To Treat or Not to Treat
LEO SEMES, OD, FAAO
her comprehensive eye examination, a 42-year-old African-American female was found
to have elevated intraocular pressure in each eye. This is a diagnostic conundrum
even before considering
the No. 1 glaucoma risk factor elevated IOP. Considering that elevated IOP
is the most important risk factor in glaucoma development, ocular hypertension (OHT),
primary open angle glaucoma (POAG) and secondary glaucomas are all possible diagnoses.
On follow-up visits the patient showed IOP readings between 24 mmHg and 36 mmHg
at varying times of day.
Additional findings revealed she had non-contributory medical
and family history. Her pachy-metry readings were 623μ and 638μ in the
right and left eyes respectively. Two visual field results were clean and repeatable
over a three-week span. The optic disc size was average with healthy rim tissue
and without retinal nerve fiber layer defects in each eye.
With normal disc and field findings, the diagnosis would be OHT.
Is treatment necessary?
A risk calculator (GRC) was published and validated based on data
from the ocular hypertension treatment study (OHTS). This model (available at discoveriesinsight.org),
the first quantitative assessment tool for ocular hypertensive patients, takes into
account structural and functional risk factors: IOP, CCT, age, C/D ratio, PSD and
diabetic status. An electronic version is available from Pfizer.
The calculator gives a risk for the conversion to glaucoma over
the next five years. One guideline is that when the risk is greater than 15 percent,
treatment would be beneficial. Given her relatively young age and the GRC result
recommending treatment, we decided to try to reduce her risk by recommending IOP-lowering
We began with latanoprost 0.005%, (Xalatan, Pfizer) evening dosing
and saw the patient three weeks later. Her IOP failed to respond, prompting an additional
three-week trial. When this additional period showed no response, we sampled travoprost
0.004% (Travatan, Alcon). Again with two three-week trial periods, the IOP remained
in the low 30s. While there are innumerable influences on IOP, because the IOP failed
to respond to either of these prostaglandin analogs (PA), we tried the remaining
member of the class, bimatoprost 0.03%, (Lumigan, Allergan). Following the first
three-week trial of evening dosing, the IOP reading at mid-morning was 22 mmHg in
each eye. This was repeatable three weeks later, and we wrote her a prescription.
One of the potential barriers to the lipid-receptor family of
IOP-lowering medications may be relatively thicker corneas. This may have been the
case with a patient whose CCT is > 600μ in each eye. CCT may be a valuable
indicator of risk for conversion from OHT to glaucoma and optic disc damage for
those who have thinner CCT (<555μ in the OHTS). Whether a thicker CCT (>588μ
in the OHTS) may be protective against glaucomatous damage remains to be proven.
What are the lessons from this case? Because IOP is the greatest
risk factor for developing glaucomatous damage, lowering it seemed essential because
it was >30 mmHg. Second, when she failed to respond to the first PA, we decided
to switch within the class rather than add medication. Finally, the GRC offered
new insights to potential clinical conundrums regarding for whom to offer treatment.
A recent comparison of glaucoma specialists with the risk calculator
suggests that glaucoma treatment recommendations would benefit from more exact methods
for determining those OHT patients who will convert to glaucoma.
For references, please visit www.clspectrum.com/references.asp
and click on document #134.
Dr. Semes is an associate
professor at the University of Alabama at Birmingham School of Optometry.
Contact Lens Spectrum, Issue: January 2007