Triamcinolone Acetonide
Triamcinolone acetonide is a synthetic, intermediate-acting **glucocorticoid** that is approximately 4 to 10 times (and up to 40 times in some models) more potent than hydrocortisone. **Clinical Pearls & Key Features:** * **Zero Mineralocorticoid Activity:** Unlike hydrocortisone or prednisone, triamcinolone lacks appreciable mineralocorticoid effects, meaning it does not cause significant sodium or water retention. * **Versatile Administration:** It is utilized systemically (oral, injectable), topically, intra-articularly (especially in equine sports medicine), and intralesionally (e.g., for esophageal strictures or lick granulomas). * **Duration of Action:** When given orally, its metabolic activity lasts 24-48 hours. However, intramuscular (IM) or subcutaneous (SC) depot injections can persist for 4 to 6 weeks (sometimes up to 8 weeks), making it useful for chronic inflammatory or allergic conditions where daily pilling is difficult, though this increases the risk of prolonged adrenal suppression. * **Equine Use:** Frequently used for intra-articular injections in high-motion joints to reduce synovitis and improve lameness. It is an ARCI Class 4 drug in racing.
Mecanismo: Triamcinolone exerts its effects via classic genomic and non-genomic glucocorticoid pathways: 1. **Genomic Pathway:** Free triamcinolone crosses the cell membrane and binds to the cytosolic **glucocorticoid receptor (GR)**. 2. The receptor-ligand complex translocates to the nucleus and binds to **Glucocorticoid Response Elements (GREs)** on DNA. 3. **Anti-inflammatory Protein Induction:** It upregulates the expression of **lipocortin-1 (annexin A1)**. Lipocortin-1 inhibits **phospholipase A2**, thereby blocking the release of arachidonic acid from membrane phospholipids. 4. **Eicosanoid Suppression:** This → halts the synthesis of pro-inflammatory prostaglandins and leukotrienes (via COX and LOX pathways). 5. **Cytokine Inhibition:** It suppresses the transcription of major inflammatory cytokines (e.g., IL-1, IL-6, TNF-α) and reduces inflammatory cell migration and capillary permeability.
Dosificación por especie
- Glucocorticoid effects · 0.25-0.5 mg PO once daily for 7 days · PO · q24h · 7 days
- Pododermatitis, feline plasmacytic pharyngitis · 2-4 mg (total dose) PO once a day or every other day 0.4-0.6 mg/kg PO once daily, then taper. · PO · q24h or q48h · Tapered
- Pemphigus complex · 0.4-0.8 mg/kg/day PO · PO · q24h
- General therapy (Tablets) · 0.11 mg/kg PO initially once a day, may increase to 0.22 mg/kg PO once daily if initial response is unsatisfactory. As soon as possible, but not later than 2 weeks, reduce dose gradually to 0.028-0.055 mg/kg/day · PO · q24h · Taper within 2 weeks
- Inflammatory, allergic, or dermatological disorders (Injectable) · 0.11-0.22 mg/kg for inflammatory or allergic disorders, and 0.22 mg/kg for dermatological disorders. · IM/SC · As needed · Effects generally persist for 7-15 days · If symptoms recur, may repeat or institute oral therapy.
- Intralesional injection · Usual dose is 1.2-1.8 mg; inject around lesion at 0.5-2.5 cm intervals. Do not exceed 0.6 mg at any one site or 6 mg total dose. · Intralesional · As needed · May repeat as necessary.
- To prevent re-stricture after esophageal dilation · Using an endoscopically directed needle, inject 0.5-1 mL of Vetalog (2 mg/mL) submucosally at time of dilation procedure. Infiltration is done circumferentially at four points around the site. · Submucosal · Once at time of procedure
- Adjunctive treatment of miliary dermatitis · 0.2-0.6 mg/kg PO once daily for 10-14 days, then tapered. · PO · q24h · 10-14 days, then taper
Vías de administración
Contraindicaciones
- Systemic fungal infections
- Viral infections
- Active tuberculosis
- Peptic ulcers
- Corneal ulcers
- Acute psychoses
- Cushingoid syndrome
- Idiopathic thrombocytopenia (IM administration)
- Hypersensitivity to the drug
Efectos adversos
- Polyuria (PU)
- Polydipsia (PD)
- Polyphagia (PP)
- Weight gain
- Panting (dogs)
- Dull, dry haircoat
- Vomiting and diarrhea
- Elevated liver enzymes (e.g., ALP)
- Pancreatitis
- Gastrointestinal ulceration
- Lipidemias
- Insulin resistance / Activation of diabetes mellitus
- Muscle wasting
- Behavioral changes (depression, lethargy, viciousness)
- Iatrogenic hyperadrenocorticism (Cushing's syndrome) with chronic use
- Laminitis (horses)
Interacciones farmacológicas
- Amphotericin B · May cause hypokalemia when administered concomitantly
- Opiate Analgesics / Local Anesthetics (Epidural) · Combination in epidurals has caused serious CNS injuries and death; restrict volume to very small intrathecal test doses
- Anticholinesterase Agents (e.g., pyridostigmine) · May lead to profound muscle weakness in myasthenia gravis patients; discontinue 24h prior if possible
- Aspirin · Glucocorticoids may reduce salicylate blood levels
- Barbiturates · May increase the metabolism of glucocorticoids and decrease blood levels
- Cyclophosphamide · Glucocorticoids may inhibit hepatic metabolism of cyclophosphamide; dosage adjustments may be required
- Cyclosporine · May mutually inhibit hepatic metabolism, increasing blood levels of both drugs
- Potassium-depleting Diuretics (e.g., spironolactone) · May cause hypokalemia
- Erythromycin, Clarithromycin · May increase triamcinolone levels
- Estrogens · May potentiate the effects of triamcinolone
- Insulin · Insulin requirements may increase due to glucocorticoid-induced insulin resistance
- Isoniazid · Triamcinolone may decrease isoniazid levels
Monitoreo
- Weight, appetite, signs of edema
- Serum and/or urine electrolytes
- Total plasma proteins, albumin
- Blood glucose
- Growth and development in young animals
- ACTH stimulation test if necessary
Sobredosis
Short-term administration of massive doses is unlikely to cause harmful effects, though one case of acute CNS effects in a dog after accidental ingestion has been reported. If acute clinical signs occur, provide supportive treatment. **Chronic Toxicity:** Chronic overdosage or prolonged use leads to serious adverse effects, primarily manifesting as iatrogenic hyperadrenocorticism (Cushing's syndrome), immunosuppression, and adrenal axis suppression.
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