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Biomedical subjects

Ruth Sapir-Pichhadze

Publications and source records attributed to Ruth Sapir-Pichhadze.

2 recordsLinked to original sources

[The medical treatment of glaucoma].

Chronic open angle glaucoma is a one of the leading causes of irreversible blindness. Elevated intraocular pressure is a major risk factor for the progression of this disease. At present, most patients suffering from open angle glaucoma have started medical therapy. The goal is to reduce the intraocular pressure to an individualized target pressure in an effort to delay the progression of damage to the optic nerve. Until a decade ago, topical beta-adrenergic antagonists, adrenergic agonists, miotics and oral carbonic anhydrase inhibitors comprised the common medications in use. In the past decade many new drugs have been introduced. These drugs exert less systemic side effects and are very effective in lowering the intraocular pressure and furthermore, are easier to comply with. These include: local carbonic anhydrase inhibitors, prostaglandin F2á analogues and á2 adrenergic selective agonists. Due to lack of consensus as to the initial medication of choice for the commencement of treatment, the traditional tendency to initiate treatment with a local beta adrenergic antagonist persists. This review attempts to familiarize the reader with the new arsenal of glaucoma medications.

Adrenergic Agonists↗

[Steroid induced glaucoma].

Steroid treatment has gained notoriety due to its tendency to induce multiple side effects, including a variety of ocular side effects. Administration of local, regional, inhalation or systemic steroids may induce the development of ocular hypertension, which might even result in subsequent open angle glaucoma. About one in every three people is considered a potential "steroid responder". A significant elevation of intraocular pressure might result in these patients in response to steroid treatment. Included in this group are patients with first degree relatives suffering from open angle glaucoma. Morphologic changes in the trabecular meshwork (which serves as the site of aqueous humor drainage from the eye) are suggested as the proposed mechanism through which steroid treatment results in glaucoma. Steroids are said to induce the expression of a gene that is located on chromosome 1 and is known as TIGR or GLCIA. its product is a protein called myocilin. Ocular hypertension secondary to steroid treatment is usually reversible, when treatment is limited to a period of less than 12 months. The fear of ocular hypertension, which is usually unnoticed by the patient, obligates regular ophthalmologic follow-up examinations, including tonometry, visual fields and optic disc examinations.

Chromosome Mapping↗