disc areas experienced moderate vi-
7 sual loss.5 Large-spot TTT with the
6 used in the present study did not ap-
5 cult choroidal neovascularization.
Patients, No.
4
3
2 Richard F. Spaide, MD
1 Lawrence A. Yannuzzi, MD
0
–15 –14 –13 –12 –11 –10 –9
Figure 2. Bar graph showing the number of patients and the change in visual acuity from baseline.
nal lipid (P = .076) at baseline; the
need for retreatment (P=.36); or the
need for subsequent photody-
namic therapy with verteporfin
(P=.89); but was correlated with the
initial acuity (Spearman ␳ = -0.38,
P=.02) such that those with better
initial acuity lost more acuity over
the follow-up period. Ten eyes
(28.6%) suffered 6 or more lines of
visual acuity loss.
Comment. This study retrospec-
tively examined 35 patients treated
with TTT using an 810-nm diode la-
ser with a power of 800 mW for 90
seconds and a 4500-µm spot size for
occult CNV ranging in size from
3000 µm to 4500 µm in diameter.
After a mean follow-up period of
13.5 months, most patients (60%)
experienced a moderate visual acu-
ity loss. A lens providing ⫻1.5 mag-
nification of the spot size was em-
ployed, which supplied a maximum
spot size of 4500 µm given the
3000-µm maximum beam size. The
patients were treated with 800 mW
for 90 seconds, which was a lower
power density but a longer expo-
sure time than some of the other pa-
tients treated in a previous study em-
ploying smaller spot sizes. 1 A
subsequent study by Mainster et al4
detailing a mathematical analysis of
TTT suggested that the laser power
should be increased linearly with the
spot size, which calculates to 1200
mW given over a period of 60 sec-
onds for the larger spot size used in
this study to theoretically match that
(REPRINTED) ARCH OPHTHALMOL / VOL 123, SEP 2005
–8 –7 –6 –5 –4 –3 –2 –1 0 1 2 3 4 5
Lines of Visual Acuity Change
given by Reichel et al1 using a 3-mm
spot size. The power density for the
spot size used in the study by Thach
et al3 for large lesions was not only
less than this suggested amount, it
was slightly less, proportionately,
than what we used in our patients.
The exact power density and dura-
tion of the laser exposure for TTT
and the incidence of any possible
long-term toxicity has not been es-
tablished through any published
studies and is not calculable math-
ematically with currently available
data. The reasons for difference in
apparent outcomes for our series and
that reported by Thach et al are not
known, but likely explanations are
that there may have been differ-
ences in patients treated; both were
small studies with incomplete fol-
low-up and there were no control
groups.
The randomized trial currently
under way evaluating TTT for CNV
is evaluating a maximum lesion size
of 3 mm, which is relatively small.
As the results from a randomized
trial of photodynamic therapy us-
ing verteporfin show, possible treat-
ment benefit for small occult le-
sions is not predictive of efficacy in
larger lesions.5 In that study, 45% of
patients treated with verteporfin
compared with 72% of placebo pa-
tients with lesions less than or equal
to 4 disc areas experienced moder-
ate visual loss after 2 years of follow-
up. On the other hand, 65% of both
the treatment and placebo groups
with occult lesions greater than 4
WWW.ARCHOPHTHALMOL.COM
1273
Downloaded from www.archophthalmol.com on January 27, 2008
©2005 American Medical Association. All rights reserved.
power levels and exposure times
pear to be effective for subfoveal oc-
Large-spot TTT should be evalu-
ated by a dose-ranging randomized
trial before introduction into our
treatment armamentarium.
Jason Slakter, MD
John Sorenson, MD
6 K. Bailey Freund, MD
Correspondence: Dr Spaide, Vitre-
ous, Retina, Macula Consultants of
New York, 460 Park Ave, Fifth Floor,
New York, NY 10022 (vrmny@aol
.com).
Financial Disclosure: Dr Slakter is
a consultant for Alcon Laboratories
Inc (Fort Worth, Tex), and Dr Yan-
nuzzi is on the Scientific Advisory
Panel for Eyetech Pharmaceuticals
Inc (New York, NY).
1. Reichel E, Berrocal AM, Ip M, et al. Transpupil-
lary thermotherapy of occult subfoveal choroi-
dal neovascularization in patients with age-
related macular degeneration. Ophthalmology.
1999;106:1908-1914.
2. Stevens TS, Bressler NM, Maguire MG, et al.
Occult choroidal neovascularization in age-
related macular degeneration: a natural history
study. Arch Ophthalmol. 1997;115:345-350.
3. Thach AB, Sipperley JO, Dugel PU, et al. Large-
spot size transpupillary thermotherapy for the
treatment of occult choroidal neovasculariza-
tion associated with age-related macular
degeneration. Arch Ophthalmol. 2003;121:817-
820.
4. Mainster MA, Reichel E. Transpupillary ther-
motherapy for age-related macular degenera-
tion: long-pulse photocoagulation, apoptosis, and
heat shock proteins. Ophthalmic Surg Lasers.
2000;31:359-373.
5. Verteporfin In Photodynamic Therapy Study
Group. Verteporfin therapy of subfoveal cho-
roidal neovascularization in age-related macu-
lar degeneration: two-year results of a random-
ized clinical trial including lesions with occult
with no classic choroidal neovascularization—
verteporfin in photodynamic therapy report 2.
Am J Ophthalmol. 2001;131:541-560.
Vision Loss Due to
Macular Edema Induced by
Rosiglitazone Treatment
of Diabetes Mellitus
Rosiglitazone is in the thiazolidine-
dione class of insulin-sensitizing
agents used for the treatment of type
2 diabetes mellitus.
Thiazolidinediones have been re-
ported to cause or exacerbate ven-
 sion in each eye during a 2-week pe-
A
Fluorescein Leakage and Edema riod. He had a history of diabetes
mellitus (diagnosed in 1987) com-
plicated by proliferative diabetic reti-
nopathy, neuropathy, and recently
discovered nephropathy. Hyperten-
sion, hyperlipidemia, and depres-
sion were also being treated.
His medications included regu-
lar insulin 3 times daily, insulin
glargine, rosiglitazone, atorvastatin
calcium, amlodipine besylate,
quinapril hydrochloride, hydrochlo-
B Resolution of Fluorescein Leakage and Edema rothiazide, and sertraline hydrochlo-
ride. He had been taking rosiglita-
zone for 3 years; the dosage had been
increased from 2 to 8 mg/d in Sep-
tember 2003, 1 month before the vi-
sion loss was noted. Peripheral edema
was also noted after the dosage of
rosiglitazone was increased.
Biochemical evidence for progres-
sive nephropathy was present. Left
ventricular function, as measured by
Figure 1. Right macular region demonstrating fluorescein leakage and edema (hyperfluorescence) after ultrasonography, was normal.
increased rosiglitazone dosage to 8 mg/d (A) and resolution (with improved vision) 3 weeks after In July 2003 (before the in-
decreased dosage to 2 mg/d (B). creased rosiglitazone dosage), his vi-
sual acuity was 20/30 OD and 20/25
OS, and there was no evidence of
A
macular edema. In October 2003, 1
month after rosiglitazone was in-
creased to 8 mg/d, his visual acuity
had declined to 20/80 OD and 20/70
OS, associated with bilateral macu-
lar edema. Three weeks after the
rosiglitazone dosage was decreased
to 2 mg/d, his visual acuity had im-
proved to 20/25 OU, and macular
edema had resolved ( Figure 1 and
Figure 2).

B Comment. The thiazolidinediones

have been reported to be associated
with the development of dose-
related peripheral edema, espe-
cially when used with insulin.3
In addition to peripheral edema,
diuretic-resistant pulmonary edema
Resolution of Fluorescein Leakage and Edema has been reported with thiazolidine-
dione treatment.3
Patients with depressed left ven-
Figure 2. Left macular region demonstrating fluorescein leakage and edema (hyperfluorescence) after tricular function and/or renal insuf-
increased rosiglitazone dosage to 8 mg/d (A) and resolution (with improved vision) 3 weeks after ficiency have an increased potential
decreased dosage to 2 mg/d (B).
for edema when receiving thiazo-
lidnedione treatment. Postulated
tricular failure, pulmonary edema, to rosiglitazone-induced macular mechanisms for the induction of
and peripheral edema, especially in edema, which reversed on dosage re- dose-related edema in patients tak-
patients with left ventricular dys- duction. ing thiazolidinediones include in-
function or chronic renal insuffi- creased renal sodium absorption, in-
ciency.1,2 This case report describes Report of a Case. A 55-year-old man creased plasma volume, sympathetic
vision loss in a diabetic patient due noted an insidious decrease in vi- activation, intestinal ion transport al-

(REPRINTED) ARCH OPHTHALMOL / VOL 123, SEP 2005 WWW.ARCHOPHTHALMOL.COM

1274
Downloaded from www.archophthalmol.com on January 27, 2008
©2005 American Medical Association. All rights reserved.
terations, and increased production
of vascular endothelial growth fac-
tor (which induces increased vascu-
lar permeability).3
Although the case reported is the
first report, to our knowledge, of the
development of reversible macular
edema with vision loss in a patient
taking rosiglitazone, this is probably
not a rare event. A retrospective medi-
cal record review of 30 patients given
at the annual meeting of the Ameri-
can Academy of Ophthalmology in
2003 by Edwin Ryan, MD, sug-
gested that glitazone use may be
linked to the existence of macular
edema in patients with diabetes melli-
tus.4 Because the administration of
thiazolidinediones like rosiglitazone
has been associated with the devel-
opment of edema, the observation of
macular edema with vision loss with
rosiglitazone administration, revers-
ible when taking a decreased dos-
age, is not unexpected. Physicians
prescribing rosiglitazone (and other
thiazolidinediones) should be aware
of the possibility of decreased vision
associated with the development of
macular edema due to the thiazoli-
dinedione. Caution should be exer-
cised when thiazolidinediones are
used in those with nephropathy (or
congestive heart failure). Options for
the management of rosiglitazone (or
thiazolidinedione)-induced macular
edema with vision loss include dose
reduction and discontinuation.
Michael Colucciello, MD
Correspondence: Dr Colucciello,
South Jersey Eye Physicians, 509 S
Lenola Rd, Suite 11, Moorestown, NJ
08057 (michael@macula.us).
Financial Disclosure: None.
Previous Presentation: This study
was presented at the 130th anniver-
sary meeting of the Department of
Ophthalmology, University of Penn-
sylvania, Scheie Eye Institute; May
22, 2004; Philadelphia, Pa.
1. Kermani A, Garg A. Thiazolidinedione-asso-
ciated congestive heart failure and pulmonary
edema. Mayo Clin Proc. 2003;78:1088-1091.
2. Niemeyer NV, Janney LM. Thiazolidinedione-
induced edema. Pharmacotherapy. 2002;22:924-
929.
3. Mudaliar S, Chang AR, Henry RR. Thiazolidine-
diones, peripheral edema, and type 2 diabetes:
incidence, pathophysiology, and clinical
implications. Endocr Pract. 2003;9:406-416.
4. Harby K. Glitazone use may be associated with
macular edema in diabetes. Available at: http:
//www.medscape.com/viewarticle/464732. Ac-
cessed July 7, 2004.

Correction

Error in Table. In the Laboratory Sciences article by Stitzel et al titled “Blunt Trauma of the Aging Eye: Injury Mechanisms
and Increasing Lens Stiffness,” published in the June issue of the ARCHIVES (2005;123:789-794), there was an error in Table 3.
Line A2 was printed on top of line A1. The table is reproduced correctly as follows. The journal regrets the error.

Table 3. Stress Data for Impact Simulations*

Stress, MPa
Age
Simulation No. Object Group, y Corneoscleral Shell Ciliary Body Zonules
F1 Foam 16-35 7.82 ↑ 2.83 ↑↑ 16.40
F2 Foam 36-65 7.77 2.75 14.75
F3 Foam ⱖ66 7.82 2.58 12.83
W1 Wheel 16-35 12.76 4.25 ↑↑ 37.86
W2 Wheel 36-65 12.83 6.28 35.25
W3 Wheel ⱖ66 12.77 ↓↓ 9.35 31.62
A1 Air bag 16-35 ↑ 15.30 8.81 ↑↑ 33.04
A2 Air bag 36-65 15.13 8.88 28.34
A3 Air bag ⱖ66 15.10 ↓ 9.36 24.01

Abbreviation: MPa, megapascals.

*Arrows indicate increasing stress; up arrows decrease with age, and down arrows increase with age. Double arrows indicate high sensitivity (⬎1 MPa
per age group), whereas single arrows indicate low sensitivity (⬍1 MPa per age group).

(REPRINTED) ARCH OPHTHALMOL / VOL 123, SEP 2005 WWW.ARCHOPHTHALMOL.COM

1275
Downloaded from www.archophthalmol.com on January 27, 2008
©2005 American Medical Association. All rights reserved.