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Ocular Hypertension: When to Treat?

Ocular Hypertension: When to Treat?

Figure
Figure

Glaucoma is
the leading
cause of
blindness in
the United
States.1Nearly 3 million
persons have the disease,
and about 100,000 new
cases are diagnosed each
year.1 Between 3 and 6 million
Americans are thought
to be at increased risk for
glaucoma because of elevated
intraocular pressure
(IOP).2

To treat glaucoma, the
IOP must be lowered by either
pharmacologic or surgical
intervention to reduce
aqueous humor production
or to increase its outflow.3
Although optic nerve head
and optic nerve fiber layer
imaging have enhanced
the diagnosis of glaucoma,4,5
the question of when
to begin treatment in a patient
with ocular hypertension
(and in whom an elevated
IOP is the only sign
of possible glaucomatous
damage) has gone largely
unanswered.

Some practitioners
postpone therapy and
monitor patients regularly.
The rationale for this approach
is that withholding
treatment spares patients
the inconvenience of taking
medication or the risks
of surgery. In addition, the
potentially serious ocular
and systemic side effects
that are associated particularly
with older agents,
such as epinephrine and
β-blockers, and the financial
burden of medication
can be avoided. A recent
study found that the cost
of maximum, multipledrug
glaucoma therapy
can consume up to 11% of
an elderly patient's annual
income.6

Physicians who prefer
to initiate treatment sooner
point to histologic studies
of patients with ocular hypertension
who sustained a
diffuse loss of 40% of optic
nerve fibers even though
their visual fields remained
normal.7Thus, by the time
evidence of glaucoma damage
is documented, significant
optic nerve fiber loss
has already occurred and
the involved nerve fibers
may be even more susceptible
to damage.

AN IMPORTANT
NEW STUDY

The results of the recent
Ocular Hypertension
Treatment Study (OHTS)
reassure physicians of the
benefit of early medical intervention
in patients who
are at moderate to high
risk for glaucoma. Further,
the results indicate that
this approach may prevent
the disease.8

The multicenter study
included 1636 patients between
the ages of 40 and 80
years who had elevated
IOP (24 mm Hg or greater
in at least 1 eye) and no
other signs of glaucoma.
Their IOP was between 24
and 32 mm Hg in 1 eye and
between 21 and 32 mm Hg
in the other eye. Half the
group were randomly assigned
to receive daily
pressure-lowering eyedrops;
the other half were
given no medication and
observed. The IOP of the
medicated patients decreased
by 22.5% 9.9%.

After 5 years, the cumulative
probability of primary
open-angle glaucoma
in those who used pressure-
lowering eyedrops
was reduced by 60%. Glaucoma
developed in 36 patients
(4.4%) in the medication
group and in 89
patients (9.5%) in the observation
group. The results
clearly demonstrate that
treatment delays or prevents
glaucomatous visual
field loss, optic nerve damage,
or both. Furthermore,
patients in the medication
group reported no adverse
ocular or systemic symptoms
associated with therapy;
this suggests that the
pressure-lowering drops
available today, such as selective
α2-adrenergic agonists,
prostaglandins,
prostamide analogs, and
carbonic anhydrase inhibitors,
are safe and well
tolerated.

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