To Treat or Not to Treat
BY LEO SEMES, OD, FAAO
During 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 medication.
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.