Steroid induced glaucoma pdf

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandrosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Nadia: Sorry for your troubles. You have just described the course of a steroid responder. Your pressure was fine for the first few weeks, but after being on a corticosteroid for several weeks your pressure began to rise. If inflammation is well controlled, most surgeons stop the steroid or switch to a weaker steroid if the pressure is hard to control. If you are on a non-steroidal anti inflammatory (NSAID), it makes it easer to get off of the steroid since these drops will still help control inflammation when the steroid is stopped. Sometimes it takes several months for the steroid pressure elevation to resolve. During that time, maximum medical management is attempted. If a patient already has weakened nerves from glaucoma, sometimes a glaucoma surgery must be used to lower the pressure and protect vision.
God Bless,
Gary Foster

Q: Please, explain the use of calcium channel blockers in glaucoma treatment. Do they replace other medications such as beta-blockers or are they used in conjunction with other glaucoma medication? Is it more dangerous to the patient to use calcium channel blockers when the patient is being treated for other health problems such as heart disease?
A: Calcium channel blockers represent an entirely new approach to the treatment of glaucoma. Hopefully, the advent of these drugs marks only the beginning of a trend in finding new approaches to the treatment of glaucoma over the coming years.
  Previously, the only form of treatment of glaucoma has involved lowering intraocular pressure (IOP), even when IOP is normal to begin with. Although the evidence is not all in yet, calcium channel blockers have been reported to increase blood flow to the eye and to stabilize the visual field. Thus, instead of lowering IOP (although they appear to do this also), calcium channel blockers increase the resistance of the eye to glaucomatous damage. Because they represent an entirely new approach to the treatment of glaucoma, they do not replace other medications that are used in conjunction with them.
  There are different types of calcium channel blockers. Some primarily affect the strength with which the heart contracts, while others affect peripheral blood vessels, making them dilate so that more blood can pass through. The calcium channel blockers used in the treatment of glaucoma ideally would be those which increase blood flow to the brain, since the eye and the brain share a common blood supply.
  It remains to be determined just which patients will be helped and which will not be helped, or even perhaps harmed, by calcium channel blockers. Calcium channel blockers can also lower blood pressure, and a low blood pressure predisposes to glaucomatous damage. Therefore, we do not use these drugs at the present time in patients who have low blood pressure, but only in those with normal or high blood pressure. The patient's internist or family physician should be consulted with regard to the treatment plan.

The most common side effect of topical corticosteroid use is skin atrophy. All topical steroids can induce atrophy, but higher potency steroids, occlusion, thinner skin, and older patient age increase the risk. The face, the backs of the hands, and intertriginous areas are particularly susceptible. Resolution often occurs after discontinuing use of these agents, but it may take months. Concurrent use of topical tretinoin (Retin-A) % may reduce the incidence of atrophy from chronic steroid applications. 30 Other side effects from topical steroids include permanent dermal atrophy, telangiectasia, and striae.

Steroid induced glaucoma pdf

steroid induced glaucoma pdf

The most common side effect of topical corticosteroid use is skin atrophy. All topical steroids can induce atrophy, but higher potency steroids, occlusion, thinner skin, and older patient age increase the risk. The face, the backs of the hands, and intertriginous areas are particularly susceptible. Resolution often occurs after discontinuing use of these agents, but it may take months. Concurrent use of topical tretinoin (Retin-A) % may reduce the incidence of atrophy from chronic steroid applications. 30 Other side effects from topical steroids include permanent dermal atrophy, telangiectasia, and striae.

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