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GENERAL REVIEW

Anterior uveitis夽
J. Gueudry ∗, M. Muraine

Service d’ophtalmologie, hôpital Charles-Nicolle, CHU de Rouen, 1, rue de Germont, 76031

Rouen cedex, France

Received 1st September 2017; accepted 14 November 2017

KEYWORDS Summary Anterior Uveitis is the most common form of uveitis. There are several known and
Uveitis; many possible etiologies for anterior uveitis. After examining the posterior segment and ruling
Iridocyclitis; out masquerade syndromes, the main step of etiologic diagnosis is clinical characterization. It is
Herpetic uveitis; essential to establish the presence or absence of unilateral versus bilateral and granulomatous
HLA B27; features. Subsequently, a directed work-up may be obtained which then helps to confirm diag-
Juvenile idiopathic nostic hypotheses based on the detailed history and clinical examination. The priority is to rule
arthritis out an infection. Treatments are adapted according to etiology and disease severity. Finally, bio-
logics have greatly changed the management and prevention of some forms of anterior uveitis, in
particular uveitis associated with HLA-B27 and juvenile idiopathic arthritis-associated anterior
uveitis.
© 2017 Elsevier Masson SAS. All rights reserved.

Introduction ination along with simple ancillary testing allow a directed

Uveitides are relatively rare diseases of variable causes.
They are potentially sight threatening, representing 10% of
legal blindness in industrialized countries [1]. The uveitis
may be just the tip of the iceberg and may be the present-
ing sign of a systemic disease. Anterior uveitis is the most
frequent. Certain routine steps on the initial clinical exam-
夽 See this article unabridged, illustrated and detailed, with elec-
tronic enhancements in EMC-Ophtalmologie: Gueudry J. Uvéites
antérieures. EMC — Ophtalmologie 2017:1—13 [Article 21-220-A-40].
∗ Corresponding author.
E-mail address: julie.gueudry@chu-rouen.fr (J. Gueudry).
approach to further testing and treatment by avoiding cer-
tain pitfalls.
Definition of anterior uveitis
The current classification of uveitis is an anatomic classifi-
cation, as set forth by the International Uveitis Study Group
(IUSG) then confirmed by the Standardization of Uveitis
Nomenclature (SUN) work group [2,3]. This classification
is based upon the concept of the ‘‘primary’’ or ‘‘initial’’
site of inflammation. It is thus based on the place where
the inflammation predominates. It distinguishes between

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anterior uveitis with iris and ciliary body involvement, inter-
mediate uveitis with peripheral chorioretinal involvement,
posterior uveitis with choroidal and retinal involvement and
panuveitis. The associated complications do not change the
type of uveitis. For example, an HLA-B27 positive anterior
uveitis complicated by macular edema remains classified
as anterior uveitis. The SUN also allows for distinguishing
uveitides as a function of their presentation, sudden-onset
or insidious, as well as their progression; acute, in the case
of a sudden, brief episode; recurrent, in the case of mul-
tiple episodes separated by quiet periods of 3 months or
more without treatment; chronic, in the case of a persis-
tent episode with relapses occurring less than 3 months after
treatment is discontinued.
Epidemiology of anterior uveitis
In 2016, in over 4 million Americans, the prevalence
of uveitis was found to be 133/100,000 inhabitants and
121/100,000 inhabitants just for non-infectious causes.
Among these, 80% represented anterior uveitis [1]. The
clinical entities found most frequently in series in western
countries are HLA-B27 positive uveitis, Fuchs heterochromic
iridocyclitis and herpetic uveitis [4].
Etiologic diagnosis
Clinical characterization of anterior uveitis
The key to etiologic diagnosis of uveitis is the clinical exam-
ination. The characterization of a case of uveitis allows
the patient to be integrated into a clinical context, which
points quickly toward certain etiologies (Table 1) [5]. The
anatomic characterization of uveitis, its mode of progres-
sion and its unilaterality or bilaterality are thus necessary
for a targeted diagnosis and appropriate treatment. Finally,
it is necessary to define whether the involvement is granu-
lomatous, which allows the number of possible etiologies
to be filtered down, even if it is not always easy. Any
uveitis may begin as non-granulomatous. Thus, it has been
described that over half of patients with biopsy-proven sar-
coidosis presented initially with non-granulomatous uveitis
[6].
The typical symptoms, which lead to consultation, are
pain, redness, photophobia and decreased visual acuity.
However, certain patients may remain asymptomatic, for
example in the case of Fuchs heterochromic iridocyclitis or
uveitis associated with juvenile idiopathic arthritis (JIA).
One must also keep in mind that the contrast between
the appearance of intraocular inflammation in a ‘‘white
eye’’ is suggestive of masquerade syndromes, notably in

Table 1 Principal diagnoses to consider according to the clinical presentation of anterior uveitis, adapted from Zierhut
M, Carlos E. Pavesio and Debra A. Goldstein.
Ophthalmologic clinical signs Diagnostic consideration
Laterality Unilateral: HSV/VZV; CMV; PSS
Bilateral: Sarcoidosis; TB; Behçet’s disease. . .
Alternating: HLA-B27
Granulomatous keratic precipitates Central/paracentral: HSV/VZV; CMV; PSS
Diffuse: FHI; HSV/VZV
Inferior: Sarcoidosis, TB, MS. . ..
Corneal involvement HSV/VZV; Syphilis; Lyme; TB; Cogan syndrome; Leprosy
Ocular hypertension HSV/VZV; CMV; PSS; FHI; Syphilis; Sarcoidosis; Tuberculosis; Leprosy
Steroid response
Lens-associated uveitis; UGH
Iris transillumination Sectoral: HSV/VZV
Diffuse: FHI; Moxifloxacin
Iris heterochromia FHI
Posterior synechiae FHI ruled out (except in postoperative period)
Hypopyon HLA-B27; Spondylarthropathy; Sarcoidosis; TB; Behçet’s disease
HSV/VZV; Syphilis; Leptospirosis
Masquerade syndromes
Hyphema HSV/VZV
UGH
Amsler’s sign in FHI
Associated scleritis Chronic atrophic polychondritis; Granulomatosis with polyangiitis (Wegener’s
granulomatosis); IBD; HLA-B27
HSV/VZV; Syphilis; Sarcoidosis; TB
‘‘White eye’’ JIA; FHI; Masquerade syndromes
M. Zierhut et al. Anterior uveitis. Intraocular Inflammation. Springer; 2016.
HSV: herpes simplex virus; VZV: varicella-zoster virus; CMV: cytomegalovirus; PSS: Posner-Schlossman syndrome; TB: tuberculosis; MS:
multiple sclerosis; FHI: Fuchs heterochromic iridocyclitis; UC: ulcerative colitis; JIA: juvenile idiopathic arthritis; UGH: uveitis glaucoma
hyphema syndrome,IBD: inflammatory bowel disease.

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neoplastic pseudo-uveitis, since cellular infiltrates actually
simulate visible inflammatory elements.
A ciliary flush may be present. Slit lamp examination
identifies and quantifies the cellular and/or protein Tyn-
dall effect and looks for the presence or absence of keratic
precipitates and iris nodules. They define the granuloma-
tous nature of the uveitis. The appearance and location of
the keratic precipitates are a large help toward a correct
diagnosis (Fig. 1).
Granulomatous precipitates may be:
• fine and spiculated, distributed over the entire posterior
surface of the cornea (such as in Fuchs heterochromic
iridocyclitis);
• of medium size, more or less central, such as in herpes,
often gray or brown, with a ‘‘leopard skin’’ distribution;
• of large size, in a triangular distribution (such as in
sarcoidosis or tuberculosis), sometimes referred to as
‘‘mutton fat’’.
Iris nodules are referred to as Koeppe nodules, situated
at the pupillary margin, or Busacca nodules, situated within
the iris stroma (Fig. 2). Their presence must be assessed
prior to dilation.
On the other hand, fine, dust-like keratic precipitates and
fibrin in the anterior chamber suggest non-granulomatous
uveitis. This fibrin may organize within the anterior
chamber in the form of a membrane and partially or
completely occlude the pupil. A hypopyon is a mass of
inflammatory cells, which settle inferiorly due to gravity
(Fig. 3). It is an indicator of the severity of uveitis more
so than an element of the etiologic diagnosis. Classically,
it is described in HLA-B27 positive uveitis, Behçet’s disease,
rifabutin uveitis, or in cases of infectious uveitis such as her-
petic uveitis [7]; however, any severe uveitis may present
with a hypopyon.
Certain uveitides are typically bilateral, such as sarcoido-
sis. Unilaterality suggests infection and alternating laterality
is characteristic of HLA-B27 positive uveitis.
An increase in intraocular pressure as the uveitis pro-
gresses may result from multiple causes such as a steroid
response, clogging of the trabecular meshwork, extensive
posterior synechiae resulting in iris bombé, or the pro-
gression of anterior synechiae. However, the intraocular
pressure change may occur at the onset of the episode,
suggesting an etiologic diagnosis. Hypotony is possible with
episodes of anterior uveitis due to ciliary body shutdown,
with a return to normal upon resolution of the inflamma-
tion. It is frequently observed with HLA-B27 positive uveitis.
However, chronic inflammation may provoke permanent
hypotony without recovery of the secretory function of the
ciliary body. On the other hand, ocular hypertension suggests
infectious uveitis such as viral uveitis, Posner—Schlossman

Figure 1. Appearance of granulomatous keratic precipitates. ‘‘Mutton fat’’ precipitates (a); distribution in an inferiorly based triangle in
sarcoidosis (b); stellate whitish appearance with diffuse, regular distribution to the top of the cornea, suggestive of Fuchs heterochromic
iridocyclitis (c and d); few, central, clear precipitates in Posner—Schlossman syndrome (e and f); central or paracentral gray precipitates
with paving-stone appearance, of herpetic uveitis (g and h).

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Figure 2. Granulomatous anterior uveitis and iris nodules. Appearance of multiple iris nodules at the pupillary margin (Koeppe nodules)
and iris stroma (Busacca nodules) (a); isolated Koeppe nodule in anterior uveitis associated with multiple sclerosis (b); angular iris nodule
in sarcoidosis and its appearance on gonioscopy (c and d).
Figure 3. HLA-B27 positive non-granulomatous uveitis. Note the
fibrin present on the anterior lens and the dust-like cellular deposit
inferiorly (a); note the fibrin on the anterior lens, persistent poste-
rior synechia, hypopyon and absence of keratic precipitates (b).
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syndrome and Fuchs heterochromic iridocyclitis in unilat-
eral cases, but also sarcoidosis or tuberculosis in bilateral
cases. Lens-induced uveitis also often raises the intraocular
pressure.
Keratouveitis first suggests herpetic or zoster involve-
ment, which may occur in the absence of concomitant
skin involvement. Corneal hypesthesia or anesthesia is
also suggestive. Also, corneal examination may reveal
band keratopathy, which suggests chronic anterior segment
inflammation.
Examination of the iris prior to dilation sometimes also
aids in the etiologic diagnosis. Sectoral iris atrophy visible
on transillumination is very suggestive of herpetic or zoster
uveitis (Fig. 4). Iris heterochromia is also very suggestive of
Fuchs heterochromic iridocyclitis due to iris stromal atrophy,
as well as the loss of iris relief and disappearance of iris
crypts. After dilation, the presence of posterior synechiae
also directs the etiologic diagnosis.
A view of the ocular fundus is absolutely necessary. It
allows one to know if the involvement is strictly anterior
and if it is really unilateral or bilateral. When the fundus
cannot be seen during the initial visit, a repeat examination
after 24—48 hours of treatment allows for identification of
posterior involvement.
At the conclusion of the clinical examination, cer-
tain principles may however be applied. For example,
HLA-B27 positive uveitis and Behçet’s disease are never
granulomatous. Posterior synechiae are always absent in
Fuchs heterochromic iridocyclitis. Unilateral uveitis sug-
gests above all an infectious process, especially when it
is granulomatous and highly steroid dependent or steroid
resistant.
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Anterior uveitis
Figure 4. Sectoral iris atrophy in herpetic uveitis. Sectoral transillumination (a and b); more diffuse involvement (c); sectoral iris atrophy
causing corectopia, note the old pigmented keratic precipitates (d).
History
The history is then directed based on the differential diagno-
sis arising from the clinical examination. Certain systematic
questions are useful and will avoid errors. For example, ask-
ing the patient about oral ulcers is necessary due to the
ophthalmologic morbidity associated with Behçet’s disease,
and this will not necessarily be reported spontaneously by
the patient (Appendix 1) [8].
Ancillary testing
At the conclusion of the clinical examination, the etiologic
diagnosis may be purely ophthalmologic and not typically
require additional testing, such as for a typical herpetic
uveitis, sometimes confirmed by PCR analysis of the aque-
ous humor after anterior chamber paracentesis. However, in
the majority of cases, diagnostic hypotheses require confir-
mation. A minimal etiologic work-up will be proposed upon
initial evaluation of the uveitis (Appendix 2) [8] and will be
supplemented based on the differential diagnosis. Syphilis
serology is systematic, given the polymorphism of the asso-
ciated uveitis. Antinuclear antibodies are useful in children
to document possible juvenile idiopathic arthritis. Rheuma-
toid factor levels are not systematically necessary in adults.
Actually, rheumatoid arthritis causes scleritis much more
frequently. An extensive systematic work-up has a role for
severe chronic uveitis. Finally, numerous viruses may cause
an anterior uveitis concomitantly or subsequently to the ini-
tial infection, such as Zika, Chinkungunya or even influenza
[9].
Tests to detect production of interferon-␥ aid in the
diagnosis of tuberculosis. There are two main tests,
® ®
QuantiFERON-TB gold and T-Spot TB . These test repro-
duce in vitro in a standardized fashion the first stage in the
delayed-type hypersensitivity reaction to Mycobacterium
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5
tuberculosis. They are performed on a blood sample. In
these tests, blood T lymphocytes are stimulated in vitro
with tuberculosis antigen, and the production of interferon-
␥ is measured the next day. The particularity of these tests
is to no longer use tuberculin antigen, but antigens not
shared with the tuberculosis vaccine (BCG) or the major-
ity of atypical mycobacteria. A positive test indicates the
presence in the subject’s blood of memory T cells specific
for Mycobacterium tuberculosis. This test does not allow
for differentiation between latent tuberculosis infection and
active or treated tuberculous disease. These tests are not
recommended in France for the diagnosis of active tuber-
culosis disease except in extrapulmonary forms where the
diagnosis is difficult, such as presumed tuberculous uveitis.
In the literature, two studies in non-endemic zones have
demonstrated significance of the threshold of positivity of
®
the QuantiFERON-TB gold test, although the laboratory,
which markets it, does not indicate this. Thus, a result above
1.5 IU/mL [10] or 2 IU/mL [11], increases the success rate of
antituberculous treatment in the case of presumed tuber-
culous uveitis, most often extrapulmonary.
Anterior chamber paracentesis (ACP) is often helpful,
notably for the diagnosis of presumed viral involvement, in
order to perform aqueous humor analysis. It is performed,
under local anesthesia with tetracaine, after placing a lid
speculum most often in the operating room, by aspiration
with a 30-gauge needle, which is then capped.
Specific entities
HLA-B27 positive uveitis
HLA-B27 positive uveitis is common. It is associated with
spondyloarthritis (ankylosing spondylitis, arthritis associ-
ated with inflammatory bowel disease, psoriatic arthritis,
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reactive arthritis, undifferentiated spondyloarthropathy),
but may be isolated without arthritic symptomatology. The
frequency of the uveitis is variable, depending on the dura-
tion of the disease and the type of spondyloarthritis, rising to
30% of patients [12]. The prevalence of the uveitis is greater
in the case of ankylosing spondylitis (20—30%), than in arthri-
tis associated with inflammatory bowel disease (2—9%) or
psoriatic arthritis (7—16%).
Among those with recurrent anterior uveitis, about half
are associated with HLA-B27 or a spondyloarthropathy, and
up to 60% in a recent study of 798 patients with at least 2
episodes of anterior uveitis [13]. Anterior uveitis is thus a
frequent presenting condition of patients with the diagno-
sis of spondyloarthritis, while the rheumatologic complaints
are more easily ignored by the patient. The uveitis occurs
in a delayed fashion relative to the rheumatologic manifes-
tations; Monnet et al. have reported a delay of 8 years on
average. Recurrence is frequent, said to be alternating in
laterality, although it appears that the first eye involved is
more often affected and that the recurrences are spaced
accordingly with the progression of the disease [14].
The typical clinical presentation of HLA-B27 positive
uveitis is an acute unilateral uveitis of sudden onset, occur-
ring most often in a young subject between 20 and 40
years, and non-granulomatous. It is sometimes difficult to
differentiate this uveitis from endogenous endophthalmitis
when the fundus cannot be visualized. Posterior synechiae
are frequent. It is common to observe a few cells in the
anterior vitreous, or more rarely a true diffuse vitritis.
The most frequent complications are posterior synechiae,
cataract, glaucoma and development of chronic uveitis.
Macular edema is a complication in 10 to 30% of patients
[15]. A recent study showed that secondary glaucoma was
the most frequent cause of irreversible loss of visual acu-
ity in this type of uveitis [16]. Each episode lasts between
4 and 6 weeks, typically with complete remission between
episodes.
Anterior uveitis associated with herpes viruses
Herpes viruses are enveloped DNA viruses, which are
able to persist in a latent state within the host after
the primary infection. Reactivations and primary infec-
tions may be symptomatic. Herpes simplex virus (HSV)
uveitis is classically unilateral, recurring, granulomatous or
non-granulomatous and most often associated with ocular
hypertension. A slight hyphema is sometimes present. It
causes relatively few synechiae. The iris examination is very
suggestive in the case of associated sectoral iris atrophy.
Anterior segment manifestations associated with the HSV
virus and varicella-zoster virus (VZV) have been previously
described (further reading). We will discuss here anterior
uveitis suspected to be associated with cytomegalovirus
(CMV).
CMV anterior uveitis occurs in the immunocompetent
patient as opposed to CMV retinitis, which is reserved for the
profoundly immunocompromised. The diagnosis can only be
made by PCR analysis of the aqueous humor after ACP. The
role of CMV in Posner—Schlossman syndrome was suggested
the first time in 1987, by identification of local synthesis of
anti-CMV antibodies in the aqueous humor by Bloch-Michel
et al. [17]. In 2002, this hypothesis was confirmed by PCR in 2
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patients [18]. Other teams have since been able to find CMV
by PCR in immunocompetent patients with anterior uveitis
and no other etiologies found [19—21].
CMV anterior uveitis manifests itself as a uveitis similar
to the anterior uveitis of HSV and VZV; with brown infe-
rior keratic precipitates, marked ocular hypertension and
marked iris atrophy, associated or not with endotheliitis,
but refractory to typical medical treatment [22]; or as the
clinical picture of Posner—Schlossman syndrome. Also note
that the CMV genome has been isolated in cases of uveitis
identified as Fuchs heterochromic iridocyclitis [23].
Posner—Schlossman syndrome (PSS)
This is a unilateral uveitis typically affecting men aged
20—50 years. Patients typically present for blurred vision
related to corneal edema due to a very significant elevation
of the intraocular pressure to between 40 and 60 mmHg.
The anterior chamber reaction is minimal and a few cen-
tral gray keratic precipitates are visible. The attacks may
lead to severe glaucomatous involvement, although this syn-
drome has long been considered benign and self-limited
[24]. In PSS, it now appears useful to screen for the CMV
viral genome in the aqueous humor. Studies of the largest
numbers of patients appear to indicate that CMV is found in
approximately half of cases of PSS [23,25]. Visual field analy-
sis appears useful for evaluating optic nerve function, which
may be increasingly affected by the repeated attacks. Note
that it appears that CMV positive PSS has a poorer prognosis
than CMV negative cases. In these cases, it has been shown
recently that endothelial cell loss was more severe and fil-
tering surgery was more frequently required [25]. In CMV
positive PSS, specific local or systemic treatment may be
instituted. Classic anti-herpetic drugs such as acyclovir and
valacyclovir are ineffective. Thus, intravenous ganciclovir or
more frequently its prodrug valganciclovir, available orally,
must be utilized. There is no established protocol for the
management of these uveitides. The use of 2% ganciclovir
eye drops appears effective for treatment induction and
maintenance to limit recurrence [25]. Topical therapy has
the advantage of avoiding the toxicity (notably hematologic)
of ganciclovir and valganciclovir. In France, 0.15% ganci-
clovir gel is available; it might also have a certain efficacy
in combination with topical steroid therapy [26]. In CMV
negative forms, treatment rests on a short course of top-
ical steroids and topical glaucoma medications. However,
its recurrent nature requires repeating the search for a viral
cause, which may be identified after several attempts.
Fuchs heterochromic iridocyclitis (FHI)
This is a chronic anterior uveitis of insidious onset. It most
often affects young subjects and is most often unilateral,
although 15% of cases are actually bilateral [27]. Typically,
considered benign, the management of the secondary glau-
coma may in reality be very complex and it must not lead to
a maladapted use of steroids, which may bring about their
own complications. Typically, FHI does not cause the usual
symptoms of anterior uveitis, with redness and pain absent.
The anterior segment inflammation is characterized by a
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Anterior uveitis
moderate Tyndall effect and fine white stellate keratic pre-
cipitates distributed fairly characteristically over the entire
corneal endothelium. The other type of uveitis, which may
result in diffuse keratic precipitates, is herpetic or zoster
uveitis. A vitritis with large floaters, leading the patient
to seek consultation, is very frequent. However, the sub-
tlety of the various clinical signs may delay the diagnosis of
FHI until the time when a visually incapacitating cataract
appears. The heterochromia is seen on examination of both
irides in bright ambient light prior to dilation. It repre-
sents progressive diffuse atrophy of the iris stroma. It is
generally the lighter colored eye that is affected by the
inflammation, except for very light blue eyes, for which the
appearance of the iris pigment epithelium on the posterior
surface of the iris may make the iris appear darker than is
really is. In the bilateral case, heterochromia is difficult to
identify. In this case, certain clinical signs of iris atrophy
may help, such as diffuse and discrete zones of iris tran-
sillumination or a smoother appearance of the iris stroma
with less marked relief. The iris vessels become more appar-
ent. The fragility of the vessel walls may probably provoke
the classic hyphema upon anterior chamber paracentesis, or
Amsler’s sign [28]. Importantly and relatively pathognomon-
ically, posterior synechiae and ciliary flush are absent, as
well as macular edema in the unoperated cataract patient,
despite the chronic inflammation. Iris nodules are relatively
frequent in over 30% of cases [29].
Long-term use of anti-inflammatories in ineffective
and sometimes harmful in FHI. Management rests on
screening for and treating cataract, ocular hyperten-
sion and glaucoma. The secondary glaucoma may become
rapidly refractory to medical treatment. Glaucomatous
involvement is present in 15 to 59% of cases [30]. The
prognosis is usually good, with visual acuity of 5/10 or
greater after cataract surgery [31,32]. In the postoperative
period, posterior synechiae may form, as well as intraoc-
ular lens deposits. Thus, use of high-frequency steroids
would appear useful during this period to prevent these
complications.
While FHI is felt to be idiopathic, there are now some
reasons to associate it with rubella. The presence of ocu-
lar rubella infection has been identified by measuring the
Goldmann—Witmer coefficient in several studies [33—35]. In
addition, its incidence seems to be less since the widespread
rubella vaccination compared to an older or foreign popu-
lation [36]. Although the diagnosis is clinical, a work-up for
other etiologies as well as ACP for molecular analysis of the
aqueous humor may be considered. One particular form is
FHI associated with ocular toxoplasmosis, for which a scar
or active focus must be systematically sought [37].
Sarcoid anterior uveitis
Sarcoid uveitis is usually bilateral. Anterior uveitis is the
most frequent presentation, in 41 to 75% of cases. It is
chronic and granulomatous or not [38]. The diagnosis of sar-
coidosis is histologic, but this confirmed diagnosis is difficult
to obtain. In 2009, diagnostic criteria for ocular sarcoidosis
were published to define on clinical, laboratory and radio-
logic criteria, the diagnosis of certain, presumed, probable
or possible ocular sarcoidosis [39].
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Anterior uveitis associated with Behçet’s
disease
Uveitis is one of the diagnostic criteria for Behçet’s disease.
The anterior uveitis is rarely isolated, but the posterior seg-
ment involvement may be absent or in the initial stage. The
clinical picture is most often stormy, progressing episodi-
cally. The involvement is non-granulomatous, accompanied
rather frequently by a hypopyon. This anterior involvement
rarely affects the prognosis.
Anterior uveitis associated with multiple
sclerosis
The prevalence of uveitis is patients with multiple sclerosis
is about 1% and the prevalence of multiple sclerosis is cases
of uveitis is also about 1%, based on large studies. Although
intermediate uveitis is the most frequent, the occurrence
of anterior uveitis is possible, between 14.3 and 28.6% [40].
Granulomatous uveitis appears to be the most frequent [41].
Uveitis and medications
Immunotherapies used in the management of metastatic
cutaneous melanoma are responsible for intraocular inflam-
matory side effects. Anterior uveitis has been reported with
BRAF inhibitors, notably vemurafenib [42], and with ipili-
mumab, which is designed to stimulate the existing T-cell
immune response [43]. Whether anti-TNF␣ may cause de
novo occurrences of uveitis remains debated. Lim et al.
report, however, 26 cases of uveitis possibly associated with
the use of anti-TNF␣ for whom no existing disease pre-
disposing to uveitis was known [44]. However, side effects
paradoxically causing uveitis are possible, such as the devel-
opment of sarcoidosis.
More classically, biphosphonates (treatment for the pre-
vention of osteoporosis, treatment of bone metastases) and
rifabutin (treatment for atypical mycobacteria) may engen-
der anterior uveitis complicated or not by a hypopyon.
Treatment of the anterior uveitis rests on local steroids. Dis-
continuation of the causative medication is to be weighed
against its benefits. Brimonidine may also provoke a picture
masquerading as granulomatous anterior uveitis, paradox-
ically associated with ocular hypertension, after at least
12 months of instillation. This uveitis may be associated
with allergic conjunctivitis, which appears to precede the
uveitis [45]. Moxifloxacin has also been incriminated in the
occurrence of pseudo-uveitis in association with pigment
dispersion and diffuse iris atrophy [46].
Anterior uveitis in children
Uveitis in children represents 5 to 10% of all intraocular
inflammation. The majority of pediatric uveitis is bilateral
and non-infectious [47]. All the etiologies of adult ante-
rior uveitis may affect children, but JIA associated uveitis
is the most frequent and is specific to an onset in childhood.
The subgroups of JIA complicated by uveitis are essentially
the pauciarticular forms with positive antinuclear antibod-
ies. The frequency of JIA associated uveitis is estimated
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JFO-1835; No. of Pages 11 ARTICLE IN PRESS
8 J. Gueudry, M. Muraine
between 4 and 38% [48]. This uveitis has the particularity of
being asymptomatic with a white eye and non-painful until
complications arise. Typically, it is a chronic anterior uveitis,
granulomatous or not, and bilateral. In about 5% of cases,
the uveitis precedes the onset of the arthritis.
Differential diagnosis: masquerade syndromes
Certain non-inflammatory pathologies may mimic a large
number of diagnostic elements of anterior uveitis and divert
the etiologic diagnosis toward uveitis when there is not any.
Thus, when faced with an anterior uveitis resistant to the
usual treatment, one must re-evaluate the diagnosis before
escalating therapy [49].
Primary infiltration of the anterior segment (extension of
a retinoblastoma or vitreoretinal lymphoma into the ante-
rior segment) or secondary infiltration (metastases from
leukemia, systemic lymphoma, solid tumor) may give the
appearance of anterior uveitis. Thus, acute lymphoblastic
leukemia is the primary cause of hypopyon in children [50].
Chronic ocular ischemic syndrome of atheromatous or
arteritic origin is secondary to chronic hypoperfusion of
the globe due to involvement of the carotid arterial sys-
tem. It may present a clinical picture similar to anterior
uveitis by breakdown of the blood-aqueous barrier, which
may induce a Tyndall effect and more rarely keratic pre-
cipitates. However, there is frequently rubeosis iridis with
little or no elevation of the intraocular pressure, due to
ciliary body ischemia. The anterior segment signs may be
isolated; however, posterior segment involvement is most
frequent and leads to diagnosis most often due to tortuous
arteries, cotton-wool spots and blot hemorrhages in the mid-
periphery. Carotid Dopplers are necessary and fluorescein
angiography aids in the diagnosis [51].
Pigmentary glaucoma is frequently mistaken for refrac-
tory anterior uveitis. The diagnosis is clinical, emphasizing
the pigmented nature of the Tyndall effect, the presence
of a Krukenberg spindle (vertical pigmented keratic precipi-
tates), as well as engorgement of the anterior chamber angle
with pigment on gonioscopy.
Iridocorneal-endothelial or ICE syndromes have no rec-
ognized etiology (Fig. 5). They may, due to the induced
ocular hypertension, iris atrophy and unilaterality, mimic
a herpetic uveitis. However, there is no anterior chamber
inflammation nor keratic precipitates. Specular microscopic
analysis with an inverted appearance of the endothelial
mosaic confirms the diagnosis.
Figure 5. Differential diagnosis of anterior uveitis. Appearance of ICE syndrome, which may mimic herpetic uveitis (a); inverted appear-
ance of the endothelial mosaic confirms the diagnosis on specular microscopy (b) compared to the healthy eye (c).
Please cite this article in press as: Gueudry J, Muraine M. Anterior uveitis. J Fr Ophtalmol (2017),
https://doi.org/10.1016/j.jfo.2017.11.003
Neovascular glaucoma and unrecognized intraocular for-
eign body are also causes of masquerade syndromes.
Therapeutic strategy
The treatment of anterior uveitis has as its primary goal
the treatment of the acute inflammatory episode, which
will then be adapted if the condition becomes chronic or
if required to prevent recurrences.
In the case of non-infectious uveitis, after having elim-
inated a masquerade syndrome, especially in a child,
the cornerstone of treatment rests on steroid eye drops.
Only the inflammation associated with FHI should be
untreated. The frequency of installation must at first be
sustained and adapted according to the suspected etiol-
ogy and the clinical severity. Initially, hourly instillation
of dexamethasone drops is prescribed during the day; an
antibiotic-steroid ointment may be added at bedtime in the
acute phase, as well as mydriatic drops for pain relief and to
break posterior synechiae. After 48 hours, the frequency of
instillation is reduced progressively over several weeks.
In the case of severe or refractory inflammation, subcon-
junctival dexamethasone injections are used, typically for
3 to 5 consecutive days. Resorting to systemic steroids is
exceptional. In the case of systemic involvement associated
with anterior uveitis requiring systemic treatment, this most
often results in resolution of the anterior uveitis. A ther-
apeutic strategy for unilateral or bilateral non-infectious
anterior uveitis is proposed (Fig. 6) [52]. In the case of ocular
hypertension, prostaglandins should be avoided even though
their potential harm has not been demonstrated [53]. In the
case of posterior segment complications, notably macular
edema, peri or intraocular depot steroids may be utilized
[54]. Patients with chronic anterior uveitis not requir-
ing systemic steroids most often benefit from long-term
reduced-dose steroid drops. The side effects of long-term
topical steroid therapy must of course be kept in mind.
More recently, therapeutic advances based on several bio-
logic agents, notably anti-TNF ␣, allow better long-term
control of uveitis. Recommendations published in 2014 advo-
cate the use of infliximab or adalimumab for steroid sparing
in cases of refractory chronic uveitis associated with spondy-
loarthropathies or HLA-B27 [55]. However, anti-TNF ␣ agents
do not have market approval for the management or pre-
vention of anterior uveitis, as opposed to treatment of
refractory intermediate or posterior uveitis, for which they
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JFO-1835; No. of Pages 11 ARTICLE IN PRESS
Anterior uveitis
are already approved in Europe [56]. Their use in the set-
ting of uveitis takes place in France in collaboration with
internists, and adult or pediatric rheumatologists.
In children, uveitis, although less frequent than in adults,
is responsible for significant morbidity with potentially
blinding long-term complications, constituting a veritable
therapeutic challenge. Regarding the management of JIA
associated uveitis, systemic steroid treatment is limited due
to its side effects, notably on growth. It may be necessary for
short periods in cases of poor control of uveitis by local treat-
ment while waiting for the effect of other drugs. Regarding
local steroid therapy, it is estimated that a threshold of
steroid dependence over 3 drops per day of dexametha-
sone is detrimental. Above this dose, the risk of cataract
over a mean period of 4 years is clearly elevated [57].
Thus, it is preferable to begin systemic immunosuppres-
sive therapy, not necessarily with systemic steroid therapy.
As first-line therapy, methotrexate is used. Its efficacy in
the treatment of JIA is well known. Approximately 75% of
patients may achieve improvement in the intraocular inflam-
mation on methotrexate [58]. Anti-TNF␣ agents, infliximab
® ®
(Remicade ) and adalimumab (Humira ) have revolutionized
the management of severe pediatric uveitis [59,60]. How-
®
ever, etanercept (Enbrel ) is effective in the control of the
arthritis, without, however, appearing to be effective for
uveitis [61].
In cases of infectious uveitis, systemic treatment adapted
to the identified etiology is combined with local steroid
treatment. Multidisciplinary management is necessary in
cases of bacterial uveitis, especially since there is no defined
therapeutic protocol, particularly in the case of tuberculous
uveitis, which most often remains a presumptive diagnosis,
and because of the possible side effects of certain drugs
used. A therapeutic strategy is proposed in Table 2 [62—65].
The value of anti-TNF␣, particularly infliximab and adal-
imumab, in the prevention of HLA-B27 positive uveitis has
been demonstrated [66].
Figure 6. Therapeutic management of non-infectious anterior
uveitis adapted from LeHoang, P. The gold standard of noninfectious
uveitis: corticosteroids. Dev Ophthalmol 2012.
Please cite this article in press as: Gueudry J, Muraine M. Anterior uveitis. J Fr Ophtalmol (2017),
https://doi.org/10.1016/j.jfo.2017.11.003
9
Complications
Each episode of anterior uveitis or development of chronic
uveitis sets the stage for potentially blinding complications.
Posterior segment complications are possible, notably the
occurrence of optic disc or macular edema. The occur-
rence of chronic ocular hypertension and then secondary
glaucoma is a major complication of anterior uveitis.
Cataract, encouraged by local or systemic steroid treat-
ment, frequently complicates anterior uveitis due to the
chronicity of the inflammation and the presence of posterior
synechiae. It is most often a posterior subcapsular cataract.
Its surgical management requires certain precautions so as
to avoid rebound inflammation extremely deleterious to the
visual prognosis.
Conclusion
Anterior uveitis is the most frequent and has multiple
causes. The key step in etiologic diagnosis is the clinical
characterization of the anterior uveitis, notably its charac-
terization as granulomatous or not. Progress in molecular
biology has allowed identification of certain viruses at the
origin of uveitides, which were thought to be idiopathic.
Biologic therapies, after multidisciplinary conferences, have
greatly changed the management and prevention of certain
uveitides, notably severe HLA-B27 positive uveitis, but have
above all revolutionized the management of JIA associated
pediatric uveitis [67].
Table 2 Anti-infectious treatment in cases of diagnosed
viral or bacterial anterior uveitis.
Viral uveitis
HSV/VZV uveitis
Valacyclovir 3 g/day then progressive taper for
maintenance
CMV uveitis
Valganciclovir 900 mg 2 times per day 21 days
then 900 mg 1 time per day for maintenance
Possible trial of ganciclovir ophthalmic gel
topically
Bacterial uveitis
Tuberculosis
Triple or quadruple therapy (2 months)
Isoniazid 5 mg/kg/day
Rifampicin 10 mg/kg/day
Pyrazinamide 30 mg/kg/day
± Ethambutol 15 mg/kg/day
Then bitherapy (4 months)
Isoniazid 5 mg/kg/day
Rifampicin 10 mg/kg/day
Syphilis
Penicillin G IV for 14 to 21 days
Lyme disease
Ceftriaxone IV 2 g/day for 14 to 21 days
HSV: herpes simplex virus; VZV: varicella-zoster virus; CMV:
cytomegalovirus.
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JFO-1835; No. of Pages 11 ARTICLE IN PRESS
10
Appendix A. Supplementary data
Supplementary data associated with this article can be
found, in the online version, at http://www.sciencedirect.
com and https://doi.org/10.1016/j.jfo.2017.11.003.
Disclosure of interest
J.G.: consultant or clinical investigator or speaker for Abb-
Vie, UCB, Allergan, Théa laboratories.
M.M.: consultant or clinical investigator or speaker for Théa,
Horus, Dompé, Alcon laboratories.
References
[1] Thorne JE, Suhler E, Skup M, Tari S, Macaulay D, Chao J,
et al. Prevalence of noninfectious uveitis in the united states:
a claims-based analysis. JAMA Ophthalmol 2016;134:1237—45.
[2] Jabs DA, Nussenblatt RB, Rosenbaum JT. Standardization
of uveitis nomenclature for reporting clinical data. Results
of the First International Workshop. Am J Ophthalmol
2005;140:509—16.
[3] Bloch-Michel E, Nussenblatt RB. International Uveitis Study
Group recommendations for the evaluation of intraocular
inflammatory disease. Am J Ophthalmol 1987;103:234—5.
[4] Miserocchi E, Fogliato G, Modorati G, Bandello F. Review
on the worldwide epidemiology of uveitis. Eur J Ophthalmol
2013;23:705—17.
[5] Zierhut M, Pavesio CE, Goldstein DA. Anterior uveitis. In: Zier-
hut M, Pavesio C, Ohno S, Oréfi ce F, Rao NA, editors. Intraocular
inflammation. Springer; 2016. p. 503—16.
[6] Evans M, Sharma O, LaBree L, Smith RE, Rao NA. Differ-
ences in clinical findings between Caucasians and African
Americans with biopsy-proven sarcoidosis. Ophthalmology
2007;114:325—33.
[7] Ramsay A, Lightman S. Hypopyon uveitis. Surv Ophthalmol
2001;46:1—18.
[8] Bodaghi B, Wechsler B, Du-Boutin LT, Cassoux N, LeHoang
P, Piette JC. Uvéites chroniques sévères : classification,
démarche diagnostique et principes thérapeutiques. Rev Med
Interne 2003;24:794—802.
[9] Bodaghi B. Les uvéites virales. J Fr Ophtalmol 2004;27:528—37.
[10] Agrawal R, Gonzalez-Lopez JJ, Nobre-Cardoso J, Gupta B,
Grant R, Addison PK, et al. Predictive factors for treatment
failure in patients with presumed ocular tuberculosis in an area
of low endemic prevalence. Br J Ophthalmol 2016;100:348—55.
[11] Gineys R, Bodaghi B, Carcelain G, Cassoux N, Boutin le TH,
Amoura Z, et al. QuantiFERON-TB gold cut-off value: impli-
cations for the management of tuberculosis-related ocular
inflammation. Am J Ophthalmol 2011;152:433—40 [e1].
[12] Zeboulon N, Dougados M, Gossec L. Prevalence and charac-
teristics of uveitis in the spondyloarthropathies: a systematic
literature review. Ann Rheum Dis 2008;67:955—9.
[13] Juanola X, Loza Santamaria E, Cordero-Coma M. Description
and prevalence of spondyloarthritis in patients with anterior
uveitis: the SENTINEL Interdisciplinary Collaborative Project.
Ophthalmology 2016;123:1632—6.
[14] Monnet D, Breban M, Hudry C, Dougados M, Brezin AP. Oph-
thalmic findings and frequency of extraocular manifestations
in patients with HLA-B27 uveitis: a study of 175 cases. Oph-
thalmology 2004;111:802—9.
[15] Pathanapitoon K, Dodds EM, Cunningham Jr ET, Rothova A. Clin-
ical spectrum of HLA-B27-associated ocular inflammation. Ocul
Immunol Inflamm 2017;25:569—76.
Please cite this article in press as: Gueudry J, Muraine M. Anterior uveitis. J Fr Ophtalmol (2017),
https://doi.org/10.1016/j.jfo.2017.11.003
J. Gueudry, M. Muraine
[16] Verhagen FH, Brouwer AH, Kuiper JJ, Ossewaarde-van Norel J,
Ten Dam-van Loon NH, de Boer JH. Potential predictors of poor
visual outcome in human leukocyte antigen-B27-associated
uveitis. Am J Ophthalmol 2016;165:179—87.
[17] Bloch-Michel E, Dussaix E, Cerqueti P, Patarin D. Possi-
ble role of cytomegalovirus infection in the etiology of
the Posner—Schlossmann syndrome. Int Ophthalmol 1987;11:
95—6.
[18] Markomichelakis NN, Canakis C, Zafirakis P, Marakis T, Mallias I,
Theodossiadis G. Cytomegalovirus as a cause of anterior uveitis
with sectoral iris atrophy. Ophthalmology 2002;109:879—82.
[19] Chee SP, Bacsal K, Jap A, Se-Thoe SY, Cheng CL, Tan BH. Clinical
features of cytomegalovirus anterior uveitis in immunocompe-
tent patients. Am J Ophthalmol 2008;145:834—40.
[20] de Schryver I, Rozenberg F, Cassoux N, Michelson S, Keste-
lyn P, Lehoang P, et al. Diagnosis and treatment of
cytomegalovirus iridocyclitis without retinal necrosis. Br J Oph-
thalmol 2006;90:852—5.
[21] van Boxtel LA, van der Lelij A, van der Meer J, Los LI.
Cytomegalovirus as a cause of anterior uveitis in immunocom-
petent patients. Ophthalmology 2007;114:1358—62.
[22] Koizumi N, Suzuki T, Uno T, Chihara H, Shiraishi A, Hara Y, et al.
Cytomegalovirus as an etiologic factor in corneal endotheliitis.
Ophthalmology 2008;115:292—7 [e3].
[23] Chee SP, Jap A. Presumed fuchs heterochromic iridocyclitis and
Posner—Schlossman syndrome: comparison of cytomegalovirus-
positive and negative eyes. Am J Ophthalmol 2008;146:883—9
[e1].
[24] Jap A, Sivakumar M, Chee SP. Is Posner—Schlossman syndrome
benign? Ophthalmology 2001;108:913—8.
[25] Su CC, Hu FR, Wang TH, Huang JY, Yeh PT, Lin CP, et al. Clinical
outcomes in cytomegalovirus-positive Posner—Schlossman syn-
drome patients treated with topical ganciclovir therapy. Am J
Ophthalmol 2014;158:1024—31 [e2].
[26] Wong JX, Agrawal R, Wong EP, Teoh SC. Efficacy and safety
of topical ganciclovir in the management of cytomegalovirus
(CMV)-related anterior uveitis. J Ophthalmic Inflamm Infect
2016;6:10.
[27] Fearnley IR, Rosenthal AR. Fuchs’ heterochromic iridocyclitis
revisited. Acta Ophthalmol Scand 1995;73:166—70.
[28] Bloch-Michel E, Frau E, Chhor S, Tounsi Y. Amsler’s sign associ-
ated significantly with Fuch’s heterochromic cyclitis (FHC). Int
Ophthalmol 1995;19:169—71.
[29] Rothova A, La Hey E, Baarsma GS, Breebaart AC. Iris nod-
ules in Fuchs’ heterochromic uveitis. Am J Ophthalmol
1994;118:338—42.
[30] Mohamed Q, Zamir E. Update on Fuchs’ uveitis syndrome. Curr
Opin Ophthalmol 2005;16:356—63.
[31] Tejwani S, Murthy S, Sangwan VS. Cataract extraction outcomes
in patients with Fuchs’ heterochromic cyclitis. J Cataract
Refract Surg 2006;32:1678—82.
[32] Javadi MA, Jafarinasab MR, Araghi AA, Mohammadpour M,
Yazdani S. Outcomes of phacoemulsification and in-the-bag
intraocular lens implantation in Fuchs’ heterochromic iridocy-
clitis. J Cataract Refract Surg 2005;31:997—1001.
[33] Quentin CD, Reiber H. Fuchs heterochromic cyclitis: rubella
virus antibodies and genome in aqueous humor. Am J Ophthal-
mol 2004;138:46—54.
[34] Suzuki J, Goto H, Komase K, Abo H, Fujii K, Otsuki N, et al.
Rubella virus as a possible etiological agent of Fuchs het-
erochromic iridocyclitis. Graefes Arch Clin Exp Ophthalmol
2010;248:1487—91.
[35] de Visser L, Braakenburg A, Rothova A, de Boer JH. Rubella
virus-associated uveitis: clinical manifestations and visual
prognosis. Am J Ophthalmol 2008;146:292—7.
[36] Birnbaum AD, Tessler HH, Schultz KL, Farber MD, Gao W, Lin P,
et al. Epidemiologic relationship between fuchs heterochromic
+Model
JFO-1835; No. of Pages 11 ARTICLE IN PRESS
Anterior uveitis
iridocyclitis and the United States rubella vaccination program.
Am J Ophthalmol 2007;144:424—8.
[37] Jad A, Celine T, Bahram B, Phuc L, Nathalie C. Fuchs’ het-
erochromic cyclitis: a post-infectious manifestation of ocular
toxoplasmosis? Int Ophthalmol 2013;33:189—94.
[38] Jamilloux Y, Kodjikian L, Broussolle C, Seve P. Sarcoidosis and
uveitis. Autoimmun Rev 2014;13:840—9.
[39] Herbort CP, Rao NA, Mochizuki M. International criteria for the
diagnosis of ocular sarcoidosis: results of the first International
Workshop On Ocular Sarcoidosis (IWOS). Ocul Immunol Inflamm
2009;17:160—9.
[40] Olsen TG, Frederiksen J. The association between multiple
sclerosis and uveitis. Surv Ophthalmol 2017;62:89—95.
[41] Lim JI, Tessler HH, Goodwin JA. Anterior granulomatous
uveitis in patients with multiple sclerosis. Ophthalmology
1991;98:142—5.
[42] Guedj M, Queant A, Funck-Brentano E, Kramkimel N, Lellouch
J, Monnet D, et al. Uveitis in patients with late-stage cuta-
neous melanoma treated with vemurafenib. JAMA Ophthalmol
2014;132:1421—5.
[43] Rousseau A, Labetoulle M. Ocular manifestations of Ebola virus
disease: what we learned from the last epidemic. J Fr Ophtal-
mol 2015;38:758—63.
[44] Lim LL, Fraunfelder FW, Rosenbaum JT. Do tumor necrosis fac-
tor inhibitors cause uveitis? A registry-based study. Arthritis
Rheum 2007;56:3248—52.
[45] Byles DB, Frith P, Salmon JF. Anterior uveitis as a side effect of
topical brimonidine. Am J Ophthalmol 2000;130:287—91.
[46] Duncombe A, Gueudry J, Massy N, Chapuzet C, Gueit I, Muraine
M. Pseudo-uvéite sévère associée à l’utilisation de moxi-
floxacine. J Fr Ophtalmol 2013;36:146—50.
[47] Bodaghi B, Terrada C, Lehoang P, Quartier P, Kone-Paut I. Diag-
nostic des uvéites pédiatriques. Arch Pediatr 2009;16:524—5.
[48] Levy-Clarke GA, Nussenblatt RB, Smith JA. Manage-
ment of chronic pediatric uveitis. Curr Opin Ophthalmol
2005;16:281—8.
[49] Labalette P. Refractory anterior uveitis. J Fr Ophtalmol
2011;34:122—6.
[50] Yi DH, Rashid S, Cibas ES, Arrigg PG, Dana MR. Acute uni-
lateral leukemic hypopyon in an adult with relapsing acute
lymphoblastic leukemia. Am J Ophthalmol 2005;139:719—21.
[51] Terelak-Borys B, Skonieczna K, Grabska-Liberek I. Ocular
ischemic syndrome — a systematic review. Med Sci Monit
2012;18:RA138—44.
[52] LeHoang P. The gold standard of noninfectious uveitis: corti-
costeroids. Dev Ophthalmol 2012;51:7—28.
[53] Chang JH, McCluskey P, Missotten T, Ferrante P, Jalaludin
B, Lightman S. Use of ocular hypotensive prostaglandin ana-
logues in patients with uveitis: does their use increase
anterior uveitis and cystoid macular oedema? Br J Ophthalmol
2008;92:916—21.
[54] Thach AB, Dugel PU, Flindall RJ, Sipperley JO, Sneed SR. A
comparison of retrobulbar versus sub-Tenon’s corticosteroid
therapy for cystoid macular edema refractory to topical med-
ications. Ophthalmology 1997;104:2003—8.
[55] Levy-Clarke G, Jabs DA, Read RW, Rosenbaum JT, Vitale
A, Van Gelder RN. Expert panel recommendations for the
use of anti-tumor necrosis factor biologic agents in patients
Please cite this article in press as: Gueudry J, Muraine M. Anterior uveitis. J Fr Ophtalmol (2017),
https://doi.org/10.1016/j.jfo.2017.11.003
11
with ocular inflammatory disorders. Ophthalmology 2014;
121:785—96 [e3].
[56] Jaffe GJ, Dick AD, Brezin AP, Nguyen QD, Thorne JE, Kestelyn P,
et al. Adalimumab in patients with active noninfectious uveitis.
N Engl J Med 2016;375:932—43.
[57] Thorne JE, Woreta FA, Dunn JP, Jabs DA. Risk of cataract
development among children with juvenile idiopathic arthritis-
related uveitis treated with topical corticosteroids. Ophthal-
mology 2010;117:1436—41.
[58] Simonini G, Paudyal P, Jones GT, Cimaz R, Macfarlane GJ. Cur-
rent evidence of methotrexate efficacy in childhood chronic
uveitis: a systematic review and meta-analysis approach.
Rheumatology (Oxford) 2013;52:825—31.
[59] Foeldvari I, Nielsen S, Kummerle-Deschner J, Espada G, Horneff
G, Bica B, et al. Tumor necrosis factor-alpha blocker in
treatment of juvenile idiopathic arthritis-associated uveitis
refractory to second-line agents: results of a multinational
survey. J Rheumatol 2007;34:1146—50.
[60] Saurenmann RK, Levin AV, Rose JB, Parker S, Rabinovitch T,
Tyrrell PN, et al. Tumour necrosis factor alpha inhibitors in
the treatment of childhood uveitis. Rheumatology (Oxford)
2006;45:982—9.
[61] Schmeling H, Horneff G. Etanercept and uveitis in patients
with juvenile idiopathic arthritis. Rheumatology (Oxford)
2005;44:1008—11.
[62] Gaudio PA. Update on ocular syphilis. Curr Opin Ophthalmol
2006;17:562—6.
[63] Mikkila HO, Seppala IJ, Viljanen MK, Peltomaa MP, Karma A.
The expanding clinical spectrum of ocular lyme borreliosis.
Ophthalmology 2000;107:581—7.
[64] Ang M, Chee SP. Controversies in ocular tuberculosis. Br J Oph-
thalmol 2017;101:6—9.
[65] Sobolewska B, Deuter C, Doycheva D, Zierhut M. Long-
term oral therapy with valganciclovir in patients with
Posner—Schlossman syndrome. Graefes Arch Clin Exp Ophthal-
mol 2014;252:117—24.
[66] Gueudry J, Thorne JE, Bansie R, Braun J, van Hagen PM,
Bodaghi B. Biologic therapy for HLA-B27-associated ocular dis-
orders. Ocul Immunol Inflamm 2016:1—10.
[67] Gueudry J. Uvéites antérieures. EMC - Ophtalmol 2017:1—13
[Article 21-220-A-40].
Further reading
See this article, unabridged, illustrated and detailed, with
electronic enhancements, in EMC-Ophtalmologie: Gueudry
J. Uvéites antérieures. EMC - Ophtalmologie 2017:1-13
[Article 21-220-A-40].
Labetoulle M, Rousseau A, Bourcier T. Atteintes herpétiques du
segment antérieur de l’œil : aspects épidémiologiques, cliniques
et diagnostiques. EMC—Ophtalmologie 2014;11(1):1—10 [Article 21-
200-D-20].
Labetoulle M, Rousseau A, Bourcier T. Atteintes herpé-
tiques du segment antérieur de l’œil : aspects thérapeutiques.
EMC—Ophtalmologie 2014;11(1):1—8 [Article 21-200-D-21].