Rituximab as a monotherapy or in combination therapy for the treatment of non-paraneoplastic autoimmune retinopathy
rituximab as a monotherapy or in combination therapy for the treatment of non-paraneoplastic autoimmune retinopathy
arash Maleki 1 2
n eerav lamba 1 2
lina Ma 1 2
stacey lee 1 2
alexander schmidt 1 2
C stephen Foster 2
0 harvard Medical school , Boston, Ma, Usa
1 Ocular immunology and Uveitis Foundation , Waltham
2 Massachusetts eye r esearch and surgery institution , USA
8 1 0 2 - l u J - 2 1 n o 2 7 1 . 3 6 1 . 7 3 . 4 5 y b / m o c . rsseep l.yon PowerdbyTCPDF(ww.tcpdf.org) Purpose: To examine the efficacy of rituximab as a monotherapy or in combination therapy for the treatment of patients with non-paraneoplastic autoimmune retinopathy. Methods: Twelve eyes of six patients with non-paraneoplastic autoimmune retinopathy who were treated with rituximab and had at least 6 months of follow-up were included. Demographic data, clinical data, visual field parameters, electroretinography parameters, and anti-retinal and anti-optic nerve autoantibody bands were collected from the Massachusetts Eye Research and Surgery Institution database between September 2010 and January 2015. Changes in visual acuity, visual field parameters, electroretinography parameters, and anti-retinal and anti-optic nerve autoantibody bands from the initial visit to the most recent visit were examined. Results: From the initial visit to the last visit, visual acuity was stable in eight (66.7%) eyes. Visual field was stable in six (50%) eyes and improved in two (16.7%) eyes. Electroretinography was stable or improved in eight (66.7%) eyes. The average number of anti-retinal and anti-optic nerve antibody bands was reduced. Conclusion: Stabilization and/or improvement of visual acuity, visual field parameters, and electroretinography parameters were observed in a high number of patients (75%) on rituximab, as a monotherapy (one patient) or in combination therapy.
Autoimmune retinopathy (AIR) is an immune-mediated retinopathy that can cause
acute, subacute and chronic vision loss, visual field defects, photopsias, nyctalopia, and
color vision defects.1,2 AIR is characterized by the presence of circulating anti-retinal
antibodies that are believed to damage photoreceptors in the retina; however, the exact
mechanism is not entirely understood.3,4
AIR is subdivided into paraneoplastic (cancer-associated retinopathy and
melanomaassociated retinopathy) and non-paraneoplastic categories. Non-paraneoplastic
AIR is composed of a large group of autoimmune retinopathies with features similar
to those of carcinoma-associated retinopathy, but without any known underlying
malignancy. Non-paraneoplastic AIR is usually diagnosed at a younger age,4 in people
with a known personal and/or familial history of autoimmune diseases.2,5,6
Long-term immunosuppressive therapy is considered the mainstay of treatment
for AIR.7 Different regimens of immunomodulatory therapy, such as corticosteroid,8
plasmaphoresis,9 intravenous immunoglobulin,10 cyclosporine,6 and mycophenolate
mofetil,6 have been used in the treatment of paraneoplastic and non-paraneoplastic AIR.
Clinical Ophthalmology 2017:11 377–385 377
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However, the rarity of this entity combined with difficulty
in confirming the diagnosis and monitoring the response
to treatment makes treatment challenging.5 Rituximab, a
cluster of differentiation 20 molecule inhibitor (CD20), has
been used as a treatment option for carcinoma-associated
retinopathy in limited studies.11,12 There is also a case report
using rituximab in the treatment of non-paraneoplastic AIR.13
The aim of this study is to examine the efficacy of rituximab
as a monotherapy or in combination therapy in preserving
or improving visual function parameters in patients with
This was a single-center, retrospective interventional case
series of patients with non-paraneoplastic AIR who were
treated at the Massachusetts Eye Research and Surgery
Institution (MERSI) between September 2010 and January 2015.
Each patient had at least 6 months of follow-up from when
rsseep l.yon the diagnosis of non-paraneoplastic AIR was made. Ethical
.vdo lsue approval for this study was obtained through the New England
ttsphwww rsopenoaF iIfnnofrsotriretmutrteoiodsnpcaeolcnRtisveeevnictehwbaarBsteordeavrodien,wwssht.aiTnchdhaiissrdssutuoeddpyearwawtaiansivgpeeprrrfooofcrwmedreiutdtreeinns
accordance with the Declaration of Helsinki and was Health
Insurance Portability and Accountability Act compliant.
Diagnosis of AIR was made based on four essential
criteria with subjective symptoms as supportive criteria.5
Essential criteria included no evidence of systemic
malignancies or infections after a complete history was taken
and a physical examination and appropriate testing were
performed; no evidence of a preexisting degenerative eye
disease; confirmed progressive abnormality on repeated
electroretinography and/or visual field; and the presence of
anti-retinal and/or anti-optic nerve antibodies. Supportive
criteria were the acute or subacute presence of symptoms,
such as decreased vision, visual field defects, nyctalopia,
photoaversion, photopsia, and color vision deficits in patients
without active anterior or posterior uveitis.
Blood samples and pertinent medical history of each
patient were collected at MERSI and were sent to the
commercially available testing center at Oregon Health Sciences
University. Western blots were used to evaluate the presence
of the anti-retinal and anti-optic nerve antibodies. These tests
were repeated every 6 months.
All patients underwent fluorescein angiography,
indocyanine green (ICG) angiography, full-field
electroretinography, and automated perimetry. Optical coherence tomography
was obtained as part of the initial examination or follow-up
examinations in all patients with clinical evidence of decreased
central visual acuity at any time or angiographic suspicion of
Patient demographics, including personal and family
histories of autoimmune diseases, were collected. Best
corrected visual acuity and related logarithm of the minimum
angle of resolution (LogMAR) were recorded for every
patient at the initial and most recent visits. Humphrey
visual field (HVF; Carl Zeiss Meditec, Inc., Dublin, CA,
USA) and Ganzfeld electroretinography (SG-2002, LKC
Technologies, Gaithersburg, MD) were also performed on
all patients at the initial and most recent visits. Anti-retinal
and anti-optic nerve autoantibody bands, reported based on
their molecular weights (kDa), were recorded at the initial and
most recent visits. Furthermore, anti-retinal and anti-optic
nerve antibodies were divided into pathologically proven
and nonspecific groups, as based on the previous studies.2,5,14
After a thorough analysis of the patient’s records, treatment
regimens, the duration of each regimen, reported clinical
and laboratory (blood and urine) side effects, and reasons for
premature termination of a treatment regimen and its related
date were recorded for every patient in the study.
Visual fields were analyzed with the Humphrey Visual
Field Analyzer (Carl Zeiss Meditec, Inc.) under 24-2
FASTPAC or Swedish Interactive Threshold Activity (SITA)
fast strategy for all patients, except those with a previous
diagnosis of birdshot retinochoroidopathy. Short-wavelength
automated perimetry (SITA-SWAP) was used to evaluate
the visual fields of patients with a previous diagnosis of
birdshot retinochoroidopathy as it has been shown to be
more accurate in these patients.15 Visual field parameters
recorded were total deviation, pattern deviation, mean
deviation, and pattern standard deviation. The standardized visual
field criteria of the Optic Neuritis Treatment Trial protocol
were used to interpret visual field patterns.16,17 A field defect
was defined as three or more significant (P,0.05) non-edge
contiguous points, with at least one at the (P,0.01) level on
the same side of the horizontal meridian.18,19 Ganzfeld
electroretinography (SG-2002, LKC Technologies) parameters
included scotopic b-wave amplitude, maximal combined
a-wave and b-wave amplitudes, 30-Hz flicker amplitude,
and 30-Hz flicker implicit time. The percentage of each of
these parameters to the mean normal control values were
calculated for statistical analysis.
The treatment protocol for rituximab was 375 mg/m2
every week for 8 weeks, then 375 mg/m2 monthly.20,21 Oral
cyclophosphamide was used at a dose of 2 mg/kg/day.
Bortezomib was the other medication, used at a dose of
1.3 mg/m2 through the subcutaneous route at days 1, 4, 8,
and 11; this was repeated every 21 days. All patients were
monitored closely for occult side effects of all medications
via a complete review of systems at each visit and periodical
blood tests, including blood cell counts, blood urea
nitrogen, creatinine, and liver function tests. In patients
on cyclophosphamide, urine samples were analyzed for
hematuria every other month. The decision for rituximab
monotherapy or in combination therapy was made based on
the severity of the disease.
Severe disease was defined as visual acuity 20/200 or
worse; or mean deviation worse than -12 dB, .50% of
points depressed ,5% level and .25% depressed ,1%
level on pattern deviation plot, any point within 5° of
fixation 0 dB. Both hemifield contain point(s) ,15 dB within
5° of fixation;22 or flat or near flat 30-Hz flicker amplitude
and/or combined a-wave and b-wave amplitudes.
We looked for stability or improvement of visual acuity,
HVF patterns and parameters (total deviation, pattern
deviation, mean deviation, and pattern standard deviation),
and electroretinography parameters (scotopic rod response
amplitude, maximal combined a-wave and b-wave
amplitudes, 30-Hz flicker amplitude, and 30-Hz flicker implicit
time) at the most recent visit. Stability in visual acuity was
defined as a visual acuity that was similar to the first visit
(within one line on the Snellen chart). Improvement in visual
acuity was defined as visual acuity that improved by at least
two lines on the Snellen chart from the first visit. Stability
of visual field was defined as the patient having the mean
deviation and pattern standard deviation within the same
category based on probability symbols on HVF printout.
Visual field patterns were considered improved if scotomas
in the field became more localized or less dense in the final
visit than in the initial visit. Finally, electroretinography
parameters were considered stable when they were within
25% (minimum reported for stability) of the baseline values
or better,23 respectively, from the first to the last visit.
As there were multiple parameters in the HVF and
electroretinography tests, stability or improvement in each test
was defined as stability or improvement in .50% of the
parameters of that test. Parameters included total deviation,
pattern deviation, mean deviation, and pattern standard
deviation in HVF; and scotopic rod response amplitude,
maximal combined a-wave and b-wave amplitudes, 30-Hz
flicker amplitude, and 30-Hz flicker implicit time in
electroretinography. The test was determined to be
inconclusive when 50% of the parameters were worse and the other
50% were stable or better.
Statistical Package for the Social Sciences (SPSS) 16.0 (IBM
Corp., Armonk, NY, USA) and MedCalc software 126.96.36.199
(MedCalc®, Mariakerke, Belgium) were used for statistical
There were six patients (12 eyes) who met all inclusion
criteria. The median age at initial presentation was 49 years
and initial consultation was 10.5 months (range, 2–44). The
median duration of follow-up was 18 months (range, 8–49).
Of the six patients, five (83.3%) were females. All patients
were of a non-Hispanic Caucasian ethnicity. One patient
had a previous diagnosis of systemic lupus erythematosus
(patient 3), two patients had a previous diagnosis of birdshot
retinochoroidopathy (patients 5 and 6), and one patient had
a previous diagnosis of HLA-B27-positive panuveitis and
vasculitis (patient 2). All patients’ family histories were
negative for any systemic autoimmune, ocular autoimmune,
and hereditary degenerative diseases.
At the initial visit, the mean LogMAR visual acuity was
0.58±0.6 (20/70–20/80). The presenting symptoms included
progressive decreased vision in four eyes of two patients,
progressive decreased vision and visual field defects in
four eyes of two patients, and only progressive visual field
defects in two eyes of one patient. Two eyes of one patient
with birdshot retinochoroidopathy were found,
incidentally, during regular monitoring with impressive changes
in his visual field and electroretinography tests after almost
4 years of being in remission off medications and without
any intraocular inflammation. None of the eyes had active
uveitis at the initial visit. Two of the six patients (four eyes)
had abnormal funduscopy examinations; one of them (two
eyes) showed disc pallor, arterial narrowing, and diffuse
retinal and retinal pigment epithelium atrophy, whereas the
other patient (two eyes) showed isolated generalized retinal
and retinal pigment epithelium atrophy. All other patients
had normal funduscopy examinations bilaterally.
Fluorescein angiography did not reveal any abnormalities
in any of the 12 eyes at the initial visit. ICG angiography
was normal in eight eyes of four patients and was considered
stable in patients who had previous diagnoses of birdshot
retinochoroidopathy. Macular optical coherence tomography
was obtained in four patients due to decreased visual acuity.
Results of this testing showed decreased macular thickness
with no macular edema or cystic changes in the macula in
eight eyes of these four patients.
All patients received immunomodulatory therapy. Four
patients with underlying systemic or ocular autoimmune
diseases were already on conventional immunomodulatory
therapy, which included methotrexate, cyclosporine,
mycophenolate mofetil, and adalimumab. All of these medications
were stopped before using the AIR treatment protocol.
Rituximab was started in all the patients in the study. Oral
cyclophosphamide was used in three patients. One patient
rsseep l.yon received bortezomib in combination with rituximab as the
.vdo lsue initial therapy. Cyclophosphamide was replaced with
bort://www rsnoa ezomTriebaitnmoennet pwaatisenptrbemecaatuusreeloyf dstoocpupmeednitnedtlweuokpoapteineniat.s.
ttsph ropeF One patient discontinued treatment due to intolerable side
from effects of the medications: rituximab, cyclophosphamide, and
edd bortezomib. This patient experienced dermatitis (1 month
loan after starting treatment), leukopenia (6 months after starting
odw treatment), and peripheral neuropathy (2 months after
lyog starting treatment) with rituximab, cyclophosphamide, and
lom bortezomib, respectively. The other patient discontinued
tahh treatment due to issues in insurance coverage (5 months after
lpO starting treatment). One patient, who was on rituximab and
cyclophosphamide combination therapy, had to discontinue
cyclophosphamide due to leukopenia (10 months after
treatment), but was able to continue treatment with
rituximab. The mean number of medications used to treat
was 1.83 (range, 1–3). The average duration of treatment was
14.1±5.07 months (range, 8–20). Table 1 shows the details
of the treatment regimens in each patient.
Changes in vision, visual field patterns and parameters,
and electroretinography parameters from the initial visit to
the most recent visit are shown in Table 2 and Figure 1.
From the initial visit to the last visit recorded, visual acuity
was found to be stable in eight (66.7%) eyes and decreased
in four (33.3%) eyes. Visual field as a single test showed
stability in six (50%) eyes, improvement in two (16.7%) eyes,
and worsening in one (8.33%) eye. It was inconclusive in
three eyes (25%). Figure 2 shows the improvement of mean
deviation and stability of pattern standard deviation in one
of the patients who responded to rituximab.
Electroretinography as a single test showed improvement in two (16.7%)
eyes, worsening in four (33.3%) eyes, and stability in two
(16.7%) eyes. In four (33.3%) eyes, electroretinography
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showed stability/improvement (50% of electroretinography
parameters were stable and the other 50% improved).
Figure 3 shows improvement in 30-Hz flicker amplitude and
after treatment. One eye developed negative waveforms
during the treatment. Table 3 shows changes in visual acuity,
the HVF, and electroretinography as a single test modality
from the initial visit to the last visit. Nine (75%) eyes of five
(83.5%) patients showed stability or improvement in at least
two test modalities, including visual acuity, visual field, and
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At the initial visit just before starting rituximab, all patients
were positive for anti-retinal and anti-optic nerve
antibodies. The average number of anti-retinal antibody bands was
2.83±2.31 (range, 1–7). All but one had at least one
pathologically proven anti-retinal antibody band (mean, 1.5±1.04;
range, 0–3). The average number of anti-optic nerve antibody
bands was 2.33±1.03 (range, 1–3). The pathologically proven
anti-optic nerve antibody band was found only in one patient.
At the most recent visit, the average number of anti-retinal
antibody bands was 2.33±1.96 (range, 1–6), and the average
number of anti-optic nerve antibody bands was 1.66±1.36
(range, 0–4). After treatment, the average number of
pathologically proven anti-retinal autoantibodies bands was 1±0.89
(range, 0–2); the average number of nonspecific anti-optic
nerve antibodies was the same, although the number of
bands decreased in five patients and increased in one patient.
Interestingly, in three out of five patients with pathologically
proven anti-retinal antibodies, at least one pathogenically
proven band disappeared after treatment; however, one of
these patients developed a new pathologically proven band.
Table 4 describes pathologically proven and nonspecific
anti-retinal and anti-optic nerve antibodies at the initial and
most recent visits.
On the basis of the presumed antibody-mediated mechanism2,5,6
and our personal experience regarding the failures of
conventional immunomodulatory therapy (four patients in this
cohort), we evaluated the efficacy of rituximab as a
monotherapy or in combination with cyclophosphamide and/or
bortezomib to preserve or improve visual functions in patients
with non-paraneoplastic AIR. The rationale for this protocol
was to eliminate the B cells, precursors of plasma cells that
are responsible for making the autoantibodies against retinal
cells. Oral cyclophosphamide and/or bortezomib were used
in patients with severe disease.
Of the six patients, two patients (four eyes) were previously
diagnosed with HLA-A29-positive birdshot
retinochoroidopathy. These cases were in remission for a long time
(.2 years). Neither of them had active intraocular
inflammation, especially vitreous cells and vitreous haze. They had
subacute impressive visual field and visual acuity loss with
normal fluorescein angiography and stable ICG angiography.
These findings made us suspicious to AIR more than birdshot
retinochoroidopathy relapse as AIR has previously been
reported in cases with birdshot retinochoroidopathy.14 Both
of these cases responded to rituximab infusions.
In our study, vision did not improve in any patient despite
treatment; however, visual acuity was stable at the most recent
visit in eight (66.7%) eyes. Ferreyra et al showed improved
vision in three eyes of three patients out of 15 patients with
non-paraneoplastic AIR who responded to
immunosuppressive therapy.6 Two patients in their study had cystoid macular
edema that improved after treatment, which can explain the
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improvement in visual acuity.6 However, none of our patients
tested with fluorescein angiography and optical coherence
tomography had cystoid macular edema. Jampol and Fishman
reevaluated and reanalyzed their data in patients with
nonparaneoplastic AIR without cystoid macular edema; they
observed stability or improvement in 60% of studied eyes.24
In our study, four patients had previous retinal, choroidal,
and retinal vasculature problems, which might explain why
018 their vision did not improve despite treatment. Moreover,
l-u2 three eyes of two patients with worsening of visual acuity
-J12 were in the group in which the treatment was prematurely
.2no71 stopMpeodstdoufethtoe psirdeveieofufsecsttusdoiresinesmurpahnacseiziesdsuGeos.ldman
perim.136 etry for peripheral visual changes; however, central and
para.734 central scotomas have been reported in patients with AIR.5 In
yb5 addition, electroretinography shows peripheral retinal function
/om accurately; therefore, we performed 24-2 FASTPAC or
SITA.c FAST or SITA-SWAP strategy in our patients as these tests
rsseep l.yon can also indicate optic nerve involvement. Different strategies
.vdo lsue were used based on the underlying problems in our patients;
www snoa for example, we obtained SITA-SWAP data in patients with
//: r birdshot retinochoroidopathy.15 This does not interfere with
ttsph ropeF the interpretation of the results, as we compared the status of
from patients at their most recent visit with their own baseline
mealdedao tswuroempaetnietns.tsI.nOouurrrsetsuudltys,avriesunaolt faisefldaviomrapbroleveadstihnotswe ofoeuynedsboyf
lltooham upeseridmtehteryH, VthFe mteestth,wodhuicshedhabsy mFeorrreeypraaraemtael.teOrsurthfianndGinoglsdwmearne
phO consistent with Jampol and Fishman reanalysis of Ferreyra et al’s
ililcanC rweistuhltIsV,-in4-tehatatrtgheetyifnouhnadlf noof cthheanpgaetiienntGs.o24ldTmhaensepefrinimdientgrys
make our results superior to that study when taking into
account our strict criteria. Moreover, all of our patients had
autoimmune-related retinopathy and optic neuropathy
syndrome, which might make the prognosis poorer than that of
The major advantage of this study, as opposed to previous
studies on this disorder, was the comprehensive evaluation
of electroretinography parameters and their changes from
the initial to the final visit while considering inter-test
variability.6,11,12,20 The majority of parameters were stable or
improved in eight eyes (66.7%). The four eyes with
worsening of the majority of the parameters on
electroretinography belonged to two patients in whom the treatment was
stopped prematurely due to insurance issues or side effects.
Only limited case reports and small case series reported
electrophysiological data with no pathognomonic findings; in
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addition, most of our patients were asymptomatic in the most
recent visit. As such, the importance of this finding is not
completely clear. The largest cohort of non-paraneoplastic
AIR patients, performed by Ferreyra et al, did not include
electroretinography parameters in the improvement criteria
in all of their patients.6
We divided anti-retinal and anti-optic nerve antibodies
into pathologically proven and nonspecific groups based
on the previous studies.2,5,14 The importance of nonspecific
anti-retinal and anti-optic nerve antibodies is unclear. Half
of our patients showed elimination of at least one
pathologically proven anti-retinal antibody band (Table 4). This can
indicate the efficacy of treatment; however, due to the rarity
of the disease, lack of standardization of these tests, and low
antibody-specific concordance rate, this is still an area of
debate.8,25 Although antibody titers may be more valuable than
the bands themselves in reporting efficacy of treatment, titers
were not available in antibody reports from the laboratory.
Despite all of these controversies, stability or
improvement of two or more tests in nine (75%) eyes of five (83.5%)
patients along with the reduction of pathologically proven
antibody bands (50%) can be considered a success in the
treatment of this disease, which historically has had a poor
prognosis. This becomes more significant if we consider that
all three eyes with worsening of at least two test modalities
were in the group in which the treatment was prematurely
stopped. However, due to ongoing underlying autoimmune
processes and the unpredictability of this rare disorder, the
duration of treatment and the final prognoses of these patients
are still unclear.
Our study was limited by its retrospective nature and
small sample size. Not having optical coherence tomography
data for all patients was another limitation of our study. We
were also dependent on a commercially available laboratory
for anti-retina and anti-optic nerve antibodies, and they did
not include the antibodies’ titers in their reports. Moreover,
the patient population in our tertiary referral center is skewed
toward patients with very severe intraocular disease. Thus, it
is difficult to predict from our data, the outcomes of treatment
in patients with a milder disease course. Notwithstanding
these limitations, this article describes the only cohort to date
of patients with non-paraneoplastic AIR who were treated
with rituximab as a monotherapy or in combination with
cyclophosphamide and/or bortezomib with a comprehensive
analysis of the static visual field, electroretinography, and
anti-retinal and anti-optic nerve antibodies.
Overall, stability of vision, visual field, and
electroretinography parameters were observed in a high number of eyes
(75%) who were treated with rituximab as monotherapy (one
patient) or combination therapy (four patients). However, a
prospective multi-center study with a large population and
longer follow-up would help us to standardize the use of
visual field, electroretinography parameters, and evaluation
of anti-retinal and anti-optic nerve antibody bands and titers
so that criteria can be established for a proper response to
treatment with rituximab, alone or in combination therapy.
C Stephen Foster discloses the following: consultancies with
Aldeyra Therapeutics (Lexington, MA, USA), Bausch &
Lomb Surgical, Inc (Rancho Cucamonga, CA, USA),
Eyegate Pharma (Waltham, MA, USA), Novartis
Pharmaceuticals (Cambridge, MA, USA), pSivida (Watertown, MA,
USA), and Xoma (Berkeley, CA, USA).
Grants or grants pending with Alcon (Aliso Viejo, CA,
USA), Aldeyra Therapeutics, Bausch & Lomb (Bridgewater,
NJ, USA), Clearside Biomedical (Alpharetta, GA, USA),
Dompé pharmaceutical (Milan, Italy), Eyegate Pharma, Icon
(Dublin, Ireland), Novartis Pharmaceuticals, pSivida, Santen
(Osaka, Japan), and Xoma.
Payment for lectures including service on speaking
bureaus: Alcon, Allergan (Dublin, Ireland). Stock or Stock
Options: Eyegate Pharma. The other authors report no
conflicts of interest in this work.
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