Pharmacology of Triamcinolone

Introduction/Overview

Triamcinolone is a synthetic glucocorticoid corticosteroid of significant clinical utility across multiple medical specialties. As a potent anti-inflammatory and immunosuppressive agent, it occupies a central role in the management of conditions characterized by excessive inflammation, immune dysregulation, and allergic responses. Its pharmacological profile distinguishes it from other corticosteroids, particularly due to its formulation versatility and prolonged duration of action at certain administration sites. The drug is available in several chemical forms, including triamcinolone acetonide, triamcinolone hexacetonide, and triamcinolone diacetate, each tailored for specific routes of delivery and therapeutic contexts. The clinical importance of triamcinolone stems from its ability to provide localized therapeutic effects with potentially reduced systemic exposure compared to oral corticosteroids, although systemic effects remain a consideration with all routes of administration.

The relevance of triamcinolone extends from common outpatient dermatological and rheumatological conditions to specialized use in ophthalmology, otolaryngology, and palliative care. Its application ranges from topical management of eczema and psoriasis to intralesional treatment of hypertrophic scars, from intra-articular injection for osteoarthritis to intravitreal administration for macular edema. Understanding its pharmacology is therefore essential for safe and effective prescribing, requiring knowledge of its unique pharmacokinetic properties, spectrum of therapeutic actions, and characteristic adverse effect profile.

Learning Objectives

• Describe the chemical classification of triamcinolone and its relationship to glucocorticoid receptor activity.
• Explain the molecular mechanism of action of triamcinolone, detailing genomic and non-genomic pathways leading to anti-inflammatory and immunosuppressive effects.
• Analyze the pharmacokinetic profile of triamcinolone, including how absorption, distribution, metabolism, and excretion differ between its various esterified forms and routes of administration.
• Identify the approved therapeutic indications for triamcinolone, categorizing them by route of administration, and recognize common off-label uses.
• Evaluate the major adverse effects, drug interactions, and special population considerations associated with triamcinolone therapy to mitigate clinical risk.

Classification

Triamcinolone is systematically classified within the broader category of synthetic corticosteroids. This classification can be further delineated by chemical structure, pharmacological activity, and clinical use.

Pharmacological and Therapeutic Classification

Primarily, triamcinolone is classified as a glucocorticoid. Glucocorticoids are adrenocortical steroids that predominantly influence carbohydrate, protein, and lipid metabolism, and possess potent anti-inflammatory and immunosuppressive properties. They are distinct from mineralocorticoids, which primarily regulate electrolyte and water balance. Triamcinolone exhibits high glucocorticoid receptor affinity with minimal mineralocorticoid activity, placing it among the intermediate-to-high potency synthetic glucocorticoids when compared to the endogenous reference standard, cortisol (hydrocortisone).

Chemical Classification

Chemically, triamcinolone is a fluorinated corticosteroid. Its base structure is a pregnane derivative, specifically a 9α-fluoro-11β,16α,17α,21-tetrahydroxypregna-1,4-diene-3,20-dione. The critical modifications from cortisol include:

• Fluorination at the 9α position: This substitution significantly enhances glucocorticoid receptor binding affinity and anti-inflammatory potency while typically reducing mineralocorticoid activity.
• Introduction of a 1,2 double bond in ring A: This modification, shared with prednisolone, increases glucocorticoid potency and slows metabolism.
• Hydroxylation at the 16α position: This structural feature is pivotal in virtually eliminating sodium-retaining (mineralocorticoid) activity, making triamcinolone particularly suitable for patients where fluid retention is a concern. This also contributes to its distinct pharmacological profile compared to other fluorinated steroids like dexamethasone.

The drug is commonly administered not as the free alcohol but as esterified prodrugs to modify its solubility and duration of action. Triamcinolone acetonide is a cyclic ketal derivative at the 16α,17α positions, rendering it highly lipophilic. This lipophilicity facilitates local tissue retention, making it ideal for topical, intralesional, intra-articular, and inhaled formulations. Triamcinolone hexacetonide is a di-ester with even greater lipophilicity and a markedly prolonged duration of action within joints. Triamcinolone diacetate is more water-soluble and is often used for intramuscular injection and intra-articular administration where a less persistent effect is desired.

Mechanism of Action

The therapeutic and adverse effects of triamcinolone are mediated primarily through its action as an agonist at the intracellular glucocorticoid receptor (GR), a member of the nuclear receptor superfamily. The ensuing effects are a consequence of complex genomic and non-genomic pathways that modulate gene transcription and protein function.

Glucocorticoid Receptor Activation and Genomic Mechanisms

In the absence of ligand, the GR resides in the cytoplasm as part of a multiprotein complex that includes heat shock proteins (HSPs) and immunophilins. Being highly lipophilic, triamcinolone readily diffuses across cell membranes and binds with high affinity to the ligand-binding domain of the GR. This binding induces a conformational change, causing dissociation of the chaperone proteins, receptor dimerization, and rapid translocation of the ligand-receptor complex into the nucleus.

Within the nucleus, the triamcinolone-GR complex exerts its effects through two principal genomic mechanisms:

1. Transactivation: The dimer binds to specific DNA sequences known as glucocorticoid response elements (GREs) located in the promoter regions of target genes. This binding recruits coactivators and the transcriptional machinery, leading to increased transcription of anti-inflammatory proteins. Key proteins upregulated via this mechanism include:
   • Annexin-1 (lipocortin-1): Inhibits phospholipase A₂, reducing the release of arachidonic acid, the precursor for prostaglandins and leukotrienes.
   • IκBα: The inhibitor of nuclear factor kappa B (NF-κB). Increased IκBα sequesters NF-κB in the cytoplasm, preventing its pro-inflammatory gene transcription.
   • Interleukin-10 (IL-10): A potent anti-inflammatory cytokine.
   • β₂-adrenergic receptors: May contribute to bronchodilation in asthma.
2. Transrepression: This mechanism is largely responsible for the anti-inflammatory and immunosuppressive effects. The triamcinolone-GR complex can interfere with the activity of pro-inflammatory transcription factors, such as NF-κB and activator protein-1 (AP-1), without directly binding to DNA. It does so through protein-protein interactions that either prevent these factors from binding to their response elements or by recruiting corepressor complexes that suppress gene transcription. This leads to decreased production of a wide array of inflammatory mediators:
   • Cytokines: IL-1, IL-2, IL-6, IL-8, TNF-α.
   • Chemokines.
   • Adhesion molecules (e.g., ICAM-1, VCAM-1).
   • Enzymes: Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2).

Non-Genomic Mechanisms

Some effects of triamcinolone occur too rapidly to be explained by gene transcription and protein synthesis. These non-genomic mechanisms include:

• Membrane-associated effects: Interaction with membrane-bound GRs or other receptors can rapidly inhibit signaling pathways.
• Physicochemical interactions: At very high concentrations, such as those achieved with local injections, corticosteroids may stabilize cellular membranes, including lysosomal membranes, preventing the release of inflammatory enzymes.
• Effects on second messengers: Rapid inhibition of arachidonic acid release and modulation of intracellular calcium levels have been observed.

Cellular and Systemic Effects

The molecular actions of triamcinolone translate into predictable cellular and systemic pharmacological effects:

• Anti-inflammatory: Reduces vasodilation, capillary permeability, leukocyte migration, and phagocytic activity at inflamed sites.
• Immunosuppressive: Inhibits cell-mediated immunity. Reduces lymphocyte proliferation (especially T-lymphocytes), inhibits dendritic cell maturation, and induces apoptosis of certain immune cells (e.g., eosinophils, lymphocytes).
• Metabolic: Promotes gluconeogenesis, reduces peripheral glucose utilization, stimulates protein catabolism and lipolysis, and redistributes body fat.
• Other: Potentiates vasoconstrictor response to catecholamines (important in skin blanching tests), suppresses the hypothalamic-pituitary-adrenal (HPA) axis, and alters bone and calcium metabolism.

Pharmacokinetics

The pharmacokinetics of triamcinolone are complex and highly dependent on the specific ester form and the route of administration. The esterification profoundly influences solubility, absorption rate, and local tissue retention.

Absorption

Absorption varies dramatically by formulation:

• Topical: Percutaneous absorption of triamcinolone acetonide is generally low but is influenced by the vehicle (ointment > cream > lotion), skin integrity (increased with inflammation, occlusion, or broken skin), and the surface area treated. Significant systemic absorption can occur if applied to large areas, under occlusion, or to thin-skinned regions.
• Intralesional/Intra-articular/Intrabursal: Triamcinolone acetonide and hexacetonide are formulated for local deposition and slow release. Absorption into the systemic circulation occurs gradually over weeks, with the rate inversely related to the lipophilicity of the ester (hexacetonide > acetonide > diacetate in terms of persistence).
• Intramuscular: Triamcinolone diacetate and acetonide suspensions are absorbed slowly from the injection site, providing a sustained systemic effect lasting from one to several weeks, which is useful for suppressing HPA axis activity in conditions like allergic disorders.
• Oral Inhalation/Aerosol: A fraction of the inhaled dose is absorbed from the lung alveoli into the systemic circulation. The majority is either deposited in the oropharynx and swallowed (subject to first-pass metabolism) or exhaled.
• Oral: Triamcinolone is available as a tablet (as the base or diacetate) and is well absorbed from the gastrointestinal tract.
• Intravitreal: Administered as a sustained-release implant or suspension, systemic absorption is minimal, but local ocular concentrations remain high for extended periods (months with implants).

Distribution

Once absorbed into the systemic circulation, triamcinolone distributes widely throughout body tissues. Its volume of distribution is approximately 1.0 to 1.5 L/kg. Like other corticosteroids, it crosses the placenta and is excreted in breast milk. The drug is approximately 68% bound to plasma proteins, primarily transcortin (corticosteroid-binding globulin, CBG) and, to a lesser extent, albumin. This binding is saturable, meaning the fraction of free, pharmacologically active drug may increase at higher doses. The lipophilic ester forms (acetonide, hexacetonide) exhibit high affinity for adipose tissue and sites of local injection, creating a depot effect.

Metabolism

Triamcinolone undergoes extensive hepatic metabolism, primarily via the cytochrome P450 (CYP) 3A4 isoenzyme system. The metabolic pathways include reduction of the 4,5 double bond and the 3-keto group, hydroxylation at the 6β position, and conjugation with sulfate and glucuronic acid to form water-soluble metabolites. The ester forms are first hydrolyzed by esterases in the liver and other tissues to release the active triamcinolone free alcohol. The metabolism is generally not saturable within the therapeutic dose range. Hepatic impairment may reduce clearance and prolong the half-life, potentially increasing the risk of systemic toxicity.

Excretion

The metabolites of triamcinolone are eliminated predominantly by renal excretion, with approximately 60% of a dose appearing in the urine and 40% in the feces via biliary elimination. Less than 1% of the parent drug is excreted unchanged in the urine. Renal impairment does not typically necessitate dosage adjustment for single or intermittent courses, but caution is advised with chronic therapy due to altered electrolyte balance and potential for accumulation of inactive metabolites.

Half-life and Dosing Considerations

The half-life of triamcinolone is multi-phasic and context-dependent:

• Plasma elimination half-life (t_1/2β): For the free alcohol, the biological half-life is approximately 2 to 5 hours. However, this figure is misleading for clinical effect duration.
• Biological half-life: Due to its genomic mechanism of action, the pharmacological effects persist long after the drug is cleared from plasma. The biological half-life, which reflects the duration of HPA axis suppression, is approximately 18 to 36 hours for triamcinolone, classifying it as an intermediate-acting glucocorticoid. This contrasts with short-acting hydrocortisone (8-12 hours) and long-acting dexamethasone (36-54 hours).
• Local depot half-life: For esterified forms administered locally (e.g., intra-articular acetonide), the effective duration of action at the site can range from 3 to 8 weeks, depending on the ester. Triamcinolone hexacetonide has the longest intra-articular duration.

Dosing considerations must account for the route, indication, and desired duration of effect. A key principle is to use the lowest effective dose for the shortest possible duration. For chronic conditions requiring systemic therapy, alternate-day morning dosing may be employed to minimize HPA axis suppression.

Therapeutic Uses/Clinical Applications

Triamcinolone’s therapeutic applications are extensive and route-specific, leveraging its potent anti-inflammatory and immunosuppressive properties.

Approved Indications by Route

Topical Dermatological Formulations

• Inflammatory dermatoses: Atopic dermatitis, contact dermatitis, seborrheic dermatitis, lichen simplex chronicus.
• Papulosquamous disorders: Psoriasis (particularly plaque psoriasis).
• Other: Discoid lupus erythematosus, lichen planus.

Intralesional Injection

• Hypertrophic scars and keloids.
• Alopecia areata.
• Localized inflammatory skin lesions: Granuloma annulare, necrobiosis lipoidica, cystic acne.
• Oral lichen planus and aphthous ulcers.

Intra-articular, Intrabursal, and Periarticular Injection

• Inflammatory arthritis: Rheumatoid arthritis, psoriatic arthritis, acute gouty arthritis (when colchicine or NSAIDs are contraindicated).
• Osteoarthritis: For symptomatic relief of inflamed joints.
• Bursitis (e.g., subacromial, trochanteric, olecranon).
• Tendinitis or tenosynovitis (e.g., De Quervain’s tenosynovitis, epicondylitis).
• Ganglion cysts.

Intramuscular Injection

• As a systemic corticosteroid for conditions requiring prolonged effect: Severe allergic reactions (e.g., refractory allergic rhinitis, asthma exacerbations), dermatological diseases (e.g., severe psoriasis, pemphigus), or as adjunctive therapy in certain autoimmune disorders.
• As an antiemetic in palliative care settings.

Inhalation (Oral and Nasal)

• Bronchial asthma (as a maintenance controller medication).
• Allergic rhinitis.

Ophthalmic Formulations

• Inflammatory conditions of the eye: Allergic conjunctivitis, keratitis, uveitis, iritis.
• Post-operative inflammation following ocular surgery.
• Intravitreal Injection/Implant: Diabetic macular edema, macular edema following retinal vein occlusion, non-infectious uveitis affecting the posterior segment.

Common Off-Label Uses

• Topical: Vitiligo (often in combination with phototherapy), prurigo nodularis.
• Intralesional: Prurigo nodularis, cutaneous sarcoidosis.
• Intra-articular: Adhesive capsulitis (frozen shoulder).
• Intravitreal: Cystoid macular edema from various causes, central serous chorioretinopathy.
• Systemic (Oral/IM): Autoimmune hepatitis, certain hematologic malignancies (as part of combination chemotherapy), prevention of contrast media reactions.

Adverse Effects

The adverse effects of triamcinolone are extensions of its pharmacological actions and are influenced by dose, duration, and route of administration. Systemic effects are most pronounced with oral, parenteral, and prolonged high-potency topical or extensive local use.

Common Side Effects

These effects are often predictable and dose-related:

• Local Effects (Injections): Pain at injection site, transient flare of inflammation (crystal-induced synovitis), subcutaneous atrophy (lipoatrophy), skin hypopigmentation or depigmentation, sterile abscess formation.
• Local Effects (Topical/Ophthalmic): Skin thinning (atrophy), telangiectasias, striae (with prolonged use), acneiform eruptions, perioral dermatitis, burning/stinging sensation. Ophthalmic use can cause elevated intraocular pressure (steroid-induced glaucoma), posterior subcapsular cataract formation, and increased risk of ocular infection.
• Systemic Effects (with sufficient absorption): Fluid retention and weight gain (less common with triamcinolone than with corticosteroids possessing mineralocorticoid activity), mood disturbances (euphoria, insomnia, anxiety, depression), increased appetite, dyspepsia, cushingoid habitus (moon face, buffalo hump, central obesity).

Serious and Rare Adverse Reactions

• Endocrine: Suppression of the hypothalamic-pituitary-adrenal (HPA) axis, leading to adrenal insufficiency upon withdrawal, particularly after prolonged systemic therapy. Manifestations include weakness, fatigue, hypotension, hypoglycemia, and electrolyte imbalance. Iatrogenic Cushing’s syndrome.
• Musculoskeletal: Osteoporosis and increased risk of vertebral and hip fractures. Osteonecrosis (avascular necrosis), particularly of the femoral head. Steroid myopathy, characterized by proximal muscle weakness.
• Gastrointestinal: Increased risk of peptic ulcer disease, particularly when co-administered with NSAIDs. Pancreatitis.
• Ophthalmic (Systemic or Local): As noted, glaucoma and cataracts are serious, potentially vision-threatening complications of chronic use.
• Immunological: Increased susceptibility to infections (bacterial, viral, fungal, parasitic), masking of signs of infection, potential reactivation of latent tuberculosis or hepatitis B.
• Metabolic: Hyperglycemia and worsening of pre-existing diabetes mellitus (steroid-induced diabetes). Dyslipidemia.
• Cardiovascular: Hypertension, accelerated atherosclerosis.
• Neurological/ Psychiatric: Severe psychiatric reactions (psychosis, delirium), pseudotumor cerebri (benign intracranial hypertension), especially upon withdrawal.
• Dermatological: Severe skin atrophy with ulceration, allergic contact dermatitis to the drug or vehicle.
• Injection-specific: Tendon rupture (if injected directly into a tendon), nerve damage, joint infection (septic arthritis), chalky deposit formation (from the suspension).

Black Box Warnings

Triamcinolone, as a corticosteroid, carries black box warnings common to this drug class for certain routes of administration:

• Intra-articular Use: Strict aseptic technique is mandatory. Intra-articular injection may cause systemic as well as local effects. Joint instability and increased pain shortly after injection warrant evaluation for septic arthritis.
• Systemic Use (Oral/Injectable): Corticosteroids can cause serious and fatal infections. Patients exposed to chickenpox or measles may require prophylactic treatment. Live or live-attenuated vaccines should not be given to individuals on immunosuppressive doses.
• General: Rare instances of anaphylactoid reactions have been reported with corticosteroid use.

Drug Interactions

Triamcinolone participates in several clinically significant pharmacokinetic and pharmacodynamic drug interactions.

Major Pharmacokinetic Interactions

• Enzyme Inducers: Drugs that induce CYP3A4 (e.g., phenytoin, phenobarbital, carbamazepine, rifampin, St. John’s wort) can accelerate the metabolism of triamcinolone, reducing its plasma concentration and therapeutic efficacy. Dose adjustment may be necessary.
• Enzyme Inhibitors: Drugs that inhibit CYP3A4 (e.g., ketoconazole, itraconazole, clarithromycin, ritonavir, grapefruit juice) can decrease triamcinolone metabolism, potentially increasing its plasma concentration and the risk of toxicity, including Cushing’s syndrome and adrenal suppression.

Major Pharmacodynamic Interactions

• Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) and Aspirin: Concurrent use significantly increases the risk of gastrointestinal ulceration and bleeding. The combination may also antagonize the antihypertensive effects of certain drugs.
• Anticoagulants (Warfarin): The effect is variable; corticosteroids may either increase or decrease warfarin’s anticoagulant effect. Close monitoring of the International Normalized Ratio (INR) is required.
• Antidiabetic Agents (Insulin, Oral Hypoglycemics): Triamcinolone antagonizes the glucose-lowering effects of these drugs, often necessitating increased doses of antidiabetic medication.
• Diuretics (especially potassium-depleting types like thiazides and loop diuretics): Corticosteroids can cause hypokalemia; co-administration with these diuretics exacerbates potassium loss, increasing the risk of arrhythmias.
• Cardiac Glycosides (Digoxin): Hypokalemia induced by corticosteroids potentiates the risk of digitalis toxicity.
• Live Vaccines: The immunosuppressive action of triamcinolone can diminish the immune response to live vaccines (e.g., MMR, varicella, yellow fever) and increase the risk of vaccine-strain infection. Administration is generally contraindicated in patients receiving immunosuppressive doses.
• Neuromuscular Blocking Agents: Corticosteroids may potentiate or antagonize the effects of these agents; prolonged muscle weakness has been reported.

Contraindications

Absolute contraindications to triamcinolone therapy are few but important:

• Systemic fungal infections (unless used as part of management for adrenal insufficiency in such infections).
• Known hypersensitivity to triamcinolone or any component of the formulation.
• Live virus vaccination in patients receiving immunosuppressive doses.
• Intrathecal administration is contraindicated due to the risk of severe neurotoxicity.
• Active, untreated infections at the site of intended local injection (e.g., septic arthritis, skin infection).

Relative contraindications, requiring careful risk-benefit assessment, include: active peptic ulcer disease, congestive heart failure, uncontrolled hypertension, diabetes mellitus, osteoporosis, glaucoma, psychotic disorders, and latent tuberculosis.

Special Considerations

Pregnancy and Lactation

Pregnancy (FDA Category C): Corticosteroids, including triamcinolone, have been shown to be teratogenic in animal studies at doses multiples of the human dose. Adequate and well-controlled studies in pregnant women are lacking. Use during pregnancy, especially in the first trimester, requires that the potential benefit justifies the potential risk to the fetus. Chronic use may be associated with low birth weight. Administration late in pregnancy may result in neonatal adrenal suppression. When systemic therapy is required, non-fluorinated corticosteroids (e.g., prednisone, prednisolone) are often preferred as they are more efficiently metabolized by the placental 11β-hydroxysteroid dehydrogenase type 2 enzyme, limiting fetal exposure.

Lactation: Corticosteroids are excreted in human milk. The relative infant dose is considered low (< 10% of the maternal weight-adjusted dose). However, caution is advised, particularly with high maternal doses, due to the potential for growth suppression and interference with endogenous corticosteroid production in the infant. The use of topical or inhaled formulations, which result in lower systemic levels, may be preferable when treatment during breastfeeding is necessary.

Pediatric Considerations

Children are particularly susceptible to the adverse effects of corticosteroids. Chronic use can cause growth suppression, which may not be fully reversible. Monitoring of linear growth is essential. The use of alternate-day therapy may mitigate this effect. Behavioral disturbances, including psychosis, may occur more frequently in children. Increased intracranial pressure is also more common in pediatric populations. Dosing must be carefully calculated based on body surface area or weight. The use of high-potency topical steroids on diaper areas or under occlusion should be avoided due to enhanced systemic absorption.

Geriatric Considerations

Elderly patients may be more susceptible to certain adverse effects, including hypertension, osteoporosis, hyperglycemia, and fluid retention. The risk of steroid-induced myopathy and subsequent falls is increased. Age-related decreases in hepatic and renal function may alter pharmacokinetics, potentially necessitating dose adjustments. The presence of multiple comorbidities and polypharmacy increases the likelihood of significant drug interactions.

Renal and Hepatic Impairment

Renal Impairment: Dosage adjustment is not routinely required for single doses or short courses, as renal excretion of the parent drug is minimal. However, caution is warranted in patients with severe renal impairment due to the potential for exacerbating fluid retention, hypertension, and electrolyte imbalances (hypokalemia). Monitoring of serum electrolytes is recommended.

Hepatic Impairment: Since triamcinolone is extensively metabolized in the liver, hepatic impairment can reduce its clearance, prolong its half-life, and increase systemic exposure. Dose reduction may be necessary in patients with significant liver disease (e.g., cirrhosis) to avoid steroid toxicity. Monitoring for signs of Cushing’s syndrome and adrenal suppression is prudent.

Summary/Key Points

• Triamcinolone is a synthetic, fluorinated glucocorticoid with potent anti-inflammatory and immunosuppressive activity and minimal mineralocorticoid effects, available in several esterified forms (acetonide, hexacetonide, diacetate) that dictate its pharmacokinetics and clinical use.
• Its primary mechanism of action involves binding to the intracellular glucocorticoid receptor, leading to genomic effects (transactivation and transrepression) that modulate the expression of numerous pro-inflammatory and anti-inflammatory genes, with additional rapid non-genomic effects.
• Pharmacokinetics are route- and ester-dependent. Lipophilic esters (acetonide, hexacetonide) create local depots for prolonged action, while systemic absorption can lead to HPA axis suppression and other classic corticosteroid adverse effects. It is metabolized hepatically by CYP3A4 and has an intermediate biological half-life.
• Therapeutic applications are broad and include topical treatment of inflammatory skin diseases, intralesional injection for scars and alopecia, intra-articular injection for arthritis and bursitis, intramuscular injection for systemic effect, inhalation for asthma and rhinitis, and ophthalmic use for ocular inflammation and macular edema.
• Adverse effects range from local reactions (atrophy, hypopigmentation) to serious systemic complications (HPA axis suppression, osteoporosis, infection risk, hyperglycemia, glaucoma). The risk is proportional to dose, potency, duration, and route of administration.
• Significant drug interactions occur with CYP3A4 inducers/inhibitors, NSAIDs, anticoagulants, antidiabetic drugs, diuretics, and live vaccines. Contraindications include systemic fungal infection and hypersensitivity.
• Special caution is required in pregnancy, lactation, pediatric, and geriatric populations, as well as in patients with hepatic impairment, due to altered pharmacokinetics and increased susceptibility to adverse effects.

Clinical Pearls

• When administering intra-articular triamcinolone, the hexacetonide ester provides the longest duration of symptom relief for inflammatory arthritis, while the acetonide or diacetate forms may be preferred for softer tissue injections.
• The risk of subcutaneous atrophy following intralesional injection can be minimized by using the lowest effective concentration (e.g., 2.5-5 mg/mL for keloids), avoiding superficial injection, and limiting the volume per site.
• Patients on chronic topical potent steroids should be periodically assessed for signs of skin atrophy and advised about the “finger-tip unit” method to ensure appropriate dosing and minimize systemic absorption.
• Before initiating systemic or potent local triamcinolone therapy, consider screening for latent tuberculosis (PPD or interferon-gamma release assay) and checking baseline blood glucose, blood pressure, and bone density in at-risk patients.
• A single intramuscular dose of triamcinolone can suppress the HPA axis for weeks. Patients undergoing significant stress (e.g., surgery) during this period may require supplemental corticosteroids.

References

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