Download Birdshot Chorioretinopathy

Birdshot
C Pavesio
Euretina 2012
Birdshot Chorioretinopathy
Carlos Pavesio MD, FRCOphth
Consultant Ophthalmologist
Moorfields Eye Hospital
London, UK
Background: Birdshot Chorioretinopathy (BCR) can be defined as a chronic, bilateral,
inflammatory condition, which affects the posterior segment of the eye with involvement of
the choroid and retinal vessels.
BCR is an uncommon condition, being diagnosed in 0.6-1.5% of patients with uveitis
referred to tertiary centers, accounting for 6-7.9% of patients with posterior uveitis. Females
are more frequently involved and the mean age at disease onset is reported as being 53 years.
The youngest reported patient was 25 years old, and the oldest 79.
It is found more frequently in white people of northern European origin. It seems to be much
less frequent in Asia, which may be related to the low prevalence of HLA-A29 among Asian
populations. There has been only one report of one Hispanic and one black individual with
this condition.
Ocular Picture: The presenting symptoms may vary and while some patients may present
reporting significant night blindness, others will complain of fluctuation in vision, floaters,
photopsia, glare and reduction of peripheral vision. These symptoms give a good indication
of the fact that in the early stages of the disease there is involvement of the peripheral retina,
more likely due to the retinal vasculitis than to the choroidal disease, which is not matched by
changes in central vision. Patients do not present with symptoms of pain and redness, which
reflects the fact that the examination of these patients reveals an anterior chamber with no or
minimal inflammation, and typically no posterior synechiae. A study looking into laser flare
photometry has shown no significant elevation of aqueous humor protein content.
1
Birdshot
C Pavesio
Euretina 2012
The vitreous shows cellular infiltrate in nearly all patients, which tends to be more marked in
the posterior portion, but also shows variation in its intensity tending to be more intense
during early stages of the disease.
The typical birdshot lesions, which may take as long as 8 years to appear after onset of
symptoms, are usually round or oval in shape, measuring from a quarter to half a disc
diameter, but they can become confluent and form linear lesions(Fig 1). They are normally
seen as if radiating from the optic disc to the periphery, most commonly nasally and
inferiorly to the disc.
Figure1: colour photograph, deep cream-colored elongated spots located predominantly
nasally and inferiorly to the disc.
In typical cases they appear bilaterally and tend to be quite symmetric, but striking
asymmetry can also be found. The lesions, at least initially, seem to be located in the
choroidal stroma and are associated with the large choroidal veins. The indistinct appearance
of the lesions, the lack of pigmentary changes involving the retinal pigment epithelium
(RPE), and the angiography behavior of the lesionssupport this deep location in the choroidal
stroma. The macula may also show lesions, but it is most frequently spared, which may be
related to the relative absence of large choroidal veins in this location. In later stages the
2
Birdshot
C Pavesio
Euretina 2012
lesions tend to take a more atrophic appearance and enlarge, also involving outer retina and
producing RPE pigmentary disturbance. At this stage the functional abnormalities have
become irreversible and therapy is unlikely to be of any benefit.
The involvement of the retina appears in the form of retinal vasculitis leading to
hyperpermeability of capillaries and retinal edema, especially cystoid macular edema (CME).
Peripheral vision disturbances, seen quite early in the course of the disease, seem to be
related to inner retinal abnormalities, secondary to vasculitis and possibly diffuse retinal
edema, different from late disease when the outer retina becomes affected by progressive
choroidal disease. Other findings include diffuse narrowing of retinal arterioles, vascular
tortuosity, perivascular hemorrhages and optic disc swelling.
The most common symptoms related to central vision are blurring of vision and floaters, but
visual acuity tends to be fairly good in the majority of patients at presentation (better than
20/40 in 61.8% of eyes), even if they are already showing significant complaints related to
their peripheral vision. Most patients show symmetric visual acuity disturbance, but striking
asymmetry can also be found. The most important reason for loss of central vision is the
development of CME. Until recently this finding represented the main reason to treat patients
with BCR, but the understanding that peripheral retinal insult is happening independent of
this abnormality has led to a change in treatment strategy.The relapsing and remitting nature
of the CME may lead to permanent macular damage and permanent loss of visual acuity in
later phases of the disease.
The diffuse inner retinal involvement produces symptoms of reduction of peripheral visual
field and nyctalopia, which are usually seen quite early, even before any other abnormalities
become apparent. They may be reversed by therapy.
3
Birdshot
C Pavesio
Euretina 2012
Problems with color vision have also been reported in as many as 76% of the patients, mainly
affecting both the blue-yellow and red-green axis, which is the result not only of the retinal
disease, but also of the optic disc involvement, which is frequently overlooked.The optic
neuropathy can be present without any signs of papillitis or optic disc edema. The optic disc
margins remain sharp and the pallor of the optic nerve appears insidiously. Visual field
testing is mandatory, particularly if the visual impairment cannot be explained by the retinal
involvement.
Glare, photopsia, photophobia, metamorphopsia and decreased depth perception have also
been reported.
Etiology/Pathogenesis: Even though the exact role of specific HLA associations has not
been determined, a strong association with HLA-A29 has been found. No associations were
found for HLA-DR in one study.
The HLA-A29 genotype or phenotype is found in up to 7% of Caucasians and in more than
95% of individuals with BCR. Only 4.3% of the cases of BCR reported have been HLA-A29
negative. It must be kept in mind that the use of HLA-A29 as a defining criterion for the
diagnosis of BCR may have influenced this strong association.The relative risk of BCR
among HLA-A29 positive individuals has been estimated to be between 50 and 224.
There are six described subtypes of the HLA-A29 (HLA-A*2901 through HLA-A*2906).
The HLA-A29.2 serotype has been strongly associated with the risk of developing BCR,
while it has been shown in one study that the HLA-A29.1 serotype might have a protective
role.
It is interesting to note that the HLA-A29 phenotype has also been associated with idiopathic
retinal vasculitis.
4
Birdshot
C Pavesio
Euretina 2012
Diagnosis:
a. Diagnostic Criteria
The criteria initially formulated by Ryan and Maumenne include:
1. Minimal, if any, anterior segment inflammation; 2. diffuse vitritis without snowbanking; 3.
retinal vascular leakage, particularly in the posterior pole, which may be associated with
macular edema and optic disc edema; 4. distinctive, discrete, cream coloured or depigmented
spots throughout the postequatorial fundus; and 5. a painless eye.
In the largest reported series to date of 102 cases, Priem and Oosterhuis used the criteria of:
1. bilateral birdshot spots plus 2. retinal vasculopathy or disc edema or optic atrophy or
vitreous cells.
A recent publication has reported on the research criteria for BCR, designed mainly to
facilitate clinical studies. The required characteristics included: 1. Bilateral disease; 2.
Presence of at least three peripapillary “birdshot lesions” inferior or nasal to the optic disc in
one eye; 3 Low-grade anterior segment intraocular inflammation; 4. Low-grade vitreous
inflammatory reaction. Supportive findings include a positive HLA-A29 test, retinal
vasculitis and CME. It is important to stress these criteria were created for research purposes.
The finding of keratic precipitates, posterior synechiae and the presence of infectious,
neoplastic, or other inflammatory diseases that can cause multifocal choroidal lesions,
represent exclusion criteria. These criteria showed high specificity and sensitivity as reported
by the same authors.
b. Ancillary Tests
1. Fundus Fluorescein angiography (FFA): angiographic studies with sodium fluorescein are
particularly useful for the study of retinal circulation, but are limited when assessing lesions
located primarily in the choroidal stroma. The choroidal birdshot spots are described as
5
Birdshot
C Pavesio
Euretina 2012
showing early hypofluorescence and late hyperfluorescence. In reality, considering the deep
location of these lesions, most of them are actually not well demonstrated by FFA, and we
actually see fewer lesions than those apparent by ophthalmoscopy. The profuse leakage of
fluorescein at the level of choriocapillary tends to hide the deeper lesions from sight. FFA
shows the vascular leakage from retinal vessels and also CME and disc edema, which are
very common findings (Fig 2).
Fig 2: late phase of the fluorescein fundus angiography : Cystoid Oedema of the posterior
pole with CMO.
Another finding reported during FFA in BCR is a prolongation of the arteriovenous transit
time, which was initially described by Gass [13]. The transit time was found to be prolonged
by about 20 seconds, which was felt to be due to the extensive leakage of fluorescein into the
retina from compromised blood-retinal barrier associated with vasculitis, delaying the
appearance of the dye in the venous circulation.
2. Indocyanine green angiography (ICG): the birdshot lesions appear hypofluorescent on ICG
and are associated with medium-to-large choroidal vessels. Hypofluorescence in ICG could
mean either an inflammatory infiltrate (space occupying lesion), or non-perfusion of the
choroid. The histopathologic report of an eye of a 49 year old man supports the first by
demonstrating the presence of multiple foci of predominantly lymphocytes, located at various
6
Birdshot
C Pavesio
Euretina 2012
levels of the choroid, occasionally occupying the full thickness. The choroidal lesions are
actually more visible by ICG than clinically, especially in lightly pigmented fundus (Fig 3).
Fig 3:: intermediate phase of the ICG-A (12 minutes) during active inflammation:
numerous dark spots are distributed throughout the fundus (nodular choroidal inflammation).
Active lesions tend to be become isofluorescent in the later phase of the angiogram,
indicating penetration of the dye in to the affected areas, while lesions which have become
atrophic will continue to show hypofluorescence. Another feature is the presence of a fuzzy
indistinct appearance of the stromal vessels of the choroid. Early treatment will have a
marked effect on the choroidal lesions, which tend to resolve. This finding can be used to
assess response to therapy. This is in contrast to the response of the retinal vasculopathy and
is likely to be due to a much higher concentration of the therapeutic agent in the richly
perfused choroid.
3. Electrophysiology: abnormal electroretinograms (ERG) have been found in nearly 90% of
the cases. Early reports suggested possible inner retinal dysfunction, as suggested by the
finding of a negative ERG which indicates abnormal function of the neural retina with
relative sparing of outer retina-inner choroidal complex. In later disease there is also
involvement of the outer retina, which is demonstrated by progressive decrease in a-wave and
b-wave amplitudes. It is a very useful test especially considering that the functional status of
7
Birdshot
C Pavesio
Euretina 2012
the retina cannot be reliably inferred either from subjective symptoms or clinical signs. The
most sensitive parameter for dysfunction was the 30Hz cone derived flicker response. It
seems to be quite helpful for the decision to initiate therapy and also for monitoring efficacy
of treatment.
4. Visual Fields: the observed visual fields abnormalities include peripheral constriction,
generalized diminished sensitivity, enlarged blind spot, and central or paracentral scotomas.
It is likely that visual field findings reflect what is seen by electrophysiological studies and
that in the early stages of the disease they are related to inner retinal dysfunction and that
later on an outer retinal component also plays a role. It would certainly be much simpler to
use visual fields for monitoring purposes, but there are issues regarding standardization, both
of hardware and testing strategies, which make interpretation more difficult. Proper studies
are required to establish its value, especially in comparison to electrophysiology tests.
5. Optical Coherence Tomography (OCT): this test has been quite widely used to study the
macula and for monitoring CME and atrophic changes. Ultrahigh resolution OCT and depth
enhancement imaging may become interesting adjuncts to the study of the retinal changes in
different stages of BCR.
Differential Diagnosis: It is important to remember that BCR behaves in a very special
way it involves both the choroid and the retina as primary targets. Most inflammatory
processes involving the eye tend to primarily affect one or the other. There are two other
conditions which can lead to a similar dual involvement, tuberculosis and sarcoidosis, but
they usually also present with systemic manifestations, not present in BCR.
8
Birdshot
C Pavesio
Euretina 2012
Theoretically one can list all entities producing white dots in the fundus as part of the
differential diagnosis for BCR. The concept of white dot syndromes needs be revised since
the conditions put under this heading actually involve different layers of retina/choroid and
do nothave much in common. This has been brought about by studies of these conditions
using ICG angiography. Conditions such as APMPPE (Acute Posterior Multifocal Placoid
Pigment Epitheliopathy), PIC (Punctate Inner Choroidopathy) and MEWDS (Multiple
Evanescent White Dot Syndrome)involve the inner choroid. Conditons such as VKH and
sympathetic ophthalmia, which truly involve the choroidal stroma, are also associated with
significant anterior segment involvement, not a feature of BCR. Conditions such as
sarcoidosis, tuberculosis, mentioned above, and syphilis, apart from potential anterior
segment inflammation, tend to show systemic manifestations, not a presentation proven in
BCR.
It is important not to forget the possibility of a masquerade presentation, as in the case of
intraocular lymphomas, which may present with vitritis. The subretinal lesions seen in this
condition, at least initially, are located in a sub-RPE location and not in the deep choroid.
Treatment: An important development in the management of BCR has been the
recognition that we should not wait for changes in central vision to initiate therapy.
Peripheral retinal abnormalities may be well advanced by the time visual acuity suffers a
decline, which is reflected by symptoms of peripheral field loss and nyctalopia reported by
the patients and by the findings in ERG and visual field tests. This is important because early
and aggressive management may produce reversal of these abnormalities before they become
chronic and irreversible. Also it has been proposed that serial ERGs may be useful in
monitoring response to therapy and in guiding decisions to taper medications. Sequential
9
Birdshot
C Pavesio
Euretina 2012
visual field testing may also be an alternative for monitoring these patients as mentioned
above.
Considering that BCR is a chronic, progressive disease, the objective of therapy should be of
maximum control of inflammatory activity. Steroids, either systemically or locally, have been
used, especially for the treatment of CME, but also for the management of abnormalities in
ERG and CNV. This type of treatment is likely to produce some improvement in early stages,
but will not provide sufficient control. Even though long-term control may be achieved with
low doses of systemic steroids, this is likely to be more an exception and they should be used
more to manage acute exacerbations. Periocular injections and intravitreal triamcinolone
have a temporary effect and do not achieve overall control. A more stable delivery of
intraocular steroids is achieved by the use of intraocular devices, such as the fluocinolone
acetonide device (Retisert). Unpublished data shows also good control of the implanted eyes
but with high risk of cataract and ocular hypertension, requiring filtering procedure.
Agents such as cyclosporine, mycophenolate mofetil, azathioprine, oral methotrexate and
daclizumab have been used with reported success, but no data regarding superior efficacy of
any strategy is currently available.Their use is actually recommended early in the
management so as to provide the best chance of maintaining long-term retinal function and
visual acuity.
Another form of therapy reported deals with the use of intravenous immunoglobulin in 18
patients previously treated with systemic steroids but not with immunosuppressive agents.
The results showed favorable response in terms of resolution of macular edema, visual acuity,
visual fields and lowering of the corticosteroid-dependence threshold. Even though it is an
interesting option, it must be kept in mind that it is a small series and patients had better
initial vision when compared to other reports, not allowing us to conclude that this represents
an option in poorly responsive cases.
10
Birdshot
C Pavesio
Euretina 2012
Prognosis: The most common complication seems to be chronic CME, affecting around
50% of the cases. Epiretinal membranes occur in nearly 10% of cases and may progress with
significant contraction. Choroidal neovascular membranes are uncommon occurring in less
than 6% of cases. Neovascularization of the retina and disc are uncommon.
Most patients reported in the literature show progressive decline in vision, mainly due to
chronic CME. Other causes of decreased vision include: CNV, progressive choroidal atrophy,
vitreous opacity, cataract, epiretinal membrane, optic atrophy and central retinal vein
occlusion. A final visual acuity of 20/40 or better, in the better-seeing eye, was reported in
75.1% of patients. Legal blindness as defined by visual acuity of 20/200 or worse was found
in 9.8% of patients.
Longfollow-up of these patients show that there is progressive enlargement of the choroidal
lesions, which is associated temporally with visual loss. There are progressive pigmentary
changes involving the RPE, and consequently photoreceptors, and in later stages, due to
vasculitis, it may result in a pale disc and attenuated retinal vessels, reflecting the loss of
retinal function.
With early therapy, guided by sequential ERGs, it may be possible to retain visual function,
but this needs to be confirmed by long-term monitoring of patients who have been offered
this strategy.
11
Birdshot
C Pavesio
Euretina 2012
References:
References
Aaberg TM. Diffus inflammatory salmon patch choroidopathy syndrome. Presented at
the International Fluorescein Macula Symposium. Carmel, CA :1979.
Amalric P, Cuq G. Une forme très particulèire de chorio-retinopathie en grains the riz.
Bull Soc Ophthalmol Fr 1981 ;81 :131-134.
Barondes MJ, Fastenberg DM, Schwartz PL, Rosen DA. Peripheral reinal
neovascularization in birdshot retinochoroidopathy. Ann Ophthalmol 1989;21:306-8.
Bloch-Michel E, Frau E. Birdshot retinochoroidopathy and HLA-A29+ and HLAA29- idiopathic retinal vasculitis:comparative study of 56 cases. Can J Ophthalmol
1991;26:361-6.
Brucker AJ, Deglin EA, Bene C, et al. Subretinal choroidal neovascularization in
birdshot retinochoroidopathy. Am J Ophthalmol 1985;99:40-4.
Bouchenaki N, Cimino L, Auer C et al. Assessment and classification of choroidal
vasculitis in posterior uveitis using indocyanine green angiography. Klin Monatsbl
Augenheikd 2002;219(4):243-9.
12
Birdshot
C Pavesio
Euretina 2012
de Courten C., Herbort CP. Potential role of computerized visual field testing for the
appraisal and follow-up of birdshot chorioretinopathy. Arch Ophthalmol 1998;116:
1389-91.
de Waal LP, Lardy NM, van der Horst AR, et al. HLA-A29 subtypes and birdshot
chorioretinopathy. Immunogenetics 1992;35:51-3.
Donvito B, Monnet D, Tabary T, et al. Different HLA Class IA region Complotypes
for HLA-A29.2 and –A29.1 Antigens, Identical in Birdshot Retinochoroidopathy
Patients or Healthy Individuals. Invest Ophthalmol Vis Sci 2005;46:3227-32.
Fardeau C, Herbort CP, Kullmann N, Quentel G, LeHoang P. Indocyanine Green
Angiography in birdshot chorioretinopathy. Ophthalmology. 1999 Oct;106(10):192834.
Franceschetti A, Babel J, La chorio-retinite en “tâches de bougie,” manifestation de la
maladie de Besnier-Boeck. Ophthalmologica 1949 ;118 :701-710.
Gash At, Smith JA, Whitcupp SM. Birdshot retinochoroidopathy. Br J Ophthalmol
1999;83:241-9.
Gass JDM. Vitiliginous chorioretinitis. Arch Ophthalmol 1981;99:1778-1787.
Gaudio PA, Kaye DB, Crawford JB. Histopothology of birdshot retinochoroidopathy.
Br J Ophthalmol 2002;86:1439-41.
13
Birdshot
C Pavesio
Euretina 2012
Godel V, Barush E, Lazar M. Late development of chorioretinal lesions in birdshot
retinochoroidopathy. Ann Ophthalmol 1989;21:49-52.
Guex-Crosier Y, Pittet N, Herbort CP. Sensitivity of laser flare photometry to monitor
inflammation in uveitis of the posterior segment. Ophthalmology 1995;102:613-21.
Guex-Crosier Y, Herbort CP. Prolonged retinal arterio-venous circulation time by
fluorescein but not by indocyanine green angiography in birdshot chorioretinopathy.
Ocul Immunol Inflamm 1997;5:203-6.
Heaton JM, Mills RP. Sensorineural hearing loss associated with birdshot
retinochoroidopathy. Arch Otolaryngol Head Neck Surg 1993;119:680-1.
Herbort CP, Probst K, Cimino L, Tran VT. Differential inflammatory involvement in
retina and choroids in birdshot chrorioretinopathy. Klin Monatsbl Augenheilkd
2004;221:351-6.
Hesse S, Berbis P, Chemila JF, et al. Psoriasis and birdshot chorioretinopathy:
response to aromatic retinoids. Dermatology 1993;187:137-9.
Hirose T, Katsumi O, Pruett RC et al. Retinal function in birdshot
reinochoroidopathy. Acta Ophthalmol 1991;69:327-37.
14
Birdshot
C Pavesio
Euretina 2012
Holder GE, Robson AG, Pavesio C, Graham EM. Electrophysiological
characterization and monitoring in the management of birdshot chorioretinopathy. Br
J Ophthalol 2005;89:709-18.
Howe LJ, Stanford MR, Graham EM, et al. Choroidal abnormalities in birdshot
chorioretinopathy: an indocyanine green angiography study. Eye 1997;11(Pt 4):554-9.
Kaplan HJ, Aaberg TM. Birdshot retinochoroidopathy. Am J Ophthalmol
1980;90:773-82.
Kiss S, Ahmed M, Letko E, Foster CS. Long-term follow-up of patients with birdshot
retinochoroidopathy treated with corticosteroid-sparing systemic immunomodulatory
therapy. Ophthalmology 2005;1112:1066-71.
LeHoang P, Girard B, Deray G, et al. Cyclosporine in the treatment of birdshot
retinochoroidopathy. Transplant Proc 1988;20:128-30.
LeHoang P, Ozdemir N, Benhamou A, et al. HLA-A29.2 subtype associated with
birdshot retinochoroidopathy. Am J Ophthalmol 1992;113:33-35.
LeHoang P, Cassoux N, George F, et al. Intravenous immunoglobulin (IVIg) for the
treatment of birdshot retinochoroidopathy. Ocul Immunol Inflamm 2000;8:49-57.
Levinson RD, Gonzales CR. Birdshot retinochoroidopathy: immunopathogenesis,
evaluation, and treatment. Ophthalmol Clin N Am 2002;15:343-50.
15
Birdshot
C Pavesio
Euretina 2012
Levinson RD, Rajalingam R, Park MS, et al. Human Leukocyte Antigen A29
Subtypes Associated with Birdshot Retinochoroidopathy. Am J Ophthalmol
2004;138:631-4.
Levinson RD, Brezin AB, Rothova A, Accorinti M, Holland GN. Reserch criteria for
the diagnosis of Birdshot chorioretinopathy: results of an international consensus
conference. Am J Ophthalmol 2006;141:185-7.
Marsh SGE, Parham P, Barber LD. The HLA factsbook. San Diego: Academic Press,
2000:130.
Martidis A, Duker JS, Puliafito CA. Intravitreal triamcinolone for refractory cystoid
macular edema secondary to birdshot retinochoroidopathy. Arch Ophthalmol
2001;119:1380-3.
Noble KG, Greenberg J. Appearance of birdshot retinochoroidopathy in a patient with
myelodysplasia syndrome. Am J Ophthalmol 1998;125:108-9.
Nussenblatt RB, Mittal KK, Ryan S, et al. Birdshot retinochoroidopathy associated
with HLA-A29 antigen and immune responsiveness to retinal S-antigen. Am J
Ophthalmol 1982;94:147-58.
Oh KT, Christmas NJ, Folk JC. Birdshot retinochoroiditis: long term follow-up of a
chronically progressive disease. Am J Ophthalmol 2002;133:622-9.
16
Birdshot
C Pavesio
Euretina 2012
Priem HA, Oosterhuis JA. Birdshot chrorioretinopathy : clinical characteristics and
evolution. Br J Ophthalmol 1988;72:646-659.
Priem HA, Kijlstra A, Noens L, et al. HLA typing in birdshot chorioretinopathy. Am J
Ophthalmol 1988;105:182-5.
Priem HA, De Rouck A, De Laey JJ et al. Electrophysiologic studies in birdshot
chorioretinopathy. Am J Ophthalmol 1988;106:430-6.
Rothova A, Van Schooneveld MJ. The end stage of birdshot retinochoroidopathy. Br
J Ophthalmol 1995;79:1058-9.
Rothova A, Berendschot TTJM, Probst K, et al. Birdshot Chorioretinopathy: longterm manifestations and visual prognosis. Ophthalmology 2004;111:954-9.
Ryan SJ, Maumenee AE. Birdshot retinochoroidopathy. Am J Ophthalmol
1980;89:31-45.
Ryan SJ, Rao NA. Birdshot Retinochoroidopathy. IN: Retina. Ryan SJ, edtr. Mosby.
2006, 4th Edition. pp.1763-70.
Shah KH, Levinson RD, Yu F, Goldhardt R, et al. Birdshot Chorioretinopathy. Surv
Ophthalmol 2005 ;50 :519-41.
17
Birdshot
C Pavesio
Euretina 2012
Sobrin L, Lam BL, Liu M et al. Electroretinographic monitoring in birdshot
chorioretinopathy. Am J Ophthalmol 2005;140:52-64.
Sobrin L, Huang JJ, Christen W, Chrysanthi K, Choopong P, Foster CS. Daclizumab
for treatment of Birdshot Chorioretinopathy. Arch Ophthalmol 2008;126(2):186-191.
Soubrane G, Bokobza R, Coscas G. Late developing lesions in birdshot
retinochoroidopathy. Am J Ophthalmol 1990;109:204-10.
Tabary T, LeHoang P, Betuel H, et al. Susceptibility to birdshot chorioretinopathy is
restricted to the HLA-A29.2 subtype. Tissue Antigens 1990;36:177-179.
Vitale AT, Rodriguez A, Foster CS. Low-dose cyclosporine therapy in the treatment
of birdshot retinochoroidopathy. Ophthalmology 1994;101:822-31.
Vrabec TR, Augsburger JJ, Fischer DH, et al. Taches de bougie. Ophthalmology
1995;102:1712-21.
Witkin AJ, Duker JS, Ko TH et al. Ultrahigh resolution optical coherence tomography
of birdshot retinochoroidopathy. Br J Ophthalmol 2005;89:1660-1.
Wolfensberger TJ, Herbort CP. Indocyanine green angiography features in ocular
sarcoidosis. Ophthalmology 1999;106:285-9.
18
Birdshot
C Pavesio
Euretina 2012
Wolfensberger TJ, Piguet B, Herbort CP. Indocyanine green angiography (ICGA)
features in tuberculous chorioretinitis. Am J Ophthalmol 1999;127:350-3.
Zacks DN, Samson CM, Loewenstein J, Foster CS. Electroretinograms as an indicator
of disease activity in birdshot retinochoroidopathy. Graefe’s Arch Clin Exp
Ophthalmol 2002;240:601-7.
19