๐ ็ธฝ็ฎ้ ๏ฝ ๐ ่ฑๆๅๆ๏ผๆฌ็ฏ๏ผ ๏ฝ ๐ ๅฎๆด็ฟป่ญฏ ๏ฝ โญ ็ฒพ่ฏ็ญ่จ
Pharmacotherapy
Pharmacotherapy
While the pathophysiology of scar formation remains incompletely understood, the fibroblast is identified as an important cellular target. By inhibiting fibroblast proliferation and cell division through the use of antimitotic drugs, scars can be reduced in size and symptomatology.70 The mechanistic process by which this occurs is poorly understood, though Col-1, TGF-ฮฒ1, and MMP-2 have been identified as significant targets.71 The two major classes of antimitotic drugs are corticosteroids and antitumor agents. Although the use of intralesional corticosteroids is already common practice for many physicians, there is significant potential efficacy of combination therapy with other drugs, such as 5-FU.
Corticosteroids Intralesional corticosteroid therapy (i.e., dexamethasone, triamcinolone) has long been the standard of care for hypertrophic and keloid scarring. Multiple studies show that this drug class consistently inhibits fibroblast cell growth and at high dosages induces fibroblast apoptosis.70 However, inconsistent treatment sessions and inappropriate dosing are associated with treatment failure, scar recurrence, and undesirable side effects such as epidermal atrophy, lipoatrophy, hypopigmentation, and telangiectasia formation. If patients are treated with intralesional corticosteroid monotherapy, it is important to educate them on the need for consistent follow-up and repeated treatments. Appropriate drug concentration selection should be based upon scar thickness and location and is expected to change (i.e., use of lower concentration) as the scar begins to atrophy. The precise volume of an intralesional corticosteroid injection required to induce atrophy is yet to be defined, but the clinical endpoint used by the authors is visual blanching of the scar. A conservative and cautious approach should be employed in thick scars where injections may be made at multiple levels and blanching may not always be observed.