last injection (Fig. 2).

To our knowledge, the association of untreated CCHand CNV is rare.1,2 Because of the absence of typical signsof AMD in both eyes, in our case CNV is likely to beassociated with CCH. Polypoidal choroidal vasculopathyhas been reported 3 years after PDT treatment of CCHand responded to anti-VEGF intravitreal bevacizumabinjection.3

Leys et al. reported retinal and optic disc neovascular-ization in three eyes with untreated CCH,4 which wors-ened after PDT.

In our case, CNV was successfully treated with 9monthly intravitreal ranibizumab injections. Intravitreouspharmacotherapy with ranibizumab, a VEGF inhibitor, hasbeen shown to improve mean visual acuity safely in eyeswith neovascular AMD. Ranibizumab has showed to bemore effective than PDT for treatment of predominantlyclassic CNVs.5

Choroidal neovascularizations associated withuntreated choroidal haemangioma may be due to thesubtle inflammation and chronic ischemia associatedwith choroidal haemangioma, which may stimulatethe release of angiogenic factors. In our case a com-plete regression of the CNV and the associated

Figure 1. Fundus colour pho-tographs show a large well-circumscribed red-orange masssuperotemporal to the fovea,as well as a yellow-grey foveallesion, surrounded by a ring-shapehaemorrhage (suggesting sub-foveal choroidal neovasculariza-tion), in the right eye (a), andoverall normal findings in theleft eye (b). Fluorescein angio-graphy (c) and indocyanineangiography (d) frames showlate patchy staining of the largesuperotemporal lesion, and lateleakage of the subfoveal cho-roidal neovascularization. Spectral-domain optical coherence tomog-raphy scans show presence ofcystoid macular oedema and sub-retinal fluid within the fovea (e),and absence of any exudativechanges overlying the choroidalhaemangioma (f).

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© 2011 The AuthorsClinical and Experimental Ophthalmology © 2011 Royal Australian and New Zealand College of Ophthalmologists

exudative retinopathy was obtained during 12 monthsof follow up. Intravitreal ranibizumab could be consid-ered as an effective treatment for CCH-associated CNVs.

Giuseppe Querques MD PhD, Raimondo ForteMD PhD, Lea Querques MD and

Eric H Souied MD PhDDepartment of Ophthalmology, Hopital Intercommunal de

Creteil, University Paris XII, Paris, FranceReceived 30 January 2011; accepted 29 March 2011.

REFERENCES

1. Shields CL, Honavar SG, Shields JA, Cater J, DemirciH. Circumscribed choroidal hemangioma: clinical mani-festations and factors predictive of visual outcome in200 consecutive cases. Ophthalmology 2001; 108: 2237–48.

2. Ruby AJ, Jampol LM, Goldberg MF, Schroeder R,Anderson-Nelson S. Choroidal novascularization asso-ciated with choroidal hemangiomas. Arch Ophthalmol1992; 110: 658–61.

3. Tuncer S, Demirci H, Shields CL, Shields JA. Polypoi-dal choroidal vasculopathy following photodynamictherapy for choroidal hemangioma. Eur J Ophthalmol2009; 19: 159–62.

4. Leys AM, Silva R, Inhoffen W, Tatar O. Neovas-cular growth following photodynamic therapy for cho-roidal hemangioma and neovascular regression afterintravitreous injection of triamcinolone. Retina 2006; 26:693–7.

5. Sadda SR, Stoller G, Boyer DS, Blodi BA, Shapiro H,Ianchulev T. Anatomical benefit from ranibizumabtreatment of predominantly classic neovascular age-related macular degeneration in the 2-year anchorstudy. Retina 2010; 30: 1390–9.

Ophthalmic manifestations andrisk factors for mortality of HIVpatients in the post-highly activeanti-retroviral therapy era: comment

We read with great interest the recently published manu-script ‘Ophthalmic manifestations and risk factors formortality of HIV patients in the post-highly active anti-retroviral therapy era’.1 The authors highlight importantpoints regarding HIV patients and their ophthalmic care,and conclude with the recommendation that ‘patientsshould continue to be offered regular ophthalmic exami-nations despite being put on HAART’. Notably absentfrom their retrospective review, however, is a discussion ofhow patients were followed in their study. It would beinteresting if the authors could comment on how regularlypatients were followed in this study and whether factorssuch as presence of ophthalmic manifestations, presence ofHIV retinopathy, CD4 count or current HAART therapy,affected these decisions.

The current preferred practice patterns by The Interna-tional Council of Ophthalmology cite follow-up every3 months for patients with CD4 count <50.2 In the absenceof other HIV-related pathology, other specific follow-upguidelines are not cited. Based on our anecdotal clinicalexperience with a significant population of HIV patients,we have noted some variability in terms of patientfollow-up practices outside of the cited guideline. Coin-ciding with the authors’ review, HAART therapy has sig-nificantly reduced the incidence of opportunistic infectionsin this patient population, and have likely added to theflux in current follow-up patterns.

Conflict/competing interest: None declared.

Figure 2. Twelve months afterthe ninth intravitreal ranibizumabinjection, fluorescein angiography(a) shows intense diffuse hyper-fluorescence of haemangiomaand the closure of the choroidalneovascularization. Intermediatephase frame of indocyanine greenangiography (b) shows diffusehyperfluorescence of haeman-gioma, and late phase frameof indocyanine green angiogra-phy (c) shows wash out ofthe dye and no leakage fromthe choroidal neovascularization.Spectral-domain optical coherencetomography (d) shows absence ofintraretinal and subretinal fluid.

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