Triamcinolone was patented in 1956 and came into medical use in 1958.[8] It is available as a generic medication.[9] In 2022, it was the 102nd most commonly prescribed medication in the United States, with more than 6million prescriptions.[10][11]
The derivativetriamcinolone acetonide is the active ingredient in various topical skin preparations (cream, lotion, ointment, aerosol spray) designed to treat skin conditions such as rash, inflammation, redness, or intense itching due to eczema[15] and dermatitis.[16]
The side effects of triamcinolone are similar to other corticosteroids. In short-term treatment of up to ten days, it has very few adverse effects; however, sometimes gastrointestinal bleeding is seen, as well as acute infections (mainly viral) and impaired glucose tolerance.[4]
No acute overdosing of triamcinolone has been described.[17]
Interactions
Drug interactions are mainly pharmacodynamic, that is, they result from other drugs either adding to triamcinolone's corticosteroid side effects or working against its desired effects. They include:[4][17]
Triamcinolone and other drugs can also influence each other's concentrations in the body, amounting to pharmacokinetic interactions such as:[4][17]
Rifampicin, phenytoin, carbamazepine and other inducers of the liver enzyme CYP3A4[19] speed up metabolization of triamcinolone and can therefore reduce its effectiveness.
Conversely, CYP3A4 inhibitors such as ketoconazole and itraconazole can increase its concentrations in the body and the risk for adverse effects.
Blood concentrations of ciclosporin can be increased.
Triamcinolone is a glucocorticoid that is about five times as potent as cortisol but has very few mineralocorticoid effects.[4]
Pharmacokinetics
When taken by mouth, the drug's bioavailability is over 90%. It reaches its highest concentrations in the blood plasma after one to two hours and is bound to plasma proteins to about 80%. The biological half-life from the plasma is 200 to 300 minutes; due to stable complexes of triamcinolone and its receptor in the intracellular fluid, the total half-life is significantly longer at about 36 hours.[4][5]
A small fraction of the substance is metabolized to 6-hydroxy- and 20-dihydro-triamcinolone; most of it probably undergoes glucuronidation, and a smaller part sulfation. Three-quarters are excreted via the urine, and the rest via the faeces.[4][17]
Due to corticoids' mechanism of action, the effects are delayed as compared to plasma concentrations. Depending on the route of administration and the treated condition, the onset of action can be from two hours up to one or two days after application; and the drug can act much longer than its elimination half-life would suggest.[4][5]
Chemistry
Triamcinolone is a syntheticpregnanecorticosteroid and derivative of cortisol (hydrocortisone) and is also known as 1-dehydro-9α-fluoro-16α-hydroxyhydrocortisone or 9α-fluoro-16α-hydroxyprednisolone as well as 9α-fluoro-11β,16α,17α,21-tetrahydroxypregna-1,4-diene-3,20-dione.[20][21]
The substance is a light-sensitive, white to off-white, crystalline powder, or has the form of colourless, matted crystals. It has no odour or is nearly odourless. Information on the melting point varies, partly due to the substance's polymorphism: 260 to 263 °C (500 to 505 °F), 264 to 268 °C (507 to 514 °F), or 269 to 271 °C (516 to 520 °F) can be found in the literature.[4]
In 2010, Teva and Perrigo launched the first generic inhalable triamcinolone.[22]
According to Chang et al. (2014), "Triamcinolone acetonide (TA) is classified as an S9 glucocorticoid in the 2014 Prohibited List published by the World Anti-Doping Agency, which caused it to be prohibited in international athletic competition when administered orally, intravenously, intramuscularly or rectally".[23]
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