in the behavioral pathology of eating
disorders.
Akio Inui, MD, PhD
Akihiro Asakawa, MD, PhD
Masato Kasuga, MD, PhD
Kobe University Graduate
School of Medicine
Kobe, Japan
Shuji Kamikawa, MD
Tokyo Women’s Medical University
Tokyo, Japan
Masaharu Uemoto, MD, PhD
Kobe City College of Nursing
Kobe, Japan
Tomoyuki Watanabe, PhD
Sumitomo Chemical Co., Ltd.
Osaka, Japan
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vosa—an excess of both orexigenic and an-
orexigenic signalling? Mol Psychiatry. 2001;
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anatomy scanning (SAS) in intracranial
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ANTERIOR ISCHEMIC
OPTIC NEUROPATHY
CAUSED BY INTERFERON
ALPHA THERAPY
To the Editor:
Interferons are glycoproteins with
antiviral, antitumoral, and antiangio-
genic effects. Interferon alpha (IFN-
␣
), alone or in combination with
ribavirin, is so far the only effective
treatment for chronic hepatitis C
(1,2). Ocular complications rarely oc-
cur with interferon therapy and in-
clude trichomegaly and retinopathy
(3,4). We present a case of anterior
ischemic optic neuropathy due to
IFN-
␣
therapy in a patient with
chronic hepatitis C.
A 64-year-old white man pre-
sented with complaints of sudden,
painless blurring of vision in the right
eye after awakening in the morning.
He denied jaw claudication, neck
pain, trauma, or headache. His past
medical history consisted of well-
controlled hypertension, and chronic
hepatitis C, for which he had been re-
ceiving IFN-
␣
and ribavirin for 8
months. His visual acuity was 20/100
in the right eye and 20/20 in the left. A
relative apparent pupillary defect of
0.3 to 0.6 log was found in the right
eye; the left was normal. Humphrey
perimetry testing showed a cecocen-
tral scotoma in the right eye and a full
field in the left. Fundus examination
revealed nasal disc hemorrhage, with
superior segment disc edema in the
right eye (Figure). Fluorescein an-
giography confirmed optic disc
edema and peripapillary hemorrhage
in the right eye. Visual evoke poten-
tial demonstrated an absent response
in the right eye and a normal response
in the left. A complete blood count,
blood chemistry, sedimentation rate,
C-reactive protein level, human im-
munodeficiency virus titer, rapid
plasma regain test, angiotensin-con-
verting enzyme titer, and antinuclear
factor were normal, as were magnetic
resonance imaging of the head, echo-
cardiogram, and carotid Doppler
study. A diagnosis of anterior isch-
emic optic neuropathy due to IFN-
␣
therapy was made, and the drug was
discontinued. A follow-up 4 weeks
later showed a marked improvement
of visual acuity and the scotoma, and
resolution of disc hemorrhage and
edema.
The prompt resolution of anterior
ischemic optic neuropathy after dis-
continuation of IFN-
␣
in our patient
suggests a causal relation. We ruled
out other etiologies, such as vasculi-
tis, demyelination, infection, connec-
tive tissue disorder, and embolism.
Some studies have described onset
of IFN-
␣
-induced optic neuropathy
soon after starting therapy (5,6),
whereas another reported that the
likelihood of IFN-
␣
-induced retinop-
athy increased with time, with 11% of
patients affected after 2 weeks and
71% after 6 months (7), which is sim-
ilar to the late-developing neuropa-
thy that we observed.
The mechanism by which IFN-
␣
-
induced anterior ischemic optic neu-
ropathy is unknown. Ischemia may
be caused by the deposition of circu-
lating immune complexes in optic
disc vessels, or by interferons, which
inhibit proliferation and migration
of endothelial cells (8). Nocturnal
arterial hypotension also affects the
pathogenesis of the disease (9). In-
Figure. Fundus photograph showing peripapillary hemorrhage and disc edema.
Letters to the Editor
June 1, 2002 T
HE
A
MERICAN
J
OURNAL OF
M
EDICINE
Volume 112 683