Drug – bio-affecting and body treating compositions – Lymphokine – Interferon
Patent
1998-08-24
2000-07-11
Fitzgerald, David L.
Drug, bio-affecting and body treating compositions
Lymphokine
Interferon
424 854, 424 856, A61K 3821
Patent
active
060868694
DESCRIPTION:
BRIEF SUMMARY
TECHNICAL FIELD
The present invention relates to a novel remedy or preventive which is useful for retinal edema, and particularly for cystoid macular edema.
BACKGROUND ART
Vision is the most important of the senses, and diseases affecting visual function, such as reduced vision or blindness are important physical disabilities. In particular, it is expected that diseases affecting visual function will increase with age as an anticipated problem related to an aging society. In treating a patient whose daily life has been hindered, the importance of improving the quality of life (QOL) of the patient has been recently proposed. In ophthalmologic disease, improving and maintaining visual function are essential elements for improving QOL, hence establishing a therapy for achieving this is an exigency.
Serious reduced visual acuity or blindness can be caused by various factors, and some direct factors are chorioretinopathy such as retinal circulatory obstruction, inflammation, atrophy, and retinal detachment. Therapies adopted for these diseases include certain drug therapies, photocoagulation using laser, and vitreous surgery; however the performance of these has not been satisfactory, and thus other therapies are eagerly awaited. Although drug therapies have some worthy advantages, that is, reduced invasiveness and ease of administration compared with photocoagulation and vitreous surgery, which are inevitably invasive, only a few useful drugs are currently available.
On the other hand, progress of recent basic and clinical studies has clarified pathologically chorioretinopathy, that is, impairment of nerve fiber and obstruction of retinal circulation, and morbidity and pathology of the retinal pigment epithelium, as well as morbidity of the visual cells in the retina.
Among them, it is known that the occurrence of retinal edema directly results in visual loss, and the following mechanism has been proposed. The retina has blood-retinal barriers composed of tight junctions of endothelial cells of a retinal capillary and epithelial cells of the retinal pigment. These inner and outer blood-retinal barriers selectively regulate the transport of materials and water from blood to extracellular cavities of nerve cells. If these barriers are injured by any occasion, blood and exudate will deflux to the extracellular cavities of the retina. The defluxed water and the like are egested by a pumping effect of the retinal pigment of epithelial cells, vascular endothelial cells, and Muller's cells. If they are defluxed in amounts larger than the pumping capacity they are stored in the exterior of the cells causing the retinal edema.
The retina has a thin region consisting of only an outer nuclear layer, which is called a fovea, at the region of the macula, and an inner nuclear layer and a ganglion cell layer lie on the periphery. A non-vascular region lies in the center, and the retina has a larger thickness on its periphery. The central photoreceptor cells have long axons connecting with the cells in the inner nuclear layer. The layer of the axons of the photoreceptor cells corresponds to Henle's fiber layer lying in the outermost layer of the outer plexiform layer.
The Henle's fiber layer is a convergence of photoreceptor cell axons radially distributing from the fovea. In the reticular layers at the other portions, axons intertwine with each other in various directions, whereas in the macula section an interstitial gap readily becomes larger when the exudate is stored, and the increased gap causes further inflow of the exudate. Such storing of a large amount of exudate in the macula section in the retina is called cystoid macular edema (CME).
The macula section is the most important section for sight, and prolonged edema causes progressive obstruction of nerve fibers and visual cells (cell death), atrophy of the retinal pigment epithelium, and thus external obstruction of visual function. If the inner limiting membrane of the cyst including the fovea breaks, a lamellar macular hole will be formed. Further progression
REFERENCES:
patent: 5721206 (1998-02-01), Tobe et al.
patent: 5846526 (1998-12-01), Cummins
Gillies, M. C. (1996) Invest. Ophthalmol. Vis. Sci 37(3): S590, abst. No. 2720-B565, Apr. 1996.
Sanchez Roman, J., et al. (1996) Rev. Clin. Esp. 196 (5): 293-98, May 1996.
Tata, F., et al. (1988) Rec. Prog. Med. (Italy) 79 (3): 135-37, Mar. 1998.
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Kijima Atsushi
Sone Saburo
Takahashi Kanji
Utsumi Jun
Uyama Masanobu
Fitzgerald David L.
Miller Austin R.
Toray Industries Inc.
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