Triamcinolone (Nasacort® AQ; Kenalog®)

Classification:
Dermatological Agents

Topical Antiinflammatory Agents
- Corticosteroids

Hormones and Hormone Modifiers

Adrenal Agents
- Corticosteroids

Musculoskeletal Agents

Antiinflammatory Agents
- Corticosteroids

Oropharyngeal Agents

Antiinflammatory Agents

Oropharyngeal Agents

Dental and Peridontal Agents

Respiratory Agents

Respiratory Antiinflammatory Agents
- Corticosteroids

Description: Triamcinolone and its derivatives are synthetic glucocorticoids used as antiinflammatory or immunosuppressive agents. Triamcinolone has little mineralocorticoid activity and is therefore not used to manage adrenal insufficiency unless a more potent mineralocorticoid is administered concomitantly. Topical triamcinolone preparations are considered medium or high potency (0.5% cream and ointment only). Since triamcinolone is resistant to metabolism in the skin, repeated applications may lead to a depot effect and prolonged actions, increased side effects, and an increased risk of systemic absorption. High potency topical corticosteroids may be used in areas with thickened skin due to chronic conditions but should only be used on the face or intertriginous areas for a short duration. Triamcinolone is commercially available in oral, nasal, parenteral, topical, and aerosol formulations. Triamcinolone was first approved by the FDA in 1957.

Mechanism of Action: Corticosteroids exhibit anti-inflammatory, antipruritic, and vasoconstrictive properties. At the cellular level, corticosteroids induce peptides called lipocortins. Lipocortins antagonize phospholipase A₂, an enzyme which causes the breakdown of leukocyte lysosomal membranes to release arachidonic acid. This action decreases the subsequent formation and release of endogenous inflammatory mediators including prostaglandins, kinins, histamine, liposomal enzymes and the complement system.

Early anti-inflammatory effects of topical corticosteroids include the inhibition of macrophage and leukocyte movement and activity in the inflamed area by reversing vascular dilation and permeability. Later inflammatory processes such as capillary production, collagen deposition, keloid (scar) formation also are inhibited by corticosteroids. Clinically, these actions correspond to decreased edema, erythema, pruritus, plaque formation and scaling of the affected skin.

In the treatment of asthma, corticosteroids block the late phase allergic response to allergens. Mediators involved in the pathogenesis of asthma include histamine, leukotrienes (slow releasing substance of anaphylaxis, SRS-A), eosinophil chemotactic factor of anaphylaxis (ECF-A), neutrophil chemotactic factor (NCF), cytokines, hydroxyeicosatetraenoic acids, prostaglandin-generating factor of anaphylaxis (PGF-A), prostaglandins, major basic protein, bradykinin, adenosine, peroxides, and superoxide anions. Different cell types are responsible for release of these mediators including airway epithelium, eosinophils, basophils, lung parenchyma, lymphocytes, macrophages, mast cells, neutrophils, and platelets. Corticosteroids inhibit the release of these mediators as well as inhibit IgE synthesis, attenuate mucous secretion and eicosanoid generation, up-regulate beta-receptors, promote vasoconstriction, and suppress inflammatory cell influx and inflammatory processes. Clinical effects in asthma include a reduction in bronchial hyperresponsiveness to allergens, a decreased number of asthma exacerbations, and an improvement in FEV1, peak-flow rate, and respiratory symptoms. Since corticosteroid effects take several hours to days to become clinically noticeable, they are ineffective for primary treatment of severe acute bronchospastic attacks or for status asthmaticus. Inhaled corticosteroids have no bronchodilatory properties.

Aristocort A Cream(Cream 0.1 %)

Pharmacokinetics: Triamcinolone is rapidly absorbed following an oral dose. Peak effects following oral administration occur within 1 - 2 hours. The onset and duration of action of triamcinolone suspensions depend on the route of administration and the extent of the local blood supply. Bioavailability of triamcinolone following topical application is dependent on the condition of the skin at the application site. Absorption of topical preparations is increased in areas of skin damage, inflammation, or occlusion, or where the stratum corneum is thin such as the eyelids, genitalia, and face. There may be a small extent of systemic absorption of the topical solutions, especially via the oral mucosa. Systemic absorption from the lungs is equivalent to that absorbed from the GI tract.

Following oral inhalation, triamcinolone is deposited extensively in the mouth and throat, and is distributed throughout the hilar areas of the lung. The distribution kinetics of an intranasal dose of triamcinolone are unknown. The circulating drug binds weakly to plasma proteins, and only the unbound portion of a dose is active. Systemic triamcinolone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Corticosteroids distribute into breast milk and cross the placenta.

Topical preparations of triamcinolone are metabolized in the skin, and systemic triamcinolone is metabolized by the liver to inactive metabolites. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine.

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[ Revised 2/23/2006 9:31:00 AM ]

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