Intralesional steroids for alopecia areata

Cutaneous lichen planus may resolve spontaneously within one to two years, although lichen planus affecting mucous membranes may be more persistent and resistant to treatment. Recurrences are common, even with treatment. Table 4 summarizes the treatment of nongenital cutaneous lichen planus lesions. High-potency topical corticosteroids are first-line therapy for cutaneous lichen planus. 14 – 16 Oral antihistamines (., hydroxyzine [Vistaril]) may be used to control pruritus. Hypertrophic lesions are treated with intralesional triamcinolone acetonide (Kenalog), 5 to 10 mg per mL injection ( to 1 mL per 2-cm lesion). 14

Andreoli, . et al. (1997): Cecil Essentials of Medicine; (4-th ed.)- Company,.
Fauci, . et al. (1998): Harrison’s principles of internal medicine; (14-th ed.)-The McGraw-Hill Companies INC.,.
Shiau, ., Toren, . (2006): The Toronto Notes 2006: Comprehensive Medical References, 26-nd Ed., Canada.
Tierney, . (1997): Pocket guide to the essentials of diagnosis and treatment; (1-th ed.)- Lange medical book, .
Younger-Lewis,C.; Complete home medical guide;Canadian Medical Association (1-st ed.), Dk Publishing Inc.

Healthy, young adults can usually tolerate corticosteroid pills with few side effects. However, doctors do not prescribe corticosteroid pills as often as other treatments for alopecia areata, because of the health risks and side effects associated with using them for a long period of time. It’s important to talk to your doctor about your goals for treatment and possible side effects of the medication, to be sure the benefits of using corticosteroid pills in your case are greater than the risks. As with other options, hair regrown with corticosteroid use may fall back out once treatment is stopped.

We hypothesize that the fibroblast, or the myofibroblast, or both are the key cells responsible for keloid and hypertrophic scar formation. These cell types produce the bulk of extracellular matrix components during normal wound healing. In fact, experimental evidence suggests that hy­pertrophic scars and keloids result from excessive amounts of collagen and proteoglycan production or from lack of remodeling of these moie­ties.''-" We also hypothesize that wound tension is a major factor in the formation of both the hypertrophic scar and the keloid, which occurs sec­ondary to direct biochemical changes induced by this mechanical factor. Most likely these changes are a direct result of the effect of wound tension on the metabolism of the fibroblast or myofibroblast. Fibroblasts have been shown to increase cell proliferation in response to mechanical tension in Mechanical stretch alone has been shown to raise the number of myofibroblasts in mouse dermis in Presumably, mechanical ten­sion is also responsible for a positive balance in the collagen and proteo­glycan production-degradation cycle in the wound healing under exces­sive tension. We are currently studying the effects of mechanical tension on wound healing at the biochemical level. The cause-effect relationship between hypertrophic scar and keloid formation as well as other etiologic factors, such as the age and race of the patient, remain more highly spec­ulative and are not discussed here.

Intralesional steroids for alopecia areata

intralesional steroids for alopecia areata

We hypothesize that the fibroblast, or the myofibroblast, or both are the key cells responsible for keloid and hypertrophic scar formation. These cell types produce the bulk of extracellular matrix components during normal wound healing. In fact, experimental evidence suggests that hy­pertrophic scars and keloids result from excessive amounts of collagen and proteoglycan production or from lack of remodeling of these moie­ties.''-" We also hypothesize that wound tension is a major factor in the formation of both the hypertrophic scar and the keloid, which occurs sec­ondary to direct biochemical changes induced by this mechanical factor. Most likely these changes are a direct result of the effect of wound tension on the metabolism of the fibroblast or myofibroblast. Fibroblasts have been shown to increase cell proliferation in response to mechanical tension in Mechanical stretch alone has been shown to raise the number of myofibroblasts in mouse dermis in Presumably, mechanical ten­sion is also responsible for a positive balance in the collagen and proteo­glycan production-degradation cycle in the wound healing under exces­sive tension. We are currently studying the effects of mechanical tension on wound healing at the biochemical level. The cause-effect relationship between hypertrophic scar and keloid formation as well as other etiologic factors, such as the age and race of the patient, remain more highly spec­ulative and are not discussed here.

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