ReeCure

Macular Degeneration

Also called: Age-related macular degeneration (AMD) is a leading cause of vision loss in Americans aged 60 and older. It is a disease that destroys your sharp, central vision. You need central vision to see objects clearly and to do tasks such as reading and driving.

AMD affects the macula, the part of the eye that allows you to see fine detail. It does not hurt, but it causes cells in the macula to die. In some cases, AMD advances so slowly that people notice little change in their vision. In others, the disease progresses faster and may lead to a loss of vision in both eyes. Regular comprehensive eye exams can detect macular degeneration before the disease causes vision loss. Treatment can slow vision loss but it does not restore vision.

Retinitis Pigmentosa

Retinitis pigmentosa (RP) is a group of genetic eye conditions. In the progression of symptoms for RP, night blindness generally precedes tunnel vision by years or even decades. Many people with RP do not become legally blind until their 40s or 50s and retain some sight all their lives. Others go completely blind from RP and in some cases as early as childhood. Progression of RP is different in each case.

RP is a type of progressive retinal dystrophy, a group of inherited disorders in which abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina lead to progressive visual loss. Affected individuals first experience defective dark adaptation or nyctalopia (night blindness), followed by reduction of the peripheral visual field (known as tunnel vision) and sometimes loss of central vision, late in the course of the disease.

Signs

Mottling of the retinal pigment epithelium with black bone-spicule pigmentation is typically indicative (or pathognomonic) of retinitis pigmentosa. Other ocular features include waxy pallor of the optic nerve head, attenuation (thinning) of the retinal vessels, cellophane maculopathy, cystic macular edema and posterior subcapsular cataract.

Diagnosis

The diagnosis of retinitis pigmentosa relies upon documentation of progressive loss in photoreceptor function by electroretinography (ERG) and visual field testing. The mode of inheritance of RP is determined by family history. At least 35 different genes or loci are known to cause "nonsyndromic RP" (RP that is not the result of another disease or part of a wider syndrome).

Corneal ulcer

A corneal ulcer, or ulcerative keratitis, or eyesore is an inflammatory or an infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and the agrarian societies. In developing countries, children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become blind in both eyes, which may persist lifelong.

Corneal anatomy of the human

The cornea is a transparent structure that is part of the outer layer of the eye. It refracts light and protects the contents of the eye. The corneal thickness ranges from 450 to 610 micrometres and on an average 550 µm thick in caucasian eyes. In Indian eyes, the average thickness is slightly less at 510 µm. The trigeminal nerve supplies the cornea via the long ciliary nerves. There are pain receptors in the outer layers and pressure receptors are deeper.

Transparency is achieved through a lack of blood vessels, pigmentation, keratin, and through tight layered organization of the collagen fibers. The collagen fibers cross the full diameter of the cornea in a strictly parallel fashion and allow 99 percent of the light to pass through without scattering.

There are five layers in the human cornea, from outer to inner:

• Epithelium
• Bowman's layer
• Stroma
• Descemet's membrane
• Endothelium

The outer layer is the epithelium, which is 25 to 40 µm and five to seven cell layers thick. The epithelium holds the tear film in place and also prevents water from invading the cornea and disrupting the collagen fibers. This prevents corneal edema, which gives it a cloudy appearance. It is also a barrier to infectious agents. The epithelium sticks to the basement membrane, which also separates the epithelium from the stroma. The corneal stroma comprises 90 percent of the thickness of the cornea. It contains the collagen fibers organized into lamellae. The lamellae are in sheets which separate easily. Posterior to the stroma is Descemet's membrane, which is a basement membrane for the corneal endothelium. The endothelium is a single cell layer that separates the cornea from the aqueous humor.

Corneal healing

An ulcer of the cornea heals by two methods: migration of surrounding epithelial cells followed by mitosis (dividing) of the cells and introduction of blood vessels from the conjunctiva. Superficial small ulcers heal rapidly by the first method. However, larger or deeper ulcers often require the presence of blood vessels to supply inflammatory cells. White blood cells and fibroblasts produce granulation tissue and then scar tissue, effectively healing the cornea. The ulcer heals by the fourth day.

Superficial and deep corneal ulcers

Corneal ulcers are a common human eye disease. They are caused by trauma, particularly with vegetable matter, chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiae, corneal dystrophy and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa and chlamydia. Bacterial keratitis is caused by Staphylococcus aureus, Streptococcus viridans, Escherichia coli, Enterococci, Pseudomonas, Nocardia and many other bacteria.

Fungal keratitis causes deep and severe corneal ulcer. It is caused by Aspergillus sp., Fusarium sp., Candida sp., as also Rhizopus, Mucor and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes Zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual. Protozoa infection like Acanthamoeba keratitis is characterized by severe pain and is associated with contact lens users and swimming in pools. Chlamydia trachomatis can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and distichiasis (inturning of eye lashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

Symptoms

Corneal ulcers are extremely painful due to nerve exposure, and can cause tearing, squinting and vision loss of the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour) and redness of the eye. An axon reflex may be responsible for uveitis formation - stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine and acetylcholine.

Diagnosis

Diagnosis is done by direct observation under magnified view of slit lamp revealing the ulcer on the cornea. The use of fluorescein stain, which is taken up by exposed corneal stroma and appears green, helps in defining the margins of the corneal ulcer and can reveal additional details of the surrounding epithelium. Herpes simplex ulcers show a typical dendritic pattern of staining. Rose-Bengal dye is also used for supra-vital staining purposes, but it may be very irritating to the eyes. In descemetoceles, the Descemet's membrane will bulge forward and after staining will appear as a dark circle with a green boundary, because it does not absorb the stain. Doing a corneal scraping and examining under the microscope with stains like Gram's and KOH preparation may reveal the bacteria and fungi respectively. Microbiological culture tests may be necessary to isolate the causative organisms for some cases. Other tests that may be necessary include a Schirmer's test for keratoconjunctivitis sicca and an analysis of facial nerve function for facial nerve paralysis.

Bacterial corneal ulcer require intensive fortified antibiotic therapy to treat the infection. Fungal corneal ulcers require intensive application of topical anti-fungal agents. Viral corneal ulceration caused by herpes virus may respond to antivirals like topical acyclovir ointment instilled at least five times a day. Alongside, supportive therapy like pain medications are given, including topical cycloplegics like atropine or homatropine to dilate the pupil and thereby stop spasms of the ciliary muscle.

Superficial ulcers may heal in less than a week. Deep ulcers and descemetoceles may require conjunctival grafts or conjunctival flaps, soft contact lenses or corneal transplant. Proper nutrition, including protein intake and Vitamin C are usually advised. In cases of Keratomalacia, where the corneal ulceration is due to a deficiency of Vitamin A, supplementation of the Vitamin A by oral or intramuscular route is given. Drugs that are usually contraindicated in corneal ulcer are topical corticosteroids and anesthetics - these should not be used on any type of corneal ulcer because they prevent healing, may lead to superinfection with fungi and other bacteria and will often make the condition much worse.

We, at ReeCure offer you therapy using stem cells using our proprietary technology.

These stem cells could be of various types viz. Hematopoetic (CD 34+), Mesenchymal stem cells (MSCs) that are processed and isolated using Good Manufacturing (GMP) and Good Lab Practices (GLP) and in accordance with AABB standards.

After years of extensive research and systematic compilation and collation of relevant data (through its research division), Reelabs is now supremely confident of not only reversing the disease process of the affected patient but also improving the quality of life manifold. Stem cells produced by Reelabs are completely safe, non-toxic, easy to administer and totally devoid of side effects with an excellent probability of homing and engraftment with parent cell, tissue or organ. The eminent panel of scientists and researchers at Reelabs work exhaustively to design accurate treatment protocols that have yielded excellent results in most cases.

These stem cells are procured from various sources including bone marrow, cord blood fat etc. as per the requirement of the patient.

The stem cells can be given intravenously, intraocular or by sub-conjuctival routes.

The benefits of stem cells are follows:

• Regeneration of the affected tissue
• Repairs the damages tissue
• Improves vascularity wherever required
• Improves eyesight
• Improves general quality of life