From Secretion to Glaucom

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In a six-month multicentric, randomized controlled trial, bimatoprost proved to be statistically and clinically superior to timolol in lowering IOP in patients with glaucoma or ocular hypertension. The most frequent side effect was trace-to-mild conjunctival hyperemia. Changes in iris pigmentation were reported in 1. A multicenter, randomized, investigator-masked, parallel-group trial bimatoprost provided lower mean pressures than latanoprost at every time point throughout the study and was statistically superior in achieving low target pressures.

Bimatoprost is available in 0.

Aqueous Humor Flow and Function

It does not require refrigeration to maintain stability. Travaprost is a synthetic prostaglandin F 2a analogue. Its chemical name is isopropyl Z [ 1 R,2 R,3 R,5 S -3,5-dihydroxy[ 1 E,3 R hydroxy[ a,a,a-trifluoro- m -tolyl oxy] butenyl]cyclopentyl]heptenoate. Following absorption into the eye, the free acid form of travaprost interacts with the endogenous FP prostanoid receptor, to enhance aqueous humor outflow and lower intraocular pressure IOP. It differs from other PGAs, which exhibit partial agonist activity, in that it is a full agonist at the PGF2a receptor.

In clinical studies, travaprost once daily produced reductions in IOP of between mmHg, from a mean baseline IOP of mmHg, an effect similar to that noted in the case of bimatoprost or latanoprost. Travaprost 0. In trial, it was observed that travaprost monotherapy had better lowering than dorzolamide 2.

Travaprost provides robust lowering of IOP with little diurnal fluctuation and results in low target pressures in a large percentage of the patients. It does not require refrigeration and protection from sunlight. Macular oedema, including cystoid macular oedema, is cited as a warning in the US product labeling for travaprost, as it is for other prostaglandin analogues. When a single therapy is not sufficient to lower the IOP, a combined treatment is indicated.

The combination therapy is also dependent upon the mechanism through which the components act to reduce IOP. When choosing an agent for combination therapy, it should be borne in mind that those drugs with complementary mechanisms of action usually work together. Fixed-combination products have the combined efficacy of two ocular hypotensive drugs and the convenience of a two-drug treatment regimen in a single container, which may aid patient adherence to treatment.

If a beta-blocking agent is used as an initial treatment, adding a topical CAI can provide an additional reduction in IOP. Available fixed-combination products consist of timolol 0.

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Brimonidine 0. A secondary choice of treatment of glaucoma is the use of laser therapy.

Argon laser trabeculoplasty ALT targets trabecular meshwork, where it allows the aqueous fluid to leave the eye more efficiently. The Nd : YAG neodymium-doped yttrium aluminium garnet laser can also be used in closed-angle glaucoma to make a small peripheral hole in the iris, to allow the aqueous fluid to flow easily. Selective laser trabeculoplasty SLT delivers energy to pigmented trabecular meshwork cells in a process called photo-thermolysis.

In this procedure, an opening is made in the trabecular meshwork, so that aqueous humor can drain into the sclera. Many patients can discontinue glaucoma medications after surgery. Approximately one-third of the trabeculectomy patients develop cataract within five years. If trabeculectomy fails, another type of surgery places a drainage tube Molteno tube in the eye, between the cornea and iris, which exits at the junction of the cornea and sclera. Cyclodestructive procedures, which lower IOP by destroying the ciliary body, are typically reserved for eyes, which are refractory to all other forms of therapy.

What Causes Glaucoma?

These procedures include cyclocryotherapy, cylcodiathermy and laser cyclophotocoagulation. In recent times, there has been an increased interest in complementary medicine. But very little research has been done on the majority of herbal remedies, with regard to their effect on glaucoma. There are several nutrients and botanicals that hold promise for the treatment of glaucoma, but most studies are preliminary, and larger, controlled studies are required.

Forskolin is a diterpine derivative of the plant Coleus forskohlii, which acts on adenylate cyclase catalytic subunit to increase intracellular cAMP. Gingko biloba extract has multiple beneficial actions, which will be helpful in the treatment of glaucoma, like increased ocular blood flow, antioxidant activity, platelet activating factor inhibitory activity, nitric oxide inhibition, and neuroprotective activity combine, suggesting that Gingko biloba extract could be used in the treatment of glaucoma.

In a recent trial in Italy, which was a randomized, placebo-controlled, double masked trial involving 27 patients, there was an improvement in the visual fields in-patient, with normal tension glaucoma after four weeks of treatment with Ginkgo biloba. Alpha lipoic acid, a powerful antioxidant, may be useful in glaucoma, because it reduces nerve cell damage from oxidative stress.

In China, the main herb-derived eye drops for glaucoma are pueraria flavonoids, areca seed extract, and alkaloids from erycibe Erycibe obtusifolia; dinggongteng aka baogongteng. These eye drops appear to work as well or better than pilocarpine, which is usually used as a comparative standard. Cannabinoids reduce intraocular pressure by enhancing uveoscleral outflow.

The development of formulation for ocular administration has not yet yielded a prescription medication. A number of potential strategies for the development of a novel therapy for glaucoma are: glutamate inhibition, NMDA receptor blockade, exogenously applied neurotrophins, open channel blockers, antioxidants, protease inhibitors and gene therapy. NMDA antagonist provides neuroprotection by blocking pathological increase in glutamate, which drives cell death by facilitating calcium entry into a cell.

Memantine, an N-methyl-D-aspartate subtype glutamate receptor antagonist is in the clinical stage of development, and, if there is proof of efficacy of memantine, it will change the treatment paradigm for glaucoma.

In addition to memantine, a number of other potential non-IOP lowering direct acting neuroprotective agents are shown to have an application in glaucoma. Many of these agents focus on other routes of overcoming glutamate cytotoxicity. Eliprodil: It is a non-competitive NMDA antagonist; providing protection from glutamate mediated cytotoxicity to retinal ganglion cells.

Riluzole: It is a presynaptic glutamate release inhibitor, which has shown to have potential neuroprotective utility. L-deprenyl: An inhibit apoptosis of serum deprived retrovirus-immortilised retinal ganglion cells in vivo, it can decrease the apoptosis index of primary mix retinal cells, when deprived of specific neurotropic factors.

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An example of a neuroprotective vaccine is R16, a peptide interphotoreceptor-retinoid binding protein derived from the RGC. Signal transducers and activators of transcription protein-3 STAT-3 play an important role in cell growth and differentiation.

They are considered important because the mRNA of this protein is upregulated in rats with glaucoma. Erythropoietin is a hematopoietic cytokine, which has been shown to possess remarkable tissue-protective and neuroprotective properties that may prevent further RGC death by inhibiting apoptosis. However, further studies are needed to fully evaluate the safety and efficacy of this neuroprotective agent in clinical trials.

Gene therapy represents an attractive approach for the treatment of eye diseases such as glaucoma. Inhibitors of apoptosis protein IAP can also reduce apoptosis by inhibiting caspase. Ocular administration of viral vectors produces localized retinal gene expression with reduced risks of side effects reported with systemic administration of viral vectors. Gene therapy delivering BIRC4 significantly promoted optic nerve axon survival in a chronic ocular hypertensive model of rat glaucoma. Blocking RGC apoptosis with caspase inhibitors represents a promising approach for treatment of human glaucoma.

Since the upregulation of iNOS-2 is harmful to neurons, its inhibition might have a neuroprotective effect. Although an unregulated level of NO can cause neuronal degeneration via apoptosis, a small amount of NO could inhibit apoptosis.

Survival of serum deprived pheochromocytoma PC cells was observed when treated with an NO donor. These results indicate that the cytoprotective effect of nipradilol in PC12 cell death was due to the caspase-3 inhibition mediated by NO-related S-nitrosylation and activation of protein kinase G. Glaucoma is a very serious eye disease that can lead to blindness if not treated early.

With early diagnosis and treatment, most patients with glaucoma can have their vision restored and enjoy a healthy life. The wide variety of topical effective antiglaucoma drugs that are available today, and a few others that are in the development stage, represent significant advancement in ocular therapeutics. Though these topical ophthalmic preparations have reduced the risk of systemic toxicity to quite an extent, their long-term use causes systemic as well as ocular toxicity.

Ideal drug candidates for glaucoma therapy will offer better IOP lowering efficacy with fewer side effects and provide additional means of vision sparing through direct protection of optic nerve. Despite new advances and techniques, it is observed that there is medically uncontrolled intraocular pressure.

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The ideal medication for this is not yet available. A patient with asthma, bradycardia, hazel eyes, cataracts, systemic allergy to sulfa drugs, and topical allergy to brimonidine might have to proceed with laser trabeculoplasty or glaucoma-filtering surgery. Research on more advanced antiglaucoma medications continues and promising new directions appear to be the Rho-kinase inhibitors, microtubule-disrupting agents, serotonergics and cannabimimetics. The research is being directed towards applying new molecular and cellular techniques to induce regeneration of mammalian central nervous axons.

This will be an important step in therapy for glaucomatous optic nerve atropy. National Center for Biotechnology Information , U. Journal List Indian J Pharmacol v. Indian J Pharmacol. Gupta , Galpalli Niranjan D. Agrawal , Sushma Srivastava , and Rohit Saxena 1.

Galpalli Niranjan D. Rohit Saxena 1 Dr. Author information Article notes Copyright and License information Disclaimer. Correspondence to: Dr. Gupta, E-mail: moc. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Abstract Glaucoma is a slow progressive degeneration of the retinal ganglion cells RGCs and the optic nerve axons, leading to irreversible blindness if left undiagnosed and untreated.

Keywords: Adrenergic blockers, carbonic anhydrase inhibitors, cholinergic agonists, intraocular pressure, prostaglandin analogs. Introduction Glaucoma is characterized by slow progressive degeneration of the retinal ganglion cells RGCs and the optic nerve axons, leading to increasing deterioration of the visual field.

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