DƯỢC LÍ Goodman & Gilman's The Pharmacological Basis of Therapeutics 12th, 2010

Table 64–7
Autonomic Drugs for Ophthalmic Use (Continued)
DRUG CLASS (TRADE NAME) FORMULATION INDICATIONS FOR USE OCULAR SIDE EFFECTS
Sympathomimetic agents
Dipivefrin (AKPRO) 0.1% solution Glaucoma Photosensitivity, conjunctival ,
hyperemia hypersensitivity
Phenylephrine (AK-DILATE, 0.12%, 2.5%, and Mydriasis,
MYDFRIN, NEO-SYNEPHRINE, 10% solution vasoconstriction,
others)
decongestion
Apraclonidine (IOPIDINE) 0.5% and Ocular hypertension
1% solution
Brimonidine 0.1%, 0.15%, and Glaucoma, ocular Same as for dipivefrin
(ALPHAGAN-P, others) 0.2% solution hypertension
Naphazoline (AK-CON, 0.012%, 0.03%, Decongestant
ALBALON, NAPHCON, others) and 0.1% solution
Tetrahydrozoline (ALTAZINE, 0.05% solution Decongestant
MURINE TEARS PLUS, VISINE,
others)
α and β adrenergic antagonists
Betaxolol ( 1
-selective)
(BETOPTIC, BETOPTIC-S, others) 0.25% and 0.5%
suspension
Carteolol ()(OCUPRESS, others) 1% solution
Levobunolol () (BETAGAN, 0.25% and 0.5% Glaucoma, ocular
others) solution hypertension
Metipranolol ()
0.3% solution
(OPTIPRANOLOL, others)
Timolol () (TIMOPTIC, 0.25% and 0.5%
TIMOPTIC XE, BETIMOL, others) solution and gel
a
Off-label use. Refer to the Physicians’ Desk Reference for Ophthalmic Medicines for specific indications and dosing information. b Mydriasis and
cycloplegia, or paralysis of accommodation, of the human eye occurs after one drop of atropine 1%, scopolamine 0.5%, homatropine 1%, cyclopentolate
0.5% or 1%, and tropicamide 0.5% or 1%. Recovery of mydriasis is defined by return to baseline pupil size to within 1 mm. Recovery of
cycloplegia is defined by return to within 2 diopters of baseline accommodative power. The maximal mydriatic effect of homatropine is achieved
with a 5% solution, but cycloplegia may be incomplete. Maximal cycloplegia with tropicamide may be achieved with a 1% solution. Times to development
of maximal mydriasis and to recovery, respectively, are: for atropine, 30-40 minutes and 7-10 days; for scopolamine, 20-130 minutes and
3-7 days; for homatropine, 40-60 minutes and 1-3 days; for cyclopentolate, 30-60 minutes and 1 day; for tropicamide, 20-40 minutes and 6 hours.
Times to development of maximal cycloplegia and to recovery, respectively, are: for atropine, 60-180 minutes and 6-12 days; for scopolamine,
30-60 minutes and 3-7 days; for homatropine, 30-60 minutes and 1-3 days; for cyclopentolate, 25-75 minutes and 6 hours to 1 day; for tropicamide,
30 minutes and 6 hours.
Study Group, 1998a; Collaborative Normal-Tension Glaucoma Study
Group, 1998b). Despite overwhelming evidence that IOP reduction is
a helpful treatment, at present the pathophysiological processes involved
in glaucomatous optic nerve damage and the relationship to aqueous
humor dynamics are not understood.
Current pharmacotherapies are targeted at decreasing the
production of aqueous humor at the ciliary body and increasing outflow
through the trabecular meshwork and uveoscleral pathways.
There is no consensus on the best IOP-lowering technique for glaucoma
therapy. Currently, a National Eye Institute–sponsored clinical
trial, the Collaborative Initial Glaucoma Treatment Study
(CIGTS), aims to determine whether it is best, in terms of preservation
of visual function and quality of life, to treat patients newly
diagnosed with open-angle glaucoma with filtering surgery or
medication. Initial results showed no difference in disease progression
rates between the two treatment groups at 5 years (Lichter
et al., 2001), but after 9 years, more subjects (25.5% versus 21.3%)
had visual field loss in the medicine arm than in the surgery arm of
the trial (Musch et al., 2009).
The CIGTS study aside, a stepped medical approach depends
on the patient’s health, age, and ocular status, with knowledge of systemic
effects and contraindications for all medications. Recall that:
• young patients usually are intolerant of miotic therapy secondary
to visual blurring from induced myopia
• direct miotic agents are preferred over cholinesterase inhibitors in
“phakic” patients (i.e., those patients who have their own crystalline
lens) because the latter drugs can promote cataract formation