Triamcinolone Acetonide Cream

Each gram of 0.1% triamcinolone acetonide cream provides 1 mg triamcinolone acetonide, respectively, in a vanishing cream base containing cetyl alcohol, cetyl esters wax, glyceryl monostearate, isopropyl palmitate, polysorbate-60, polysorbate-80, propylene glycol and purified water.

triamcinolone acetonide cream

Each gram of Triderm (Triamcinolone Acetonide Cream USP), 0.025% contains 0.25 mg triamcinolone acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Each gram of Triderm (Triamcinolone Acetonide Cream USP), 0.1% contains 1 mg triamcinolone acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Each gram of Triderm (Triamcinolone Acetonide Cream USP), 0.5% contains 5 mg triamcinolone acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Each gram contains: 1 mg Triamcinolone Acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Each gram contains: 1 mg triamcinolone acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Each gram contains 0.25 mg triamcinolone acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Each gram contains 5 mg triamcinolone acetonide USP in a cream base consisting of purified water, emulsifying wax, mineral oil, propylene glycol, sorbitol solution, cetyl palmitate, sorbic acid, and potassium sorbate.

Keloid could grow spontaneously or grow following dermal trauma with poor prognosis. The uncontrolled growth of keloid will continue to grow without regression, and the patients will experience itch, pruritis, and pain. Common occurring sites include chest, shoulder, earlobes, and upper back (4). When the fibrous keloid become big, it will lead to cosmetic disfigurement, functional impairment, and affect the quality of life (4). Since keloid has notoriously high recurrence rate after surgical excision, non-surgical means are recommended for the primary keloid treatment (5). Non-surgical means include corticosteroids injection, 5-fluorouracil (5-FU), verapamil, silicon gel sheets, cryotherapy, pulsed dye laser (PDL), and radiation. Intralesional injection of corticosteroid triamcinolone acetonide (TAC) is one of the first-line treatment modalities for keloid treatment (5). Corticosteroid is highly tolerated by the patients with a keloid. Corticosteroid could diminish the exuberant collagen synthesis and inhibit the rapid growth of keloid fibroblasts (6). In addition, corticosteroid could promote vasoconstriction in the keloid scar and control local inflammation (7). However, it is also noticed that the response rate of TAC treatment is highly varying with high recurrence rate (4, 6). TAC monotherapy may induce hypopigmentation, mixed pigmentation, fat atrophy, telangiectasias, necrosis, ulcerations, and cushingoid habitus (8). In addition, there are concern on the repeated use of corticosteroid at high-dose in patients with large and multiple keloids (4). 5-FU functions by inhibiting the synthesis of pyrimidine thymidine and interferes the DNA replication process in the rapidly dividing cells by competing with uracil (9). Verapamil functions by regulating the balance between fibroblasts and extracellular matrix remodeling (10). Silicon gel sheets could act as an occlusive layer which suppresses IL-1 and IL-6 production, thus inhibiting fibroblast synthesis (11). Cryotherapy could destruct the keloid by the formation of sharp ice crystals and the induction of ischemic necrosis (12). PDL promotes keloid regression by photothermolysis (13). The light energy emitted by PDL causes coagulation necrosis of fibroblasts. PDL also suppresses proliferation and triggers apoptosis of fibroblasts. Radiation suppresses proliferation of fibroblasts, leading to a reduction in collagen generation (14).

Triamcinolone acetonide (TAC) versus TAC with 5-FU in keloid treatment. (A) Forest plot representing difference in over 50% improvement between TAC and TAC with 5-FU. (B) Effects of treatment regime on improvement. (C) Complications of TAC and TAC with 5-FU.

Comparison of triamcinolone acetonide (TAC) with verapamil in the treatment of keloid. Forest plot showing differences in pooled scar pigmentation (A), vascularity (B), pliability (C), and height (D) between TAC and verapamil treatment.

Keloids and hypertrophic scars represent an exuberant healing response that poses a challenge for physicians. Patients at high risk of keloids are usually younger than 30 years and have darker skin. Sternal skin, shoulders and upper arms, earlobes, and cheeks are most susceptible to developing keloids and hypertrophic scars. High-risk trauma includes burns, ear piercing, and any factor that prolongs wound healing. Keloid formation often can be prevented if anticipated with immediate silicone elastomer sheeting, taping to reduce skin tension, or corticosteroid injections. Once established, however, keloids are difficult to treat, with a high recurrence rate regardless of therapy. Evidence supports silicone sheeting, pressure dressings, and corticosteroid injections as first-line treatments. Cryotherapy may be useful, but should be reserved for smaller lesions. Surgical removal of keloids poses a high recurrence risk unless combined with one or several of these standard therapies. Alternative postsurgical options for refractory scars include pulsed dye laser, radiation, and possibly imiquimod cream. Intralesional verapamil, fluorouracil, bleomycin, and interferon alfa-2b injections appear to be beneficial for treatment of established keloids. Despite the popularity of over-the-counter herb-based creams, the evidence for their use is mixed, and there is little evidence that vitamin E is helpful.

Corticosteroid injections for prevention and treatment of keloids and hypertrophic scars are perhaps the first-line option for family physicians. Corticosteroids suppress inflammation and mitosis while increasing vasoconstriction in the scar. Triamcinolone acetonide suspension (Kenalog) 10 to 40 mg per mL (depending on the site) is injected intralesionally, which, although painful, will eventually flatten 50 to 100 percent of keloids, with a 9 to 50 percent recurrence rate.9 Lidocaine (Xylocaine) may be combined with the corticosteroid to lessen pain, whereas using adjunctive cryotherapy immediately before injection may make the procedure easier by softening the scar (based on expert opinion).22 Combining cryotherapy and corticosteroid injections also improves outcomes more than either modality alone, although hypopigmentation is always a significant concern.23,24 Usually, two or three injections are given a month apart; however, therapy can continue for six months or longer.25 Newer keloids are more responsive to therapy than older, established lesions. Corticosteroid injections are more effective if combined with surgery; the sooner instituted, the greater the likelihood of success. Common adverse effects include atrophy, telangiectasias, and hypopigmentation.

Imiquimod 5% cream (Aldara), an immune response modifier that enhances healing, has also been used to help prevent keloid recurrence after surgical excision. The cream is applied on alternate nights for eight weeks after surgery. Although the trials have been small, the postsurgical recurrence rate averaged only 28 percent over a six- to nine-month follow-up period, with best results (2.9 percent recurrence) in low skin tension areas such as earlobes.12 Adverse effects include irritation and hyperpigmentation.

Intralesional fluorouracil (50 mg per mL, two to three times per week) appears to shrink keloids safely while avoiding the tissue atrophy and telangiectasia that may occur with repeated corticosteroid injections.30 Combining fluorouracil with corticosteroid injections and pulsed dye laser produced superior results more rapidly than corticosteroid injections alone or corticosteroids with fluorouracil.13 Good to excellent responses at 12 weeks as rated by a blinded observer were 15 percent for triamcinolone acetonide, 40 percent for triamcinolone plus fluorouracil, and 70 percent for all three modalities (all significant). Combining corticosteroids and fluorouracil diminished the adverse effects of corticosteroids. Rare skin complications of fluorouracil may include hyperpigmentation and wound ulceration. No systemic adverse effects (e.g., anemia, leucopenia, thrombocytopenia) occurred in this study.

Bleomycin is another useful chemotherapeutic agent; a standard approach is bleomycin tattooing 0.1 mL (1.5 IU per mL) over two to six sessions, with a maximal dose of 6 mL.31 Results of one study showed a total regression of 84 percent.18 Multiple intralesional punctures are probably safe because it is likely that less than 5 percent of the dose ever reaches the bloodstream.18 Compared with triamcinolone injections combined with cryotherapy, bleomycin tattoo performed significantly better for keloids larger than 100 mm2 (P = .03).19 Systemically administered bleomycin is capable of causing pulmonary fibrosis (at doses greater than 400 U) and various cutaneous reactions (at doses of 200 to 300 U), including hair loss, hyperpigmentation, fibrosis, and vasospasm, any of which warrants cessation of treatment.32 041b061a72