Glaucoma medical therapy: Difference between revisions
| Line 21: | Line 21: | ||
* Less-selective [[sympathomimetic]]s like [[epinephrine]] and [[dipivefrin]] (Propine) increase outflow of [[aqueous humor]] through [[trabecular meshwork]] and possibly through uveoscleral outflow pathway, probably by a [[Beta-2-adrenoreceptor agonists|beta 2-agonist]] action. A two percent [[epinephine]] solution may be used [[topical]]ly to reduce [[IOP]] in open-angle glaucoma by reducing the production of [[aqueous humor]] by [[vasoconstriction]] of the [[ciliary body]] blood [[vessel]]s. | * Less-selective [[sympathomimetic]]s like [[epinephrine]] and [[dipivefrin]] (Propine) increase outflow of [[aqueous humor]] through [[trabecular meshwork]] and possibly through uveoscleral outflow pathway, probably by a [[Beta-2-adrenoreceptor agonists|beta 2-agonist]] action. A two percent [[epinephine]] solution may be used [[topical]]ly to reduce [[IOP]] in open-angle glaucoma by reducing the production of [[aqueous humor]] by [[vasoconstriction]] of the [[ciliary body]] blood [[vessel]]s. | ||
* [[Miotic agents]] ([[parasympathomimetic]]s) like [[pilocarpine]] work by contraction of the [[ciliary muscle]], tightening the [[trabecular meshwork]] and allowing increased outflow of the [[aqueous humor]]. | * [[Miotic agents]] ([[parasympathomimetic]]s) like [[pilocarpine]] work by contraction of the [[ciliary muscle]], tightening the [[trabecular meshwork]] and allowing increased outflow of the [[aqueous humor]]. | ||
* [[Carbonic anhydrase inhibitors]] like [[dorzolamide]] (Trusopt), [[brinzolamide]](Azopt), [[acetazolamide]] (Diamox) lower secretion of [[aqueous humor]] by inhibiting [[carbonic anhydrase]] in the [[ciliary body]]. | * [[Carbonic anhydrase inhibitors]] like [[dorzolamide]] (Trusopt), [[brinzolamide]] (Azopt), [[acetazolamide]] (Diamox) lower secretion of [[aqueous humor]] by inhibiting [[carbonic anhydrase]] in the [[ciliary body]]. | ||
====Cannabis==== | ====Cannabis==== | ||
Revision as of 17:09, 29 January 2013
|
Glaucoma Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Glaucoma medical therapy On the Web |
|
American Roentgen Ray Society Images of Glaucoma medical therapy |
|
Risk calculators and risk factors for Glaucoma medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Although intraocular pressure is only one major risk factors of glaucoma, lowering it via pharmaceuticals or surgery is currently the mainstay of glaucoma treatment. In Europe, Japan, and Canada laser treatment is often the first line of therapy. In the U.S., adoption of early laser has lagged, even though prospective, multi-centered, peer-reviewed studies, since the early '90s, have shown laser to be at least as effective as topical medications in controlling intraocular pressure and preserving visual field. Some studies suggest that acupuncture can be very helpful in the treatment of glaucoma[1].
Medical Therapy
Drugs
Intraocular pressure can be lowered with medication, usually eye drops. There are several different classes of medications to treat glaucoma with several different medications in each class.
Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate these, or to communicate with the treating physician to improve the drug regimen.
Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms. Ophthalmologists have debated whether glaucoma eye drops should initially be started in both eyes or in just one eye (a binocular or monocular trial), but it appears either strategy is reasonable when properly interpreted. [2]
The possible neuroprotective effects of various topical and systemic medications are also being investigated.
Commonly used medications
- Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous humor.
- Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and betaxolol decrease aqueous humor production by the ciliary body.
- Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous production and increasing uveo-scleral outflow.
- Less-selective sympathomimetics like epinephrine and dipivefrin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta 2-agonist action. A two percent epinephine solution may be used topically to reduce IOP in open-angle glaucoma by reducing the production of aqueous humor by vasoconstriction of the ciliary body blood vessels.
- Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humor.
- Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
Cannabis
Studies in the 1970s showed that marijuana, when smoked, lowers intraocular pressure.[3] In an effort to determine whether marijuana, or drugs derived from marijuana, might be effective as a glaucoma treatment, the US National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated that some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye. Many of these studies demonstrated that marijuana— or any of its components — could safely and effectively lower intraocular pressure more than a variety of drugs then on the market. In 2003, the American Academy of Ophthalmology released a position statement asserting that "no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of marijuana use to treat glaucoma compared with the wide variety of pharmaceutical agents now available."[3]
Major Studies
- Advanced Glaucoma Intervention Study (AGIS) - large American National Eye Institute (NEI) sponsored study designed "to assess the long-range outcomes of sequences of interventions involving trabeculectomy and argon laser trabeculoplasty in eyes that have failed initial medical treatment for glaucoma." It recommends different treatments based on race.
- Early Manifest Glaucoma Trial (EMGT)-Another NEI study found that immediately treating people who have early stage glaucoma can delay progression of the disease.
- Ocular Hypertension Treatment Study (OHTS) -NEI study findings: "...Topical ocular hypotensive medication was effective in delaying or preventing onset of Primary Open Angle Glaucoma (POAG) in individuals with elevated Intraocular Pressure (IOP). Although this does not imply that all patients with borderline or elevated IOP should receive medication, clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing POAG."
- Blue Mountains Eye Study "The Blue Mountains Eye Study was the first large population-based assessment of visual impairment and common eye diseases of a representative older Australian community sample." Risk factors for glaucoma and other eye disease were determined.
References
- ↑ Clinical application of acupuncture in ophthalmology. Dabov S; Goutoranov G; Ivanova R; Petkova N Acupunct Electrother Res 1985, 10 (1-2) p79-93
- ↑ Interpretation of uniocular and binocular trials of glaucoma medications: an observational case series,[1]
- ↑ 3.0 3.1 American Academy of Ophthalmology.Complementary Therapy Assessment: Marijuana in the Treatment of Glaucoma. Retrieved August 2, 2006.