"If you've ever been sleep-deprived, you've probably had a firsthand glimpse of the blood vessels in your eyes. But what you haven't seen—and what many eye care professionals cannot see as well as they would like—are the vessels closes"...
Mechanism of Action
Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Synthetic analogs such as triamcinolone are primarily used for their anti-inflammatory effects in disorders of many organ systems.
Corticosteroids inhibit the inflammatory response to a variety of inciting agents and probably delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation associated with inflammation. There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the bio-synthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Corticosteroids are capable of producing a rise in intraocular pressure.
Intravitreal corticosteroids can down regulate the production of proinflammatory mediators, and can be used in ocular inflammatory conditions.
Aqueous humor pharmacokinetics of triamcinolone acetonide were assessed in 5 patients following a single intravitreal administration (4 mg) of triamcinolone acetonide. Aqueous humor samples were obtained from 5 patients (5 eyes) via an anterior chamber paracentesis on Days 1, 3, 10, 17 and 31 post-injection. Peak aqueous humor concentrations of triamcinolone acetonide ranged from 2,151 to 7,202 ng/mL, the half-life ranged from 76 to 635 hours, and the area under the concentrationtime curve (AUC0-t) ranged from 231 to 1,911 ng·h/mL. The mean elimination halflife was 18.7 ± 5.7 days in 4 nonvitrectomized eyes (4 patients). In a patient who had undergone vitrectomy (1 eye), the elimination half-life of triamcinolone acetonide was much faster (3.2 days) relative to patients that had not undergone vitrectomy.
Last reviewed on RxList: 7/8/2008
This monograph has been modified to include the generic and brand name in many instances.
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