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ORAL MIFEPRISTONE FOR CHRONICCENTRAL SEROUS
CHORIORETINOPATHYJARED S. NIELSEN, MD,* LEE M. JAMPOL, MD*
Background: Chronic central serous chorioretinopathy (CCSC) can result in permanent
loss of vision. Unfortunately, many cases of CCSC are not eligible or do not respond to
treatment with thermal laser or photodynamic therapy. Glucocorticoids have been
implicated in the pathogenesis of central serous chorioretinopathy. Mifepristone, an oral
glucocorticoid receptor antagonist, may be helpful in cases of CCSC.
Methods: Mifepristone 200 mg was administered orally to 16 CCSC subjects in
2 separate protocols for up to 12 weeks. Visual acuity, examination, angiography, optical
coherence tomography, and liver function were monitored during the treatment period.
Results: Favorable response to oral mifepristone was seen in CCSC patients with seven
subjects gaining five or more letters of vision and seven subjects having improved opticalcoherence tomography findings. Treatment was well tolerated without serious adverse
effects.
Conclusion: Systemic glucocorticoid receptor antagonism with daily oral mifepristone
does have a beneficial effect in treating some cases of CCSC. Further study is warranted.
RETINA 31:19281936, 2011
Central serous chorioretinopathy (CSC) is typically
a self-limited condition with favorable clinical
outcomes. A minority of cases progress to chronic
central serous chorioretinopathy (CCSC) an often
recurrent, progressive, and persistent variant that canaffect both eyes and results in permanent vision lossfrom retinal thinning with retinal pigment epithelium
(RPE) atrophy.1 Classic CSC is manifest as focal RPE
leakage, often with a pigment epithelial detachment
and accumulation of subretinal fluid. Chronic cases
usually demonstrate diffuse leakage, intraretinal cystic
changes, with extensive RPE and retinal atrophy, and
may show no or very little subretinal fluid. Choroidal
hyperpermeablity on indocyanine green (ICG) angi-
ography2 and thickened choroid best seen on enhanced
depth imaging spectral domain optical coherence
tomography (EDI-sdOCT)3 are typical CSC findings.
The precise mechanism underlying the development
of CSC remains unknown. Primary dysfunction in
CSC may reside in the choroid. Hyperpermeable
choriocapillaris drives leakage through compromised
RPE, leading to secondary retinal changes over time.
Glucocorticoids (GCs) have been implicated in the
pathogenesis of CSC,
46
and it is reasonable to surmisethat anti-GC therapy may be helpful in its treatment.4
Mifepristone (Mifeprex; Danco Laboratories, New
York, NY), more popularly known as RU-486, is an
orally bioavailable, high-affinity, GC receptor antag-
onist.7,8 It is also a potent antiprogesterone agent and is
Food and Drug Administration approved for use as an
abortifacient when coadministered with a prostaglan-
din agent. Mifepristone binds cytosolic GC receptors,
preventing coactivator recruitment rendering the
receptor complex inactive, thus preventing gene
transcription.7 Long-term oral mifepristone has
been investigated for several disorders including
meningioma, depression, Cushing disease, uterine
leiomyomata, endometriosis, diabetes, and obesity.7,8
Long-term treatment with mifepristone is generally
well tolerated and has a typically benign side effect
profile including skin rash, nausea, dizziness, fatigue,
reversible liver transaminase elevation, and endome-
trial hyperplasia.7,8 Presently, the cornerstone of
treatment for recurrent or persistent CSC is verteporfin
(Visudyne; QLT Inc., Vancouver, British Columbia,
Canada) photodynamic therapy (PDT). Laser activa-
tion of verteporfin after infusion generates local
From the *Department of Ophthalmology, Feinberg School ofMedicine, Northwestern University, Chicago, Illinois; and WolfeEye Clinic, West Des Moines, Iowa.
Supported in part by grants from The Macula Foundation, NewYork, NY, and Research to Prevent Blindness Inc., New York, NY.
The authors report no conflicts of interest.Reprint requests: Jared S. Nielsen, MD, Wolfe Eye Clinic, 6200
Westown Parkway, West Des Moines, IA 50266; e-mail: [email protected]
1928
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reactive oxygen species decreasing choroidal perfu-
sion at the target site. Photodynamic therapy may be
associated with rare but sight threatening adverse
effects including choriocapillaris ischemia and RPE
atrophy.9 Many strategies have been used to prevent
PDT-induced injury including reducing verteporfin
dose, reducing laser duration or fluence, and alteringthe timing of infusion and laser delivery.9,10 Successful
treatment rates reported in the literature range
greatly.10 Unfortunately, some patients with CCSC
are not eligible for or do not respond to PDT. We have
investigated whether mifepristone may be helpful in
cases of CCSC.
Material and Methods
Patients with CCSC were enrolled in 2 separate
institutional review boardapproved treatment proto-cols evaluating oral mifepristone 200 mg daily for up
to 12 weeks. The first protocol was a double-masked,
randomized, controlled trial comparing mifepristone
with placebo. The second protocol was an open-label
trial of daily oral mifepristone. For both studies,
eligible patients were required to have active CSC in
one or both eyes of more than 6-month duration, not
amenable or responsive to treatment by thermal laser
photocoagulation or PDT. Individuals who were
pregnant; had irregular vaginal bleeding, hypothy-
roidism, anemia, liver disease, renal disease, choroidal
neovascularization; or were less than 60 days out fromtreatment with either laser or PDT were excluded from
participation.
The two studies differed in design. The first protocol
was a small, randomized, masked, placebo-controlled
trial. Study subjects exited Protocol 1 before 12 weeks
if they did not improve at the regular 4-week
evaluation periods. The second protocol was an
open-label treatment trial and designed to have
patients exit the study only if adverse events were
encountered.
Visual acuity was assessed in both trials at
enrollment and at 4-week intervals. Snellen visual
acuity was used in Protocol 1, whereas best-corrected
Early Treatment Diabetic Retinopathy Study testing
was performed in Protocol 2. Complete ophthalmic
examination, fluorescein angiography, and optical
coherence tomography (OCT) were performed before
enrollment for all patients and repeated every 4 weeks
over the course of treatment. Indocyanine green
angiography was performed at enrollment and on
conclusion of the trial. A serum hepatic panel was
obtained for all subjects at enrollment and was
rechecked after 4 weeks of treatment and on conclusion
of the protocol or more frequently if any abnormality
was encountered. Pregnancy was ruled out by serum
beta HCG in female subjects who were also required to
use two forms of contraception throughout the protocol.
Results
Protocol 1
Eight male subjects with CCSC were enrolled in this
randomized placebo-controlled trial from January 2004
to February 2006. With 4 taking mifepristone 200 mg
daily for up to 12 weeks and 4 taking placebo. Char-
acteristics of all patients are summarized in Table 1. The
mean age was 51.4 with an average duration of 6.8 years
of CSC (2.514 years). Three had a known history of
exogenous steroids, and four were affected bilaterally.
Three subjects had previously been treated with focal
laser, and one had previously received PDT. Vision for allsubjects ranged widely from 20/20+ counting fingers 1 ft
to 2 ft in affected eyes. Initial vision in mifepristone
subjects was worse than the placebo group. Four subjects,
1 taking mifepristone and 3 taking placebo exited the
study before 12 weeks because of no improvement.
Vision changes are summarized in Table 1. Visual acuity
improved by one line in three eyes of three patients taking
mifepristone and in one eye of one patient on placebo.
Two subjects taking mifepristone demonstrated an
improvement in OCT findings, whereas one placebo
patient had some improvement in OCT findings.
Protocol 2
Thirteen white patients, 3 women and 10 men, with
CCSC were enrolled and completed a 12-week
protocol of oral mifepristone 200 mg daily between
October 2007 and January 2011. The clinical
characteristics for all patients are summarized in
Table 2. The mean age for patients was 57.5 years
(range 2081 years). Duration of CSC averaged
6.2 years (215 years). Four patients reported a known
history of corticosteroid use, three patients had been
previously treated with thermal laser, another six with
previous PDT. Four subjects had been treated with
bevacizumab. Pretreatment vision in affected eyes
ranged from 20/16+ counting fingers 3 ft to 3 ft.
Pretreatment best-corrected visual acuity is reported
for all patients in Table 3. Hepatic panel revealed
normal liver transaminase levels in all patients.
Clinical responses are summarized in Table 3. Six
subjects reported some subjective improvement in one
or both eyes at the end of treatment. Six patients were
found to have a five-letter or equivalent improvement
in visual acuity in one or both eyes. Six of the 13
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Table 1. Protocol 1 Patient Characteristics and Response to Treatment
Age (Years) Arm PMH
CSCDuration(Years)
PreviousLaser
PreviousPDT
PreviousSteroids
AffectedEye
VisualAcuity Start
ODOS
50 Placebo Gilbert syndrome 14 2 2 2 OU 20/25 + 3 220/20 + 1 2
37 4 2 2 2 OS 20/16 220/32 + 3 2
43 4 2 2 2 OS 20/20 2
20/32 + 2 240 3 2 2 + OD 20/40 + 1 2
20/20 2 3 264 Mifepristone Hypertension 10 + 2 2 OU 20/200 2
CF 2 C63 2.5 2 + + OD 20/252 2
20/252 251 Type 2 diabetes,
kidney stones10 + 2 + OU 20/20 2 2 2
20/32 2 2 263 Hypertension,
hypercholesterolemia7 + 2 2 OU 20/200 2
20/80 2
CF, counting fingers; post tx, post treatment; PMH, past medical history.
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patients experienced an improvement in retinal OCT
findings with decreased retinal edema or subretinalfluid on OCT, with 1 patient developing increased
cystoid macular edema in 1 eye over the course of
treatment. No significant changes in fluoresceinangiography or ICG angiography were found. One
patient developed choroidal neovascularization from
CCSC thought not to be related to mifepristone
treatment and underwent subsequent injection with
bevacizumab. One patient who had a favorable
response to mifepristone in Pilot 1 relapsed and
subsequently completed the Pilot 2 protocol with
a favorable response.5 He also demonstrated a dramatic
response to rechallenge with mifepristone. No patients
experienced any serious adverse events over the course
of treatment including skin rash. No patients were
found to have liver transaminase elevation throughoutthe protocol.
Case Reports
A 63-year-old white male previously reported5 with CCSC for at
least 7 years OD worse than OS with progressive vision loss. He
had been treated previously with thermal laser in the left eye. Visual
acuity was 20/200 in the right eye and 20/80 in the left eye.
Examination revealed extensive pigment atrophy in both the eyes.
Fluorescein angiography demonstrated extensive pigment atrophy
and diffuse leakage. Choroidal hyperpermeability was shown on
ICG angiography (Figure 1). Optical coherence tomography
showed widespread retinal edema and collections of subretinal
fluid. After 12 weeks of mifepristone 200 mg daily, the edema
improved. Vision improved to 20/30 in the left eye but remained 20/
200 in the right eye.5
Four months later after completion of Protocol 1, the patientreturned with complaints of visual deterioration with vision
declining to 20/40 in the left eye and remaining at 20/200 in the
right eye. Evaluation revealed return of macular edema in both the
eyes off the mifepristone. Twenty months after him completing
Protocol 1, his decline had continued. His vision declined to 20/200
in the right eye and 20/80+ in the left eye with worsening macular
edema. Angiographic findings were similar to his original
presentation: diffuse leakage on fluorescein angiography and
choroidal hyperpermeability on ICG. He was enrolled in Protocol
2 and completed another 12-week course of oral mifepristone
200 mg daily. With rechallenge, his vision improved to 20/180+ in
the right eye and 20/50+ in the left eye with complete resolution of
his macular edema (Figure 1). Residual retinal atrophy was noted
OD.OS. Just 4 months after completing the second course of
mifepristone, he again relapsed with accumulation of cystoid
macular edema and vision decline to 20/200 in the right eye and
20/80 in the left eye.
A 38-year-old white female with CCSC for 4 years and a history
of steroid use presented with enlarging scotomata in both the eyes.
Visual acuity was excellent with Early Treatment Diabetic
Retinopathy Study best-corrected visual acuity of 20/16 in the
right eye and 20/25 in the left eye. On examination, she noted to
have diffuse pigmentary changes in both eyes. Fluorescein
angiography showed large extrafoveal leakage in both eyes and
a pigment epithelial detachment in the left eye (Figure 2).
Table 2. Protocol 2 Patient Characteristics
NumberAge
(Years) Sex PMH/POHAffected
Eye Laser Avastin PDTCSC
Duration (Years) Steroids
1 47 F HTN, herniateddisk, eczema
OD 2 2 2 2 2
2 81 M CAD s/p CABG, arthritis,
kidney stones,SB for RRD OD withpoor VA
OS 2 + 2 15 +
3 65 M HTN, hyperlipidemia,previous response toprevious mifepristone
OU + 2 + 9 2
4 81 M HTN, hyperlipidemia,urinary incontinence
OU 2 2 + 10 2
5 54 M GERD, herniated disk OU 2 2 2 12 26 63 M Anxiety, HTN OU 2 2 2 30 27 48 M Depression, anxiety OU 2 2 2 17 28 76 M Osteoarthritis,
prostate cancerOU 2 2 2 10 2
9 38 F Migraines OU 2 2 2 5 +10 58 M HTN, arthritis OU + + + 10 211 20 F Bee sting
and ibuprofen allergyOD 2 + + 2 2
12 59 M Hypertriglyceridemia OU + + + 15 +13 69 M Barrett esophagus OU 2 2 + 12 +
F, female; M, male; VA, visual acuity; PMH, past medical history; POH, past ocular history; HTN, hypertension; CAD s/p CABG,coronary artery disease with bypass graft; GERD, gastroesophageal reflux disease; SB, scleral buckle.
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Choroidal hyperpermeablity was noted on ICG angiography.
Shallow collections of subretinal fluid in both eyes and a small
pigment epithelial detachment were noted on time domain OCT.
After 12 weeks of treatment, her Early Treatment Diabetic
Retinopathy Study best-corrected visual acuity improved to 20/
12.5 and 20/20. All subretinal fluid resolved in the right eye and
improved in the left eye. Ten months after completing the
mifepristone treatment, she presented with worsening of subretinal
fluid in both the eyes with a decrease in vision to 20/40 in the left
eye. She entered into an institutional review boardapproved
compassionate use mifepristone protocol and has responded with
decreased subretinal fluid in both the eyes and some improvement
in vision in the left eye to 20/30 after 12 weeks. She is continuing
this compassionate use protocol.
A 58-year-old white male presented with devastating vision loss
from 10 years of CCSC in both the eyes despite three sessions of
PDT. Vision at presentation was 20/100 in the right eye and
counting fingers 5 ft in the left eye. Severe macular pigmentary
changes and cystoid macular edema were noted on initial
evaluation. Angiography revealed extensive macular leakage in
both the eyes on fluorescein angiography (Figure 3) and choroidal
hyperpermeability in both the eyes on ICG. Large central
intraretinal cysts were demonstrated bilaterally with time domain
OCT. After 12 weeks of oral mifepristone, vision improved to 20/
200 in the left eye and remained at 20/100 in the right eye. Central
macular cystic changes nearly resolved in the left eye, with some
mild improvement in the right eye.
Discussion
Between the 2 small protocols, 16 individuals havetaken oral mifepristone for CCSC, with 1 subject
participating in both protocols. This cohort is
heterogeneous with regard to vision and clinical
severity. Overall, 8 of the 16 patients reported a sub-
jective improvement in vision. Seven subjects demon-
strated an improvement in visual acuity of five letters or
greater. Seven individuals demonstrated improvementof findings on OCT. One subject who participated in
both protocols exhibited initial response to daily
mifepristone, relapsed off the medication, and repeat
response to subsequent rechallenge.
Many of the patients entered into this protocol withadvanced or end-stage pathology. Despite a dramatic
improvement in retinal anatomy, visual improvement
was limited by retinal thinning, neuronal loss, and
RPE atrophy. Patients with less advanced CCSC
would likely benefit more substantially from a vision
standpoint. Systemic mifepristone therapy has a sub-
stantial history of safety, and no issues were revealed
during our limited investigation.
It is clear that a 12-week course of oral mifepristone
is insufficient to resolve all macular edema and
subretinal fluid even in responsive patients. We
speculate that some patients in our 12-week protocol
might have benefited further from extended treatment.
Further investigation should be designed to consider
longer duration treatment.
Endocrine abnormalities are common in patients
with CSC. Haimovici et al11 demonstrated that 38% of
individuals with active acute CSC had elevated 24-hour
urine cortisol and 29% had an abnormal diurnal patternof cortisol secretion. Response to mifepristone may be
more likely in patients with corticosteroid abnormal-
ities. We did not specifically investigate cortisol levels
either before or during mifepristone treatment. One
individual who demonstrated a response to mifepris-
tone was tested after washout and found to have normal
serum cortisol levels. Future CSC mifepristone proto-
cols should investigate whether there is a relationship
between corticosteroid dysfunction and response to
mifepristone.
There are two patients in the study who presented
with only isolated RPE detachments and no choroidal
hyperpermeability on ICG angiography. We believe
that these patients may not have typical CSC and may
represent an entirely different disease entity. No
response was seen to mifepristone.
Table 3. Protocol 2 Response to Mifepristone Treatment
Number
Enroll VisualAcuity OD
Exit VisualAcuity OD
SubjectiveChange
ImagingResults
Enroll VisualAcuity
OS
Exit VisualAcuity
OS
1 20/16 + 1 20/16 + 2 = =20/12.5 20/16 + 1
2 20/400 CF 1 ft = 220/160 + 4 20/160 + 3
3 20/160 20/160 + 4 + +20/80 + 4 20/50 + 1
4 CF 10 ft 20/200 = =20/63 + 3 20/100 + 1
5 20/40 + 4 20/20 + 2 + =20/40 20/32 + 2
6 20/100 20/160 + 2 = +20/200 + 2 20/200
7 20/16 + 4 20/16 + 2 + +CF 3 ft 20/200 2 2
8 20/200 2 4 20/200 + 2 = =20/50 + 2 20/50 + 3
9 20/16 + 3 20/12.5 = +20/25 20/20 2 1
10 20/100 + 2 20/100 2 1 + +CF 5 ft 20/200 2 3
11 20/50 + 3 20/32 + 3 + =20/20 + 1 20/20 + 1
12 20/16 + 1 20/20 + 1 = 220/200 2 1 20/200 2 2
13 20/40 + 1 20/32 + 4 + +10/50 + 4 20/40 + 3
CF, counting fingers.
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Special considerations warrant attention during
systemic mifepristone anti-GC therapy. Mifepristone
use as an abortifacient requires exceptional caution
when treating female patients with childbearing
potential. For all patients who may become pregnant,
serum beta HCG before retreatment and two separate
forms of contraception while undergoing therapy should
be used. Mifepristone can induce reversible liver
transaminase elevation. Monitoring of these enzymes
is required during treatment. Adrenal insufficiency is
another rare but potentially serious consequence of anti-
GC therapy. Physicians using systemic mifepristone
Fig. 1. A 63-year-old whitemale with CCSC in both theeyes for 7 years. Initial pre-treatment FA (A) and ICG(B). Optical coherence to-mography responses (C) to 2separate 12-week courses ofmifepristone. FA, fluorescein
angiography.
ORAL MIFEPRISTONE FOR CHRONIC CSC NIELSEN AND JAMPOL 1933
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need to be able to recognize adrenal insufficiency, make
patients aware of the symptoms, and be ready to direct
treatment if necessary.
Our study is not the first attempt to investigate
systemic anti-GC therapy for CSC. The widely
available antifungal agent ketoconazole exhibts anti-
GC effects at higher doses. Unfortunately, after some
limited initial investigation, ketoconazole has not yet
proven effective for CSC. Meyerle et al12 investigated
ketoconazole 600 mg daily for 4 weeks in 5 patients.
They were able to demonstrate a systemic anti-GC
effect by monitoring urinary cortisol in patients taking
ketoconazole. The authors felt that the results of this
short trial were inconclusive. However, one patient did
demonstrate resolution of subretinal fluid and im-
provement of vision.12 Our experience with mifepris-
tone suggests that longer treatment may be required.
Golshahi et al13 evaluated oral ketoconazole 200 mg
daily in a casecontrol study of patients with acute
CSC. They were unable to ascertain any treatment
effect after 4 weeks. Unfortunately, the 200-mg dose is
likely too low to produce a substantial anti-GC effectin most patients, and the duration of treatment again is
too short.
Fig. 2. A 38-year-old whitefemale with CCSC in both theeyes for 4 years. Baseline FA(A) and OCT responses (B) tomifepristone. FA, fluorescein
angiography.
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This study has many limitations. The inclusion of an
open-label cohort, small size, and wide range of
disease severity limit our ability to draw definitive
conclusions about mifepristone for CCSC. Some of
the clinical responses manifest in our study indicate
that mifepristone may have an important role in the
treatment of CCSC, particularly in patients who do not
respond to other treatment.
All our patients did not respond to 12 weeks of
systemic mifepristone therapy. Many of our patients
are on the more severe end of the disease spectrum and
may be recalcitrant to mifepristone therapy. Perhaps,
CSC is a heterogeneous disease. Glucocorticoid-
mediated disease may simply be a subset of all
patients afflicted with CSC. Patients who have non
GC-mediated CSC are not likely to respond to GC
antagonists.
Our limited experience supports GC receptor
antagonism with systemic mifepristone as a possible
treatment of CCSC. The precise biologic mechanism
underlying the etiology of CSC is unknown. Our
findings add evidence to implicate GCs in the
pathogenesis of CSC. Further investigation is war-
ranted to better understand the efficacy and safety of
systemic mifepristone therapy in CSC.
Key words: antiglucocorticoid therapy, central
serous chorioretinopathy, central serous retinopathy,
glucocorticoid receptor antagonism, optical coherence
tomography, mifepristone, RU-486.
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