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Thursday, 28 November 2013

Glaucoma – The Causes

Glaucoma is a medical condition of an eye disease as result of the damage of the nerve of eye’s optic over time. If left untreated, it can lead to permanently vision impair and blindness.
A. Causes
1. Gene
a. MYOC, CYP1B1, and FOXC1 mutations
In primary Glaucoma, Matrix metalloproteinases (MMPs) play an important role in remodeling of the extracellular matrix during development and growth of various tissues including the eye and the defect of MMPs (MMP1 rs1799750 (-1607 1G/2G) and MMP9 rs17576 polymorphisms) might be of value as potential gender-dependent risk factors for developing POAG and PACG, respectively, in the Pakistan’s study(6). Other study indicated that LTBP2 gene mutations in north Indian patients with PCG are not involved in the pathogenesis of primary congenital glaucoma in our patients. Thus, it is important to screen other glaucoma-associated loci and genes for involvement in congenital glaucoma in cases that are either negative or heterozygous for MYOC, CYP1B1, and FOXC1 mutations to have better insight into the disease pathogenesis(7).
b. Connective tissue growth factor (CTGF)
The most critical risk factor for optic nerve damage in cases of primary open-angle glaucoma (POAG) is an increased intraocular pressure (IOP) caused by a resistance to aqueous humor outflow in the trabecular meshwork (TM). According to the study by the University of Regensburg, the effects of CTGF on IOP appear to be caused by a modification of the TM actin cytoskeleton. CTGF-overexpressing mice provide a model that mimics the essential functional and structural aspects of POAG and offer a molecular mechanism to explain the increase of its most critical risk factor(8).
c. Alterations of this serine protease
Angle-closure glaucoma (ACG) is a subset of glaucoma affecting 16 million people. According to the study by the The Jackson Laboratory, alterations of this serine protease may contribute to a spectrum of human ocular conditions including reduced ocular size and ACG(9).
2. Iactive congenital syphilitic interstitial keratitis
Iterstitial keratitis(IK) is defined as a condition of corneal scarring as a result of chronic inflammation of corneal stroma. According to the study, there is a report of 35 cases of secondary glaucoma due to congenital syphilitic interstitial keratitis. In four cases which had no opacities in the cornea, but with positive serologic reaction for syphilis, the characteristic goniscopical features such as peripheral anterior synechia, pigment deposits in the trabeculum, and irregularity of iris configuration as observed commonly in cases with inactive congenital interstitial syphilitic keratitis(10).
3. Anatomical disorder
Chronic angle-closure glaucoma is the commonest form of glaucoma in Sino Mongaloid populations. It is an anatomical disorder of the anterior segment of the eye characterised by permanent closure of part of the filtration angle as a result of iris apposition to the trabecular meshwork. According to the study by Radcliffe Infirmary NHS Trust, two pathways lead to this condition: recurrent pupillary block and “creeping” angle closure(11).
4. Atypical ocular ischaemia
Causes of low intraocular pressure in untreated glaucoma can be due to ciliary shut down, retinal detachment, post filtering surgery and ocular ischaemia. There is a report of a case of bilateral primary angle-closure glaucoma with atypical features of ocular ischaemia(12).
5. Other causes
In the study to evaluate the incidence of glaucoma in the first 275 consecutive eyes that underwent DMEK for Fuchs endothelial dystrophy (260 eyes) or bullous keratopathy (15 eyes), showed that overall, 18 eyes (6.5%) showed postoperative glaucoma after DMEK. Seven eyes (2.5%) had an exacerbation of a pre-existing glaucoma. Eleven eyes (4%) presented with a de novo IOP elevation, associated with air bubble-induced mechanical angle closure (2%), steroid response (0.7%), or peripheral anterior synechiae (0.4%), or without detectable cause (0.7%). Two eyes (0.7%) required glaucoma surgery after DMEK. At 6 months, all eyes had a BCVA of ≥20/40 (≥0.5), and 81% reached ≥20/25 (≥0.8) (n = 16); mean ECD was 1660 (± 554) cells/mm(2) (n = 15) (P > .1)(13).
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