A 3-month safety and efficacy study of

travoprost 0.004% ophthalmic solution

compared with timolol in pediatric patients
with glaucoma or ocular hypertension
El Roy Dixon, MD,a Theresa Landry, PhD,b Subha Venkataraman, PhD,b Nancy Gustafson, MS,b
Craig Salem, OD,b Yasmin Bradfield, MD,c Leyla Ali Aljasim, MD, FRCS,d and Robert Feldman, MDe

PURPOSE To evaluate efficacy and safety of travoprost in pediatric patients with ocular hypertension
or glaucoma and demonstrate its noninferiority to timolol.
METHODS Patients aged 2 months to \18 years with glaucoma or ocular hypertension were random-
ized to receive travoprost (0.004%) or timolol eye drops (0.25% for patients aged 2 months
to \3 years and 0.5% for patients $3 years old) for 3 months in this double-masked,
parallel-group study. Intraocular pressure (IOP) was measured and patients were evaluated
at 2 weeks, 6 weeks, and 3 months after treatment. Change in IOP from baseline to
3 months was the primary endpoint, and the test of noninferiority was based on a margin
of 13.0 mm Hg using the 95% 2-sided confidence interval of the mean change.
RESULTS Of 157 patients included (mean age, 9.6 years), 77 received travoprost and 75 timolol. All
patients experienced a significant reduction in IOP in the study eye at 3 months: the
mean IOP change from baseline was 5.4 mm Hg for travoprost; 5.3 mm Hg, for timolol.
The mean difference between travoprost and timolol at month 3 was 0.1 mm Hg (95% CI,
1.5 to 1.4 mm Hg). The most common treatment-related adverse events for the travoprost
group were ocular hyperemia and eyelash growth. No serious adverse events were reported.
CONCLUSIONS This study found travoprost to be noninferior to timolol in lowering IOP in patients with
pediatric glaucoma or ocular hypertension. Travoprost was well-tolerated, and no
treatment-related systemic adverse events were reported. ( J AAPOS 2017;21:370-374)

Report of the World Glaucoma Association.2 Primary

C
hildhood glaucoma is a potentially blinding condi-
tion characterized by structural changes in the op-
tic disk and elevated intraocular pressure (IOP).1
Childhood glaucoma is divided into 2 major categories:
primary and secondary, as defined by the 9th Consensus
Author affiliations: aDixon Eye Care, Albany, Georgia; bAlcon Research Ltd, Fort Worth,
Texas; cUniversity of Wisconsin Department of Ophthalmology and Visual Sciences,
Madison, Wisconsin; dKing Khaled Eye Specialist Hospital, Riyadh, Saudi Arabia; eRobert
Cizik Eye Clinic, Department of Ophthalmology and Visual Sciences, University of Texas
Health Science Center, Houston, Texas
Study funded by Alcon Laboratories Inc, Fort Worth, Texas, and Research to Prevent
Blindness, Inc.
Disclosures: RF is a consultant for Alcon and has received research support from Alcon;
TL, CS, and SV are Alcon employees; NG was an Alcon employee at the time of the study.
The study was conducted at multiple sites in the US, Europe, Middle East, Latin America,
Caribbean, and Asia Pacific.
Presented in part at the Annual Meeting of the Association for Research in Vision and
Ophthalmology 2015, Denver, Colorado, May 3-7, 2015.
Submitted September 9, 2016.
Revision accepted May 5, 2017.
Published online September 6, 2017.
Correspondence: El Roy Dixon, MD, Dixon Eye Care, 806 N. Jefferson Street, Albany,
GA 31701 (email: elroy117@gmail.com).
Copyright Ó 2017, The Authors. Published by Elsevier Inc. on behalf of American
Association for Pediatric Ophthalmology and Strabismus. This is an open access article
under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
1091-8531
http://dx.doi.org/10.1016/j.jaapos.2017.07.202
childhood glaucoma may be caused by congenital structural
anomalies and includes but is not limited to primary
congenital glaucoma (PCG) and juvenile open-angle glau-
coma. Secondary childhood glaucoma occurs as a result of
independent disease mechanisms or trauma (ie, surgical
removal of the native lens in eyes with congenital cata-
racts).2 Pharmacologic management of childhood glau-
coma is common despite surgery being the primary
treatment.
Current IOP-lowering medications used in adults
include b-blockers, carbonic anhydrase inhibitors (CAIs),
prostaglandin analogs (PGAs), cholinergic agonists, and
a2-agonists.3 Limited data are available on the use of
common IOP-lowering agents in pediatric patients.4,5
Lower body mass and body surface area, lower renal
clearance, and decreased blood volume compared with
adults, make pediatric patients more susceptible to systemic
adverse events.6 Some adverse events, such as central nervous
system depression associated with a2-agonists, can be
life-threatening in infants and small children.7-9
Recently, travoprost 0.004% and latanoprost 0.005%
were approved for pediatric use in Europe.10,11
The first line of pharmacologic treatment in pediatric
glaucoma is often timolol. However, topical application

370 Journal of AAPOS

Volume 21 Number 5 / October 2017
of b-blockers can trigger asthma, bradycardia, heart block,
heart failure, and masking of hypoglycemia in diabetic
children.1 Latanoprost therapy, an IOP-lowering treat-
ment considered safe in adults, has been shown to produce
higher systemic exposure to its biologically active meta-
bolic product latanoprost acid in younger children. Despite
the higher exposure, latanoprost is well tolerated and can
be an effective IOP-lowering therapy in children.5,12
Travoprost 0.004% (40 mg/mL; Travatan; Alcon Labora-
tories Inc, Fort Worth, TX) has been shown to be effective
in reducing IOP and since 2001 has been approved for use in
adults with primary open-angle glaucoma or ocular hyper-
tension. In Europe travoprost was approved for use in chil-
dren in 2014.11,13 A small retrospective study in children
found that travoprost was effective and well tolerated. In
patients with pediatric glaucoma, 54% of eyes responded
to treatment and had an IOP decrease of $15% after
1 month. Eyelash growth was the most common side
effect.14 In a study of travoprost administered to pediatric
patients as an adjunct to other glaucoma medications,
60% of patients responded to travoprost, with a $10%
reduction in IOP. The most common adverse event was
conjunctival hyperemia.15 To date, there have been no
well-controlled clinical studies examining travoprost
0.004% for the treatment of pediatric patients with glau-
coma or ocular hypertension. The purpose of this investiga-
tion was to evaluate the IOP-lowering effects of travoprost
in pediatric patients and to demonstrate its noninferiority
to timolol.
Subjects and Methods
This was a 3-month multicenter, randomized, double-masked,
parallel-group phase 3 study. This study was conducted in accor-
dance with good clinical practice and in compliance with the
ethical principles that have their origins in the Declaration of
Helsinki; it was approved by each institution’s ethical review
board. This study was conducted between September 2012 and
March 2014 at 38 sites in 15 countries (see eSupplement 1 for
complete listing). For sites in the United States, the study
conformed to the requirements of the US Health Insurance
Portability and Accountability Act of 1996. Written informed
consent was provided by the parents or guardians of patients;
when required, patients provided their assent to participate.
Eligible patients were aged 2 months to \18 years, had a diag-
nosis of pediatric glaucoma or ocular hypertension, and had IOP
of $20 mm Hg in at least 1 eye during the eligibility visit.
Included in the study were patients with aphakia wearing contact
lenses and patients with conditions requiring chronic treatment
with glucocorticoids resulting in steroid-induced glaucoma,
provided the patients were on a stable dose of steroids for
$30 days before screening. Patients meeting any of the following
criteria were excluded: history of chronic, recurrent, or severe
inflammatory eye disease; ocular trauma or intraocular surgery
within 3 months of screening; clinically significant or progressive
retinal disease; severe ocular pathologies; abnormality preventing
reliable tonometry; history of congenital cardiovascular abnor-
Journal of AAPOS
Dixon et al 371
malities; reactive airway disease; severe allergic rhinitis; corneal
dystrophies; use of additional ocular hypotensive medications
during the study; \30 days stable dosing of IOP-affecting medi-
cations or therapy with another investigational agent before the
screening visit.
Treatment and Assessment
Eligible patients were stratified by primary diagnosis (PCG or
non-PCG) and baseline IOP in the study eye (\27, 27-31, or
.31 mm Hg). Patients were then randomized 1:1 using an inter-
active Web response system to receive travoprost 0.004% (once
daily in the evening and vehicle once daily in the morning to
maintain masking) or timolol (twice daily, morning and evening,
0.5% to patients $3 years and 0.25% to patients 2 months to
\3 years). Patients and their parents or legal guardians were
instructed to instill 1 drop of assigned study medication from
the bottle labeled “morning” at 9 a.m. ( 30 minutes) and 1
drop of study medication from the bottle labeled “evening” at 9
p.m. ( 30 minutes) in each eye for 3 months. The first dose of
study medication was instilled by designated staff at each center
during the eligibility visit. The morning dose at week 2 and 6 visits
was instilled at the study site 15 minutes after IOP measurement.
IOP was measured at week 2, week 6, and month 3 by calibrated
tonometry using a Goldmann applanation tonometer, a Perkins
tonometer, or a tono-pen. Two consecutive IOP measurements
were taken and averaged in each eye at each visit. All IOP
measurements for an individual patient were performed by the
same personnel using the same method at 9 a.m.  60 minutes.
Anesthesia was used at screening and month 3 visit when an
IOP measurement could not be obtained in a conscious child.
IOP measurements were recorded immediately after induction
to stage 3 anesthesia and before intubation. Anesthetics known
to elevate IOP were avoided.
The primary efficacy endpoint was change in IOP from base-
line at month 3. Supportive efficacy endpoints included IOP
changes from baseline at weeks 2 and 6, IOP and IOP percentage
change from baseline (all visits), and percentage of patients with a
$15% reduction in IOP (all visits).
Extent of exposure, adverse events, vital signs, 12-lead electro-
cardiogram (ECG), patient alertness, best-corrected visual acuity,
slit-lamp examination, automated perimetry, central corneal
thickness, corneal diameter, ocular hyperemia, and dilated fundus
examination were monitored at week 2, week 6, and month 3
visits. If necessary, additional assessments for adverse events
were performed at unscheduled visits at any time during the study
at the investigators’ discretion. Reported adverse events were
coded using the Medical Dictionary for Regulatory Activities.
Statistical Analysis
Statistical analyses were performed using SAS software (SAS
Institute, Cary, NC). The 0.5% timolol and 0.25% timolol
groups were combined for statistical analysis. Efficacy for the
primary endpoint was evaluated in the intent-to-treat (ITT) and
per-protocol (PP) analysis sets. The ITT set included all patients
who received study medication and completed $1 on-therapy
visit. The PP set comprised all ITT patients who satisfied preran-
domization inclusion and exclusion criteria.
372 Dixon et al
If only 1 eye was treated, the treated eye was used for analysis. If
both eyes were treated, the eye with the highest baseline IOP was
used for analysis. The right eye was designated as the study eye if
baseline IOP for both treated eyes was the same.
The change in IOP from baseline at month 3 was examined
using the least-squares (LS) means from an analysis of covariance,
with treatment and primary diagnosis as factors and baseline IOP
as a covariate. The test of noninferiority was based on a margin of
13.0 mm Hg using the 95% 2-sided confidence interval of the
mean change. The noninferiority margin was agreed upon by
the European Pediatric Committee as part of the pediatric inves-
tigation plan. Assuming a standard deviation of 7 mm Hg for the
mean IOP change, a 5% chance of a type 1 error, and that the
mean change for the travoprost group would be $1 mm Hg better
than the timolol group, 65 patients per group were needed to have
approximately 90% power to demonstrate noninferiority. If
noninferiority was achieved, superiority was tested at an alpha
level of 0.05; superiority was concluded if the upper limit of the
2-sided 95% confidence interval for change from baseline at
month 3 was \0 mm Hg. Supportive efficacy endpoints were
summarized descriptively using the ITT population.
Results
Of 152 patients randomized to receive travoprost (n 5 77)
or timolol (n 5 75), 145 (95%) completed the study. Six
patients in the travoprost group and 1 patient in the timolol
group discontinued because of inadequate IOP control.
One patient was excluded from the PP analysis set
(n 5 151) because of a violation of inclusion criteria. All
152 patients were included in the ITT and safety analyses.
Mean patient age was 9.6 years; 53% were female, 41%
were white, and 30% were diagnosed with PCG. A baseline
IOP of \27 mm Hg was observed in most patients (77%).
There were no clinically meaningful differences in demo-
graphics or baseline characteristics between treatment
groups (eTable 1). Before randomization, 94 patients
received IOP-lowering medications, including PGA
(n 5 20), CAI (n 5 12), or b-blocker (n 5 22) as monother-
apy. Nineteen patients received dorzolamide/timolol.
Another 21 patients received $IOP-lowering medications
in at least 1 eye. Patients stopped previous treatments
$24 hours before the eligibility visit. Anesthesia was used
to obtain IOP measurements in 11 patients in the 2 months
to\3 years group and 8 patients in the 3 to\12 years group.
For the primary efficacy endpoint, IOP in the study eye
was reduced in both groups following 3 months of treat-
ment. LS mean IOP change from baseline was 5.4 mm
Hg for travoprost and 5.3 mm Hg for timolol in the
ITT data set and 6.4 mm Hg for travoprost and
5.8 mm Hg for timolol in the PP data set (Figure 1).
The LS mean difference between travoprost and timolol
treatment groups at month 3 was 0.1 mm Hg (95% CI,
1.5 to 1.4 mm Hg) and 0.5 mm Hg (95% CI, 2.1 to
1.0 mm Hg) in the ITT and PP data set, respectively.
The difference between treatment groups was below the
defined 13.0 mm Hg upper limit margin of the 95%
Volume 21 Number 5 / October 2017
FIG 1. Least squares (LS) mean IOP change from baseline at month 3.
LS mean and standard error were calculated for change in IOP
following treatment with travoprost 0.004% or timolol 0.5% (0.25%
for patients \3 years). IOP, intraocular pressure.
confidence interval; therefore, treatment with travoprost
was established as noninferior to timolol. However,
because the upper limit of the confidence intervals did
not lie entirely below 0, superiority was not concluded.
Supportive efficacy assessments were consistent with the
primary efficacy endpoint. Mean IOP changes from base-
line were similar in the travoprost and timolol groups at
weeks 2 and 6 (Figure 2A). Mean IOP measurements
were similar between groups at each study visit (data not
shown), and mean IOP percentage changes from baseline
were generally similar at week 2, week 6, and month 3
(Figure 2B). The percentage of patients who achieved a
$15% reduction in IOP was similar between groups at
weeks 2 and 6 and was numerically greater for travoprost
at month 3 (Figure 2C). In the travoprost group, 88% of
patients without PCG vs 71% of patients with PCG had
a $15% reduction in IOP at month 3. In the timolol group,
80% of patients without PCG vs 61% of patients with
PCG had a $15% reduction in IOP at month 3. Overall,
lesser IOP reduction was achieved in patients with PCG
in both groups.
Of the 152 patients (aged 2 months to 17 years), mean
duration of exposure (with standard deviation) was
84.0  14.2 days for patients receiving travoprost and
88.3  6.6 days for patients receiving timolol. Two patients
from the timolol group experienced serious adverse events
unrelated to use of study medication (pneumonia and
bacterial keratitis in one patient and viral infection in the
other; Table 1). No serious adverse events were reported
for patients in the travoprost group. No patient discontin-
ued from the study due to an adverse event. One patient
receiving timolol had a systemic treatment–related AE of
dizziness; no such events were reported for patients
Journal of AAPOS
Volume 21 Number 5 / October 2017
FIG 2. Supportive efficacy endpoints. A, Mean IOP change from
baseline at weeks 2 and 6. B, Mean IOP percentage changes from
baseline at weeks 2 and 6 and month 3. C, Percentage of patients
who achieved a $15% reduction in IOP from baseline at weeks 2
and 6 and month 3. Patients received travoprost 0.004% or timolol
0.5% (0.25% for patients \3 years). The ITT data set was used. ITT,
intent-to-treat.
receiving travoprost. The most common treatment-related
adverse events in the travoprost group were ocular hyper-
emia (17%) and growth of eyelashes (7%). In the timolol
group, ocular hyperemia was reported for 1%, and there
were no reports of eyelash growth. Other adverse events
in patients receiving travoprost were typical for topical
Journal of AAPOS
Dixon et al 373
ocular medication: ocular discomfort, photophobia,
tearing, dry eye, and corneal surface irritation.
Discussion
Medications that lower IOP are used to treat pediatric
patients with glaucoma both before and after surgery. In
this investigation, children with primary congenital glau-
coma or other pediatric glaucomas received travoprost
0.004% or timolol for 3 months, at which point treatment
with travoprost was found to be noninferior to timolol.
Although it was not statistically significant, a numerically
greater percentage of patients receiving travoprost (83%)
achieved a $15% reduction in IOP relative to patients
receiving timolol (74%). The IOP-lowering efficacy
observed with travoprost in this pediatric population was
consistent with previous retrospective studies.14,15
A long-term retrospective study found that latanoprost,
another prostaglandin analog, significantly reduced IOP in
pediatric patients after 6 months.5 Comparable to the
results of the current report, latanoprost was noninferior
to timolol in a 12-week study.12 The most common
latanoprost-related adverse event was hyperemia.12
No increased risks were observed in pediatric patients
receiving travoprost; no serious adverse events were
reported, and no patient left the study because of an adverse
event. A higher percentage of patients in the travoprost
group experienced treatment-related adverse events
compared with patients in the timolol group, particularly
related to ocular hyperemia. Most experiencing ocular hy-
peremia while receiving travoprost had no prior exposure
to PGA therapy. Ocular hyperemia is common in patients
receiving PGAs and has been reported in adults.1,16
Absorption of antiglaucoma drugs may cause systemic
adverse events, including hypotension and bradycardia
(timolol), headaches (travoprost), metabolic acidosis
(carbonic anhydrase inhibitors), and systemic and central
nervous system–related AEs (brimonidine).1,7 Systemic
adverse events were uncommon in the current study.
There was 1 event of treatment-related dizziness associ-
ated with timolol. There were no treatment-related sys-
temic adverse events associated with travoprost,
suggesting a combination of low systemic absorption of
topical travoprost, rapid clearance, and/or lack of signifi-
cant cardiovascular effects despite systemic absorption. A
recent study of the pharmacokinetics and safety of travo-
prost 0.004% in a small population of pediatric patients
0.3-17 years of age found that the range of systemic expo-
sure in children was comparable to that in adults, and
there was no clear association between age or body sur-
face area and systemic travoprost exposure. However,
the sample size was small, and further studies are neces-
sary to evaluate the pharmacokinetics of travoprost in pe-
diatric patients.17
Other safety assessments in the current study did not
reveal an increased safety concern for the use of travoprost
in pediatric patients compared with adult patients.
374 Dixon et al Volume 21 Number 5 / October 2017

Table 1. Summary of treatment-emergent adverse events Acknowledgments

Travoprost Timolol The authors thank Kimberly Martens of Alcon Research Ltd for assis-
Adverse event category, n (%) (n 5 77) (n 5 75) tance with manuscript preparation. Medical writing assistance was
Deaths 0 0 provided by Natalia Zhukovskaya, PhD, of The CHC Group, LLC
Nonfatal serious AE 0 2 (2.7)a (Chadds Ford, Pennsylvania).
Discontinued due to an AE 0 0
Patients with $1 treatment-emergent AE 40 (51.9) 28 (37.3)
Treatment-emergent AEs $5% References
Ocular hyperemia 15 (19.5) 3 (4.0)
Headache 5 (6.5)a 2 (2.7)a 1. Moore W, Nischal KK. Pharmacologic management of glaucoma in
Growth of eyelashes 5 (6.5) 0 childhood. Paediatr Drugs 2007;9:71-9.
Conjunctival hyperemia 4 (5.2)a 1 (1.3) 2. Beck A, Chang TCP, Freedman S. Definition, Classification,
Patients with $1 treatment-related AE 20 (26.0) 9 (12.0) Differential Diagnosis. In: Weinreb RN, Grajewski AL,
Ocular hyperemia 13 (16.9) 1 (1.3) Papadopoulos M, Grigg J, Freedman S, eds. Childhood Glaucoma.
Growth of eyelashes 5 (6.5) 0 The 9th Consensus Report of the World Glaucoma Association.
Eye pruritus 1 (1.3) 1 (1.3) Amsterdam, The Netherlands: Kugler Publications; 2013:3-10.
Photophobia 1 (1.3) 1 (1.3) 3. Sultan MB, Mansberger SL, Lee PP. Understanding the importance
Eye pain 1 (1.3) 0 of IOP variables in glaucoma: a systematic review. Surv Ophthalmol
Lacrimation increased 1 (1.3) 0 2009;54:643-62.
Erythema of eyelid 1 (1.3) 0 4. McMahon CD, Hetherington J Jr, Hoskins HD Jr, Shaffer RN.
Keratitis 1 (1.3) 0 Timolol and pediatric glaucomas. Ophthalmology 1981;88:249-52.
Conjunctival hyperemia 0 1 (1.3) 5. Black AC, Jones S, Yanovitch TL, Enyedi LB, Stinnett SS,
Dry eye 0 1 (1.3) Freedman SF. Latanoprost in pediatric glaucoma–pediatric exposure
Eye irritation 0 1 (1.3) over a decade. J AAPOS 2009;13:558-62.
Foreign body sensation 0 1 (1.3) 6. Coulter RA. Pediatric use of topical ophthalmic drugs. Optometry
Ocular discomfort 0 1 (1.3) 2004;75:419-29.
Dizziness 0 1 (1.3) 7. Al-Shahwan S, Al-Torbak AA, Turkmani S, Al-Omran M, Al-Jadaan I,
Visual field defect 0 1 (1.3) Edward DP. Side-effect profile of brimonidine tartrate in children.
Ophthalmology 2005;112:2143.
AE, adverse event. 8. Enyedi LB, Freedman SF. Safety and efficacy of brimonidine in chil-
a
Not related to treatment.
dren with glaucoma. J AAPOS 2001;5:281-4.
9. Bowman RJ, Cope J, Nischal KK. Ocular and systemic side effects of
brimonidine 0.2% eye drops (Alphagan) in children. Eye (Lond) 2004;
18:24-6.
A higher rate of discontinuations was reported with travo- 10. UK MHRA. Xalatan (latanoprost) 0.005% Eye Drops Solution. Avail-
prost (n 5 6) than with timolol (n 5 1). The 6 travoprost able at: http://www.mhra.gov.uk/home/groups/spcpil/documents/
group patients discontinued early because of inadequate spcpil/con1403242957663.pdf. Accessed October 21, 2015.
IOP control. One patient (aged 3 months) demonstrated a 11. Quaranta L, Riva I, Katsanos A, Floriani I, Centofanti M, Konstas AG.
clinically relevant reduction in IOP at weeks 2 and 6 but Safety and efficacy of travoprost solution for the treatment of elevated
intraocular pressure. Clin Ophthalmol 2015;9:633-43.
was determined by the investigator to have inadequate IOP
12. Maeda-Chubachi T, Chi-Burris K, Simons BD, et al., A6111137
control, possibly because of the patient’s age. Another patient Study Group. Comparison of latanoprost and timolol in pediatric
with reduction in IOP at weeks 2 and 6 was also discontinued glaucoma: a phase 3, 12-week, randomized, double-masked multi-
by the investigator. The baseline IOP for these 2 patients was center study. Ophthalmology 2011;118:2014-21.
.31 mm Hg. One patient experienced a short-term IOP 13. Travatan (travoprost). Summary of Product Characteristics. Camber-
decrease in response to travoprost followed by IOP increase ley, UK: Novartis Europharm Limited; 2006.
14. Yanovitch TL, Enyedi LB, Schotthoeffer EO, Freedman SF. Travo-
after week 6. The remaining 3 patients did not respond to prost in children: adverse effects and intraocular pressure response.
travoprost treatment; 2 of these patients were receiving mul- J AAPOS 2009;13:91-3.
tiple IOP-lowering medications before the screening visit 
15. Helmanova I, Autrata R, Senkov  urek J. Safety and efficacy of
a K, Reh
and it is possible that travoprost alone was not sufficient to travoprost adjunctive treatment in paediatric glaucoma. Scripta
control IOP. None of the patients in the travoprost group Medica (BRNO) 2007;80(1-2):29-36.
16. Fellman RL, Sullivan EK, Ratliff M, et al., Travoprost Study Group.
were discontinued due to adverse events.
Comparison of travoprost 0.0015% and 0.004% with timolol 0.5% in
Potential limitations of the current study were the lack of patients with elevated intraocular pressure: a 6-month, masked, multi-
extended wash-out period for previous IOP-lowering center trial. Ophthalmology 2002;109:998-1008.
medications, the relatively short treatment duration 17. Stahl E, Bremond-Gignac D, Landry T, et al. Pharmacokinetics and safety
(3 months), and the small number of patients under the age of travoprost 0.004% ophthalmic solution preserved with polyquad in pe-
of 3 (16 patients). Future studies will need to address the diatric patients with glaucoma. J Ocul Pharmacol Ther 2017;33:361-5.
18. Shah M, Lee G, Lefebvre DR, et al. A cross-sectional survey of the as-
long-term effects of c8hronic travoprost treatment, including
sociation between bilateral topical prostaglandin analogue use and
prostaglandin-associated periorbitopathy reported in adult ocular adnexal features. PLoS ONE 2013;8:e61638.
patients,18,19 and further examine the efficacy and safety of 19. Nakakura S, Yamamoto M, Terao E, et al. Prostaglandin-associated
travoprost in infants and young children. periorbitopathy in latanoprost users. Clin Ophthalmol 2015;9:51-6.

Journal of AAPOS
Volume 21 Number 5 / October 2017 Dixon et al 374.e1

eTable 1. Demographic and clinical characteristics

Travoprost Timolol
Characteristic (n 5 77) (n 5 75)
Age category, n (%)
2 months to \3 years 10 (13.0) 6 (8.0)
3 to \12 years 40 (51.9) 39 (52.0)
12 to \18 years 27 (35.1) 30 (40.0)
Mean  SD, years 9.2  4.8 10.0  4.6
Range, years 0.3 17.0 0.2 17.0
Sex, n (%)
Male 37 (48.1) 35 (46.7)
Female 40 (51.9) 40 (53.3)
Race, n (%)
White 26 (33.8) 36 (48.0)
Black or African American 17 (22.1) 13 (17.3)
Asian 8 (10.4) 11 (14.7)
Other 26 (33.8) 15 (20.0)
Diagnosis, n (%)
PCG 22 (28.6) 23 (30.7)
Non-PCG, classification 55 (71.4) 52 (69.3)
Juvenile open-angle glaucoma 13 (16.9) 13 (17.3)
Ocular hypertension 12 (15.6) 15 (20.0)
Infantile aphakic 11 (14.3) 7 (9.3)
open-angle glaucoma
Secondary childhood 6 (7.8) 2 (2.7)
glaucoma
Traumatic glaucoma 4 (5.2) 4 (5.3)
Glaucoma suspect 3 (3.9) 3 (4.0)
Primary glaucomas with profound 3 (3.9) 2 (2.7)
ocular anomalies
Lens-related glaucoma 1 (1.3) 3 (4.0)
Primary glaucomas associated with 1 (1.3) 1 (1.3)
systemic diseases
Glaucoma associated with 1 (1.3) 0
increased venous pressure
Ocular hypertension after 0 1 (1.3)
lensectomy for cataracts
Pigmentary glaucoma 0 1 (1.3)
Baseline IOP category, n (%)
\27 mm Hg 59 (76.6) 58 (77.3)
27 31 mm Hg 11 (14.3) 11 (14.7)
.31 mm Hg 7 (9.1) 6 (8.0)
Mean  SD 24.7  4.6 24.2  4.0
Range 20 47 20 37
IOP, intraocular pressure; PCG, primary congenital glaucoma; SD,
standard deviation.

Journal of AAPOS