Download Corticosteroid-induced ocular hypertension and glaucoma: a brief

Corticosteroid-induced ocular hypertension and glaucoma: a brief
review and update of the literature
Relief Jones III and Douglas J. Rhee
Purpose of review
The purpose of this article is to briefly review the literature
of corticosteroid-induced ocular hypertension and
glaucoma, its risk factors, the pathophysiology, and
treatment options. In particular, literature pertaining to
glaucoma in response to intravitreal triamcinolone
acetonide will be reviewed.
Recent findings
Primary open-angle glaucoma, status as a glaucoma
suspect, and a family history of glaucoma are risk factors
for an ocular hypertensive response with the use of
corticosteroid therapy. Recent studies suggest that
younger age may also be a risk factor in patients treated
via the intravitreal route with corticosteroids. The
mechanism of elevated intraocular pressure is increased
aqueous outflow resistance owing to an accumulation of
extracellular matrix material in the trabecular meshwork.
Summary
Corticosteroid-induced ocular hypertension and glaucoma
has been recognized for more than 50 years. Knowing the
risk factors, prevalence, and pathophysiology can help the
clinician prevent, monitor, and treat corticosteroid-induced
ocular hypertension and glaucoma.
Keywords
intravitreal triamcinolone, ocular hypertension, review,
steroid-induced glaucoma
Curr Opin Ophthalmol 17:163–167. # 2006 Lippincott Williams & Wilkins.
Harvard Medical School, Department of Ophthalmology, Massachusetts Eye and
Ear Infirmary, Glaucoma Service, Boston, Massachusetts, USA
Correspondence to: Douglas J. Rhee MD, Assistant Professor of Ophthalmology,
Harvard Medical School, Department of Ophthalmology, Massachusetts Eye and
Ear Infirmary, Glaucoma Service, 243 Charles Street, Boston, MA 02114, USA
Tel.: +617 573 3670, Fax: +617 573 3707; e-mail: [email protected]
Current Opinion in Ophthalmology 2006, 17:163–167
Abbreviations
ECM
IOP
IVTA
POAG
extracellular matrix
intraocular pressure
intravitreal triamcinolone acetonide
primary open-angle glaucoma
# 2006 Lippincott Williams & Wilkins
1040-8738
Introduction
Increased intraocular pressure (IOP) can occur as a consequence of oral, intravenous, inhaled, topical, periocular, or intravitreal corticosteroid therapy [1–6,7•,8••,
9–11]. If the ocular hypertension is of a significant magnitude, not recognized, and not treated, subsequent
glaucomatous optic neuropathy can develop (that is,
steroid-induced glaucoma). Steroid-induced ocular
hypertension was first reported in 1950 when McLean
[12] reported an increase in IOP associated with the systemic administration of adrenocorticotrophic hormone
(ACTH). The first report of increased IOP caused by
the local administration of cortisone occurred four years
later [13]. Since those initial reports, corticosteroidinduced glaucoma has been studied intensively. A number of predisposing risk factors have been identified
[14–23,24••]. The intraocular potency and mode of
administration have been shown to be important in initiating an ocular hypertensive response [1–6,7•,8••,9,25].
Recently, the popular use of intravitreal triamcinolone
acetonide (IVTA) for subretinal fluid, macular edema,
and adjunctive therapy in the treatment of choroidal
neovascularization has led to an increased incidence of
corticosteroid-induced ocular hypertension from IVTA
[7•,8••,9,26–28,29•]. The molecular biological factors
contributing to increased IOP are beginning to be better
understood and these findings may lead to additional
management options in the future [30–41]. We will
review selected studies with an emphasis on glaucoma
elevations associated with IVTA.
Predisposing risk factors
for corticosteroid-induced glaucoma
When treated with topical steroids for 4–6 weeks, 5% of
the population demonstrates a rise in IOP greater
than 16 mmHg and 30% have a rise of 6–15 mmHg
[10,11]. Several variables have been identified as predisposing risk factors for steroid-induced ocular hypertension. Patients with predisposing risk factors should be
followed more diligently when receiving corticosteroids.
Primary open-angle glaucoma (POAG) patients and
glaucoma suspects were shown to be at an increased
risk for elevated IOP after treatment with corticosteroids. Studies by Armaly [14,15] revealed that approximately one-third of glaucoma suspects and more than
90% of POAG patients responded with an IOP elevation
greater than 6 mmHg after receiving a 4-week course of
163
164 Glaucoma
topical dexamethasone 0.1%. The effect was noted to be
more prominent in the eyes of older adult patients compared with the eyes of younger adult patients. A study
by Becker and Mills [16] also indicated that patients
with pre-existing glaucoma and glaucoma suspects
demonstrated large, highly significant increases in IOP
in 2–4 weeks with the use of topical betamethasone
0.1% and exhibited decreased outflow facility during
the treatment period. The IOP returned to baseline or
normal in approximately 1 week with discontinuation of
steroid treatment. Moreover, other studies showed that
simply having a first-degree relative with POAG could
make one susceptible to being a steroid-responder [18,
19].
Although older patients are at increased risk, the frequency of steroid responsiveness with age may occur
in a bimodal distribution. Children as a group have
been shown to be greater steroid-responders as compared with adults. A recent study by Lam et al. [24••]
showed that 71.2 and 59.2% of children receiving topical
dexamethasone 0.1% (four times per day and two times
per day, respectively) responded with an IOP rise
greater than 21 mmHg. Additionally, 36.4 and 21.1% of
those same two groups had an IOP rise greater than 30
mmHg. Among children under 6 years old who received
dexamethasone 0.1% four times per day, the peak IOP
was greater, the net increase in IOP was greater, and the
time required to obtain the peak IOP was less. Children
greater than 6 years old (children up to age 10 were
included in the study) had a similar net increase in
IOP, but did not show a significant difference in peak
IOP or the time required to reach the peak IOP.
Gatson et al. [20] showed that patients with connectivetissue disease tend to be steroid-responders. Men with
connective-tissue disease tended to be greater responders, although gender is not typically considered a risk
factor in people without connective-tissue disease. Additionally, patients with type-1 diabetes mellitus [20] and
high myopia [22] have also been shown to be at
increased risk to be steroid-responders.
In summary, pre-existing POAG, status as a glaucoma
suspect, or a first-degree relative with POAG are important risk factors for corticosteroid-induced ocular hypertension and glaucoma. Age may be a risk factor;
increased risk appears to occur in a bimodal distribution
peaking first at age 6. As one progresses through adulthood age may not be a factor until late adulthood when
the risk again rises. Finally, those with connective-tissue
disease, type-1 diabetes mellitus, and high myopia
should all be considered high risk, and prudent followup should be pursued during periods of corticosteroid
use.
Types of preparations and modes
of administration
Corticosteroids have been shown to exert an ocular
hypertensive response relative to the intraocular potency
of the steroid [25]. Aside from the relative ability to inhibit inflammation, the other main determinant of
intraocular potency is chemical structure. Acetates are
more lipophilic and penetrate through the cornea better
than phosphates, which are relatively hydrophilic.
Medrysone 1.0% caused a 1.0 mmHg rise in IOP,
while more potent steroids such as prednisolone acetate
1.0% and dexamethasone acetate 0.1% caused a 10 and
22 mmHg rise in IOP, respectively.
Corticosteroids have been shown to cause a elevation in
IOP through all modes of administration [1–6,7•,8••,9].
The rise of IOP usually occurs over a period of weeks if
used topically [15,16,25] and years if used systemically
[1]. There have been some reports of an elevation of
IOP within hours of initiating intensive topical steroid
use [42].
The mode of therapy becomes important when considering corticosteroid use in individuals with pre-existing
risk factors for an ocular hypertensive response. Some
modes of therapy can be discontinued easily, thereby
reducing or reversing any untoward effects on IOP.
Other modes of therapy, however, such as subtenon’s,
periocular, or intravitreal injections, are not as easily
reversed if problems are encountered.
Corticosteroid-induced ocular hypertension
associated with triamcinolone acetonide
IVTA has become a useful therapy for many conditions
including uveitis, veno-occlusive disease, diabetes, and
choroidal neovascularization. When given intravenously,
triamcinolone acetonide is 35 times more potent as an
anti-inflammatory agent than cortisol. As the list of indications and use of IVTA increases, the incidence of corticosteroid-induced glaucoma associated with IVTA will
be more common and more likely to be encountered by
ophthalmologists. In a recent meta-analysis, Jonas found
that intravitreal dosages of approximately 20 mg (the
dose more commonly used in Europe) are associated
with a 41% prevalence of an IOP elevation greater
than 21 mmHg [29•]. All but one patient was managed
with topical glaucoma medications and medications
were no longer needed about 6 months after the injection. The one patient that required surgery underwent
trabeculectomy 9 months after injection and fluid aspirations obtained during surgery contained soluble triamcinolone [43]. It was concluded that IVTA may last 9
months or longer and this fact should be considered
prior to repeating the injection.
Ocular hypertension and glaucoma Jones and Rhee
Another study, by Smithen and colleagues [7•], of 89
patients with a mean baseline IOP of 14.9 mmHg analyzed the prevalence of IOP elevation following IVTA
injection. All patients had received a 4 mg (the dosage
more commonly used in the United States) of IVTA and
were followed for 6 months. The mean pressure increase
was 8.0 mmHg and 40.4% experienced a pressure elevation of 24 mmHg or higher; the pressure elevation
occurred at a mean of 100.6 days. Patients were also
stratified into the categories of ‘no history of glaucoma’
and ‘glaucoma patient’. The patients in these two categories were subsequently divided into two additional
categories based on their baseline IOP. Patients without
a history of glaucoma and a baseline IOP of at least 15
mmHg had a 60% chance of developing a pressure of at
least 24 mmHg, whereas those with a baseline IOP less
than 15 mmHg had a 22.7% chance of developing an
IOP of at least 24 mmHg. Patients with a history of glaucoma had a 50% chance of developing an IOP of at
least 24 mmHg. Of these patients, 50% had a baseline
IOP of at least 15 mmHg. In this series, patients who
received multiple IVTA injections did not experience
an increased incidence of elevated IOP, and there was
no correlation between IOP elevation and the disease
process being treated by the injection. All patients who
experienced an IOP elevation had their pressure controlled with a mean of one glaucoma medication. Individuals who were already taking one glaucoma medication
required an average of one additional medication. No
patients in this study required surgical intervention to
control their elevated IOP.
Singh and colleagues [8••] reported a case series of early
and rapid increases in IOP following an IVTA injection
in three individuals. In all three cases, a significant rise
in IOP occurred within 1 week of IVTA for macular
edema. All of the individuals required subsequent surgical intervention to control the elevated IOP. A peculiar
finding was the presence of a white material in the angle
of one individual on gonioscopy, probably from the
injection. A common finding was that all three of these
patients were pseudophakic, which may have allowed
the medication to move into the anterior segment causing physical obstruction of the trabecular meshwork. To
prevent these complications, Vedantham [44] suggested
that pseudophakic patients and those with prior vitrectomies be followed with greater scrutiny. In addition, he
suggested that filtering the triamcinolone and instructing patients to sleep on their backs might prevent this
complication.
Most patients with elevated IOP after IVTA are successfully managed with topical glaucoma medications.
Traditional glaucoma surgical techniques can successfully control elevated IOP and are generally required
165
in less than 2% of cases. Filtration surgery is not the
only option. One group reported vitrectomy with
removal of the intraocular triamcinolone acetonide
from the vitreous cavity to treat the elevated IOP [45].
This procedure alone was capable of controlling the ocular hypertension and could also be considered as an
alternative if traditional glaucoma treatments are not
an option or fail to control the IOP.
IVTA appears to be increasingly popular to treat those
with visual loss from macular edema; thus the prevalence of its associated corticosteroid-induced ocular
hypertension will continue to rise. Clinicians should be
aware that an elevated IOP may occur in nearly half of
all cases following a single injection of IVTA. After an
injection, they should be followed with greater scrutiny.
Postinjection examinations should occur 1 day later and
approximately 1 week later for high-risk patients. Regular follow-up examinations should continue for greater
than 6 months. Weinreb et al. [42] showed that, rarely,
some patients with a prior history of glaucoma could
develop elevated IOP in a matter of hours following
topical administration. Examinations should include
monitoring of the IOP and gonioscopy for pseudophakes
and patients with prior vitrectomies to detect mechanical obstruction of the trabecular meshwork by the medication. If the IOP cannot be managed with the addition
of glaucoma medications, subspecialty care from a glaucoma specialist should be sought as some patients may
go on to require surgical intervention.
The pathophysiology of corticosteroid-induced
ocular hypertension and glaucoma
The mechanism of corticosteroid-induced ocular hypertension is increased aqueous outflow resistance. There
are a number of observations that can be simplified into
three broad categories: corticosteroids can induce physical and mechanical changes in the microstructure of the
trabecular meshwork; cause an increase in the deposition of substances in the trabecular meshwork, thereby
causing decreased outflow facility; and inhibit proteases
and trabecular meshwork endothelial cell phagocytosis
causing a decrease in the breakdown of substances in
the trabecular meshwork.
Changes in the microstructure of the trabecular meshwork may cause a decrease in outflow facility and an
increase in IOP. Clark and colleagues [30] showed that
the actin stress fibers were reorganized into actin networks that resembled geodesic-dome-like polygonal lattices in human trabecular meshwork cells cultured in the
presence of dexamethasone. Upon discontinuing dexamethasone, cross-linking of the actin networks was
reversible. The effect was thought to be mediated via
trabecular meshwork glucocorticoid receptors. In perfu-
166 Glaucoma
sion-cultured human eyes, Clark and colleagues [31]
found that steroid treatment had similar microstructural
changes and was associated with an increased outflow
resistance. The accumulated extracellular matrix
(ECM) has the potential to affect both the paracellular
(that is, the flow in-between trabecular meshwork
endothelial cells) and transcellular (that is, the flow
through pores created within a single and or between
two inner wall Schlemm’s canal cells) levels.
Corticosteroids also increase the deposition of ECM in
the trabecular meshwork leading to decreased outflow
facility. A study by Wilson et al. [32] found an increased
deposition of ECM material altering the ultrastructure
of the juxtacanalicular region. The corticosteroid dexamethasone increases glycosaminoglycan, elastin, and
fibronectin production in cultured trabecular meshwork;
the glycosaminoglycan deposition increases further with
prolonged steroid exposure [33,34]. Myocilin is a 55 kDa
protein that has also been shown to be induced in cultured human trabecular meshwork cells after exposure
to dexamethasone for 2–3 weeks [35]. Mutations in
myocilin have been shown to be associated with juvenile-onset and adult-onset POAG [36]. Controversy
exists as to if myocilin causes an increase or a decrease
in outflow facility. In studies of perfused human trabecular meshwork cell cultures, recombinant myocilin
decreased outflow facility, while studies of viralmediated transfer of myocilin in trabecular meshwork
cells caused an overexpression of myocilin and increased
outflow facility [37].
Finally, decreased outflow facility may be caused by
reduced degradation of substances in the trabecular
meshwork. Levels of tissue plasminogen activator, stromelysin [34], and metalloproteases [38,39] have been
shown to decrease in trabecular meshwork cultures treated with dexamethasone. Furthermore, dexamethasone
treatment inhibits trabecular meshwork cell arachadonic
acid metabolism [40] and reduces the phagocytic properties of the cells [38,41]. Because these cells function to
remove debris deposited in the meshwork, reduced
functional activity may lead to reduced outflow facility.
Conclusion
Corticosteroid-induced ocular hypertension and glaucoma
has been recognized for more than 50 years. A number of
risk factors have been identified for the development of
corticosteroid-induced ocular hypertension and glaucoma,
including a personal or family history of glaucoma, young
children, older adults, type-1 diabetes mellitus, connective-tissue disease, and high myopia. The intraocular
potency and mode of administration are also important
risk factors. Increasing use of IVTA will probably lead
to a greater probability that ophthalmologists will encoun-
ter steroid-induced ocular hypertension and glaucoma.
Research into the underlying mechanisms of this pathophysiological process has improved our understanding of
the phenomenon and may lead to more efficacious treatment options in the future.
References and recommended reading
.
Papers of particular interest, published within the annual period of review, have
been highlighted as:
• of special interest
•• of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (pp. 213–214).
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