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.

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, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Of 1259 cases of paediatric glaucoma presenting at our centre over 5 years, 59 children (%) were diagnosed with SIG. Of these, 51 (87%) had been prescribed topical steroids for vernal keratoconjunctivitis (VKC). The median duration of steroid use was 18 months (range 1 month to 8 years). Also, 82% of children with VKC had been prescribed steroids by the treating ophthalmologist and 52% had been on topical steroids for >1 year. Glaucomatous optic neuropathy was the cause of blindness in % (22/59) and low vision in % (14/59) children. And 27% (16/59) were unilaterally blind at presentation.

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

After the plate is attached to the globe, the tube is laid across the cornea and cut with a sharp scissors to create a beveled edge with the opening toward the cornea. The tube should extend approximately to 3 mm into the anterior chamber to minimize the risk of tube-cornea touch or retraction out of the anterior chamber. A 23-gauge needle is used to create a track through which the tube is inserted into the anterior chamber just anterior and parallel to the iris. The tube may be secured to the sclera a few millimeters anterior to the plate with 7- 0 or 8-0 Vicryl suture. This suture helps to stabilize the tube and should not be tight; otherwise, it will restrict flow in valved devices.

Steroid induced glaucoma pdf

steroid induced glaucoma pdf

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

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