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Targeted preventive measures and advanced approaches in personalised treatment of glaucoma neuropathy.

Mozaffarieh M, Fraenkl S, Konieczka K, Flammer J - EPMA J (2010)

Bottom Line: It can also be improved by decreasing blood pressure over-dips.This can be achieved by gingko, dark chocolate, polyphenolic flavonoids occurring in tea, coffee or red wine and anthocyanosides found in bilberries as well as by ubiquinone and melatonin.This review describes the individual mechanisms which may be targeted by non-IOP lowering treatment based on our pathogenic scheme.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, University of Basel, Mittlere Strasse 91, CH-4031 Basel, Switzerland.

ABSTRACT
Glaucoma is a major cause of vision loss worldwide with nearly 8 million people bilaterally blind from the disease. This number is estimated to increase over the next 10 years. The key to preventing blindness from glaucoma is effective diagnosis and treatment. The classical glaucoma treatment focuses on intraocular pressure (IOP) reduction. Better knowledge of the pathogenesis has opened up additional therapeutical approaches often called non-IOP lowering treatment. Whilst most of these new avenues of treatment are still in the experimental phase, others are already used by some physicians. These new therapeutic approaches allow a more personalised patient treatment. Non-IOP lowering treatment includes improvements of ocular blood flow, particularly blood flow regulation. This can be achieved by improving the regulation of ocular blood flow (improving autoregulation) by drugs such as carbonic anhydrase inhibitors, magnesium or calcium channel blockers. It can also be improved by decreasing blood pressure over-dips. Blood pressure can be increased by an increase in salt intake or in rare cases by treatment with fludrocortisone. Experimentally, glaucomatous optic neuropathy can be prevented by inhibition of astrocyte activation, either by blockage of epidermal growth factor receptor or by counteracting Endothelin. Glaucomatous optic neuropathy can also be prevented by nitric oxide-2 synthase inhibition. Suppression of matrix metalloproteinase-9 inhibits apoptosis of retinal ganglion cells and tissue remodelling. Upregulation of heat shock proteins protects the retinal ganglion cells and the optic nerve head. Reduction of oxidative stress especially at the level of mitochondria also seems to be protective. This can be achieved by gingko, dark chocolate, polyphenolic flavonoids occurring in tea, coffee or red wine and anthocyanosides found in bilberries as well as by ubiquinone and melatonin. This review describes the individual mechanisms which may be targeted by non-IOP lowering treatment based on our pathogenic scheme.

No MeSH data available.


Related in: MedlinePlus

Normal optic disc. a Normal optic disc in a healthy person (left), in the eye of a cadaver (middle), and a histological section (right). b Glaucomatous atrophy of the optic disc. The eye of the patient is shown on the left, of a cadaver in the middle and a histological section in the right
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Fig1: Normal optic disc. a Normal optic disc in a healthy person (left), in the eye of a cadaver (middle), and a histological section (right). b Glaucomatous atrophy of the optic disc. The eye of the patient is shown on the left, of a cadaver in the middle and a histological section in the right

Mentions: For the past century glaucoma has been considered a disease for which diagnosis and treatment was focussed mainly on intraocular pressure. Large studies such as ‘The Ocular Hypertension Treatment Study’ or ‘The European Glaucoma Prevention Study’ recognised ocular hypertension as the most important factor for the development of primary open angle glaucoma. Because elevated intraocular pressure (IOP) was associated with the development of glaucoma, and reducing IOP, reduced the risk of visual field progression, IOP was considered a good surrogate for glaucoma treatment. The focus on IOP as the only risk factor, however, left several questions unanswered: Why do the majority of people with increased IOP not develop glaucomatous optic neuropathy (GON) (Fig. 1)? On the other hand, why do we see an increasing number of patients acquiring GON who have an IOP in the normal range? Why does reduction of IOP, whilst on the average improving prognosis, not stop progression in all patients? And why do some patients need a very low IOP, indeed sometimes an even unphysiological low IOP to stop progression of this disease? These questions can be answered when considering additional risk factors such as systemic hypotension or vascular dysregulation. The elucidation of these additional factors has lead to the investigation of non-IOP lowering treatment. Whether such treatment will be an adjunctive to the conventional IOP-lowering treatment (e.g. in patients with primary open angle glaucoma (POAG)) or whether it shall be used by itself (e.g. in patients with normal-tension glaucoma (NTG)) remains to be seen.Fig. 1


Targeted preventive measures and advanced approaches in personalised treatment of glaucoma neuropathy.

Mozaffarieh M, Fraenkl S, Konieczka K, Flammer J - EPMA J (2010)

Normal optic disc. a Normal optic disc in a healthy person (left), in the eye of a cadaver (middle), and a histological section (right). b Glaucomatous atrophy of the optic disc. The eye of the patient is shown on the left, of a cadaver in the middle and a histological section in the right
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3405319&req=5

Fig1: Normal optic disc. a Normal optic disc in a healthy person (left), in the eye of a cadaver (middle), and a histological section (right). b Glaucomatous atrophy of the optic disc. The eye of the patient is shown on the left, of a cadaver in the middle and a histological section in the right
Mentions: For the past century glaucoma has been considered a disease for which diagnosis and treatment was focussed mainly on intraocular pressure. Large studies such as ‘The Ocular Hypertension Treatment Study’ or ‘The European Glaucoma Prevention Study’ recognised ocular hypertension as the most important factor for the development of primary open angle glaucoma. Because elevated intraocular pressure (IOP) was associated with the development of glaucoma, and reducing IOP, reduced the risk of visual field progression, IOP was considered a good surrogate for glaucoma treatment. The focus on IOP as the only risk factor, however, left several questions unanswered: Why do the majority of people with increased IOP not develop glaucomatous optic neuropathy (GON) (Fig. 1)? On the other hand, why do we see an increasing number of patients acquiring GON who have an IOP in the normal range? Why does reduction of IOP, whilst on the average improving prognosis, not stop progression in all patients? And why do some patients need a very low IOP, indeed sometimes an even unphysiological low IOP to stop progression of this disease? These questions can be answered when considering additional risk factors such as systemic hypotension or vascular dysregulation. The elucidation of these additional factors has lead to the investigation of non-IOP lowering treatment. Whether such treatment will be an adjunctive to the conventional IOP-lowering treatment (e.g. in patients with primary open angle glaucoma (POAG)) or whether it shall be used by itself (e.g. in patients with normal-tension glaucoma (NTG)) remains to be seen.Fig. 1

Bottom Line: It can also be improved by decreasing blood pressure over-dips.This can be achieved by gingko, dark chocolate, polyphenolic flavonoids occurring in tea, coffee or red wine and anthocyanosides found in bilberries as well as by ubiquinone and melatonin.This review describes the individual mechanisms which may be targeted by non-IOP lowering treatment based on our pathogenic scheme.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, University of Basel, Mittlere Strasse 91, CH-4031 Basel, Switzerland.

ABSTRACT
Glaucoma is a major cause of vision loss worldwide with nearly 8 million people bilaterally blind from the disease. This number is estimated to increase over the next 10 years. The key to preventing blindness from glaucoma is effective diagnosis and treatment. The classical glaucoma treatment focuses on intraocular pressure (IOP) reduction. Better knowledge of the pathogenesis has opened up additional therapeutical approaches often called non-IOP lowering treatment. Whilst most of these new avenues of treatment are still in the experimental phase, others are already used by some physicians. These new therapeutic approaches allow a more personalised patient treatment. Non-IOP lowering treatment includes improvements of ocular blood flow, particularly blood flow regulation. This can be achieved by improving the regulation of ocular blood flow (improving autoregulation) by drugs such as carbonic anhydrase inhibitors, magnesium or calcium channel blockers. It can also be improved by decreasing blood pressure over-dips. Blood pressure can be increased by an increase in salt intake or in rare cases by treatment with fludrocortisone. Experimentally, glaucomatous optic neuropathy can be prevented by inhibition of astrocyte activation, either by blockage of epidermal growth factor receptor or by counteracting Endothelin. Glaucomatous optic neuropathy can also be prevented by nitric oxide-2 synthase inhibition. Suppression of matrix metalloproteinase-9 inhibits apoptosis of retinal ganglion cells and tissue remodelling. Upregulation of heat shock proteins protects the retinal ganglion cells and the optic nerve head. Reduction of oxidative stress especially at the level of mitochondria also seems to be protective. This can be achieved by gingko, dark chocolate, polyphenolic flavonoids occurring in tea, coffee or red wine and anthocyanosides found in bilberries as well as by ubiquinone and melatonin. This review describes the individual mechanisms which may be targeted by non-IOP lowering treatment based on our pathogenic scheme.

No MeSH data available.


Related in: MedlinePlus