Stem Cell Treatment for Glaucoma

Stem Cell Treatments for Glaucoma are currently available at SIRM

GLAUCOMA

Stem cell treatment for glaucoma

Glaucoma is an eye disorder in which the optic nerve suffers damage, permanently damaging vision in the affected eye(s) and progressing to complete blindness if untreated. It is often, but not always, associated with increased pressure of the fluid in the eye (aqueous humour). The term 'ocular hypertension' is used for cases having constantly raised intraocular pressure (IOP) without any associated optic nerve damage. Conversely, the term 'normal' or 'low tension glaucoma' is suggested for the typical visual field defects when associated with a normal or low IOP.

The nerve damage involves loss of retinal ganglion cells in a characteristic pattern. There are many different subtypes of glaucoma, but they can all be considered a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma. One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.

Glaucoma can be divided roughly into two main categories

  • open angle: Open angle, chronic glaucoma tends to progress at a slower rate and patients may not notice they have lost vision until the disease has progressed significantly.
  • closed angle: Closed angle glaucoma can appear suddenly and is often painful; visual loss can progress quickly, but the discomfort often leads patients to seek medical attention before permanent damage occurs.

 

Stem Cell Treatment for Glaucoma and stem cell therapy.

Stem Cell treatment studies and stem cell protocols from the NIH database:

Related Articles Multimodal characterization of a novel mutation causing vitamin B6-responsive gyrate atrophy. Ophthalmic Genet. 2018 08;39(4):512-516 Authors: Cui X, Jauregui R, Park KS, Tsang SH Abstract PURPOSE: Gyrate atrophy (GA) is a rare chorioretinal degeneration that results in the deterioration of night and peripheral vision, eventually leading to blindness. The disorder is caused by mutations in the gene encoding ornithine aminotransferase (OAT), causing increased levels of plasma ornithine. Treatment revolves around lowering plasma ornithine levels, with vitamin B6 supplementation being the preferred treatment. Nevertheless, most patients do not respond to this therapy. Here, we report a rare case of vitamin B6-responsive GA caused by a novel mutation in OAT and characterize the presentation with multimodal imaging. METHODS: This is a single-patient case report with a clinical diagnosis based on history, multimodal retinal imaging, laboratory findings, and DNA sequencing analysis. We include a 3D structure prediction of the novel mutant protein. RESULTS: DNA sequencing analysis demonstrated that there is a homozygous, novel variant c.473A>C: p.Y158S in OAT. Upon undergoing two weeks of vitamin B6 supplementation, the patient exhibited a 28.5% reduction in plasma ornithine levels. In a follow-up visit two years later, plasma ornithine levels were reduced by 24.1% from the levels at initial presentation and disease progression was retarded based on clinical findings. CONCLUSION: One novel homozygous missense mutation in OAT was identified and considered to be pathogenic in a patient with GA. The response for the vitamin B6 supplementation was positive, which is rare in all the GA cases reported in the literature. Our data suggests that further studies regarding the relationship between genotype and responsiveness to vitamin B6 should be conducted. PMID: 29757052 [PubMed - indexed for MEDLINE]
Read more...
Related Articles The auroKPro versus the Boston type I Keratoprosthesis: 5-year Clinical Outcomes in 134 Cases of Bilateral Corneal Blindness. Am J Ophthalmol. 2019 Mar 21;: Authors: Basu S, Serna-Ojeda JC, Senthil S, Pappuru RR, Bagga B, Sangwan V Abstract PURPOSE: To compare the clinical outcomes of Boston type I keratoprosthesis (Boston Kpro) with its low-cost version, the auroKPro. DESIGN: Retrospective comparative Case series. METHODS: This study included 134 eyes of 130 patients with severe bilateral corneal blindness but with wet ocular surfaces. The patients underwent either Boston Kpro (n=78) or auroKPro (n=56) implantation based on the device availability and patient's affordability. The primary outcome measures were anatomical retention (defined as absence of device extrusion, exchange or explantation) and functional recovery of 20/200 or better visual acuity at yearly time-points until 5-years of follow-up. RESULTS: Limbal stem cell deficiency was the most common indication (60.5%) for surgery, followed by multiple failed grafts (35%). Both groups were comparable at baseline with respect to indications for surgery and associated ocular co-morbidities (p>0.05). The overall anatomical retention rates were similar in the Boston Kpro (55/78, 70.5%) and auroKPro (35/56, 62.5%) groups (p=0.11). Kaplan-Meier survival rates at 5-years of follow-up were greater for the Boston Kpro with respect to both anatomical retention (63±6% vs. 43.4±10%, p=0.057) as well as functional recovery (42.4±6% vs.32.2±7%, p=0.345), but these differences were not statistically significant. Complications like intra-operative device breakage (7%) and post-operative extrusions (12.5%) were significantly more common with the auroKPro (p=0.023). CONCLUSIONS: Both the auroKPro and the Boston Kpro are effective treatment options for patients with severe bilateral corneal blindness. The auroKpro can be considered as an alternative to the Boston Kpro when affordability or availability of the Boston Kpro is a limiting factor. PMID: 30905723 [PubMed - as supplied by publisher]
Read more...

Quick Contact Form