AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Clinical
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• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Background

Keloids are the result of an overgrowth of dense fibrous tissue that usually develops after healing of a skin injury. The tissue extends beyond the borders of the original wound, does not usually regress spontaneously, and tends to recur after excision. The first description of keloids (recorded on papyrus) concerned surgical techniques used in Egypt in 1700 BCE. Subsequently, in 1806, Alibert used the term cheloide, derived from the Greek chele, or crab's claw, to describe the lateral growth of tissue into unaffected skin.

In contrast, hypertrophic scars are characterized by erythematous, pruritic, raised fibrous lesions that typically do not expand beyond the boundaries of the initial injury and may undergo partial spontaneous resolution. Hypertrophic scars are common after thermal injuries and other injuries that involve the deep dermis.

Pathophysiology

Hypertrophic scars and keloids can be described as variations of typical wound healing. In a typical wound, anabolic and catabolic processes achieve equilibrium approximately 6-8 weeks after the original injury. At this stage, the strength of the wound is approximately 30-40% that of healthy skin. As the scar matures, the tensile strength of the scar improves as a result of progressive cross-linking of collagen fibers. At this point, the scar is usually hyperemic and it may be thickened, but it tends to subside gradually over months until a flat, white, pliable, possibly stretched, mature scar has developed. When an imbalance occurs between the anabolic and catabolic phases of the healing process, more collagen is produced than is degraded, and the scar grows in all directions. The scar is elevated above the skin and remains hyperemic. Excessive fibrous tissue is classified as either a keloid or a hypertrophic scar.

Kischer and Brody declared the collagen nodule to be the identifying structural unit of hypertrophic scars and keloids. The nodule, which is absent from mature scars, contains a high density of fibroblasts and unidirectional collagen fibrils in a highly organized and distinct orientation. In addition, keloids and hypertrophic scars differ from healthy skin by a rich vasculature, high mesenchymal cell density, and thickened epidermal cell layer. Attempts to clinically differentiate keloids from hypertrophic scars have proved to be difficult in the early phases of formation. Clinical differences become more apparent as lesions mature. The most consistent histologic difference is the presence of broad, dull, pink bundles of collagen in keloids, which are not present in hypertrophic scars.

Frequency

International

Only humans are affected by keloids, and both dominant and recessive modes of inheritance have been described. Although keloids occur in all age groups, they are rarely found in newborns or elderly persons and have the highest incidence in individuals aged 10-20 years.

Mortality/Morbidity

Keloids and hypertrophic scars located at most sites are primarily of cosmetic concern; however, some keloids or hypertrophic scars can cause contractures, which may result in loss of function if overlying a joint or in significant disfigurement if located on the face. Keloids and hypertrophic scars can be both painful and pruritic.

Keloids and hypertrophic scars are associated genetically with HLA-B14, HLA-B21, HLA-Bw16, HLA-Bw35, HLA-DR5, HLA-DQw3, and blood group A.

Race

Keloids form more frequently in Polynesian and Chinese persons than in Indian and Malaysian persons. As many as 16% of people in a random sampling of black Africans reported having keloids. White persons are least commonly affected.

Sex

The prevalence has been reported to be higher in young females than in young males, probably reflecting the greater frequency of earlobe piercing among females. Keloids and hypertrophic scars affect both sexes equally in other age groups.

Age

Onset occurs most commonly in individuals aged 10-30 years. Keloids occur less frequently at the extremes of age, although an increasing number of presternal keloids have resulted from coronary artery bypass operations and other similar procedures now undertaken in persons in older age groups.

CLINICAL

Section 3 of 11  

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History

Keloids and hypertrophic scars do not usually cause symptoms, but they may be tender, painful, or pruritic or they may cause a burning sensation. In addition to symptomatic relief, cosmetic concern is the primary reason patients seek medical intervention.

Physical

• Origins of lesions
• • Keloids manifest as exaggerated growths of scar tissue, usually in areas of previous trauma. Keloids extend past the areas of trauma, projecting above the level of the surrounding skin, but they rarely extend into underlying subcutaneous tissue.
  • Hypertrophic scars remain limited to the traumatized area and regress spontaneously within 12-24 months, although regression may not necessarily be complete.
• Clinical findings in lesions
• • Keloids range in consistency from soft and doughy to rubbery and hard. Recent studies have demonstrated how to differentiate and classify keloids according to how they feel.
  • Early lesions are often erythematous.
  • Lesions become brownish red and then pale as they age.
  • Lesions are usually devoid of hair follicles and other functioning adnexal glands.
  • Once lesions occur, the clinical course varies. Most lesions continue to grow for weeks to months and others grow for years. Growth is usually slow, but keloids occasionally enlarge rapidly, tripling in size within months. Once they stop growing, keloids do not usually cause symptoms and remain stable or involute slightly.
  • Keloids on the ears, neck, and abdomen tend to be pedunculated.
  • Keloids on the central chest and extremities are usually raised with a flat surface, and the base is often wider than the top.
  • Most keloids are round, oval, or oblong with regular margins; however, some have clawlike configurations with irregular borders.
  • Most patients present with 1 or 2 keloids; however, a few patients, especially patients with spontaneous keloids, have multiple lesions, as do patients who develop keloids as a consequence of acne or chickenpox.
  • Keloids overlying a joint can contract and restrict movement.
• Frequency of lesion sites
• • In white persons, keloids tend to be present, in decreasing order of frequency, on the face (with cheek and earlobes predominating), upper extremities, chest, presternal area, neck, back, lower extremities, breasts, and abdomen.
  • In black persons, the descending order of frequency tends to be earlobes, face, neck, lower extremities, breasts, chest, back, and abdomen.
  • In Asian persons, the descending order of frequency is earlobes, upper extremities, neck, breasts, and chest.

Causes

The exact mechanisms of keloid and hypertrophic scar pathogenesis continue to be an enigma for physicians and researchers alike, and no specific gene or set of genes has been identified; however, the increased prevalence of keloids paralleling increased cutaneous pigmentation suggests a genetic basis or, at least, a genetic linkage. Trauma to the skin, both physical (eg, earlobe piercing, surgery) and pathological (eg, acne, chickenpox), is the primary cause identified for the development of keloids. The presence of foreign material, infection, hematoma, or increased skin tension can also lead to keloid or hypertrophic scar formation in susceptible individuals.

DIFFERENTIALS

Section 4 of 11  

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Other Problems to be Considered

Acne keloidalis nuchae
Corneal keloids

WORKUP

Section 5 of 11  

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Lab Studies

• Diagnosis is usually based on clinical findings. Biopsy may confirm the diagnosis in equivocal cases.

Histologic Findings

Formation of collagen in keloids and hypertrophic scars in the inflammatory stage takes much longer than usual in healing wounds. Collagen fibers in granulation tissue are arranged in a whorled pattern. In keloids, the nodules demonstrate thick, hyalinized bands in the central portion of the nodule.

TREATMENT

Section 6 of 11  

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Medical Care

No single therapeutic modality is best for all keloids. The location, size, and depth of the lesion; the age of the patient; and the past response to treatment determine the type of therapy used. Prevention is key, but therapeutic treatment of hypertrophic scars and keloids includes occlusive dressings, compression therapy, intralesional corticosteroid injections, cryosurgery, excision, radiation therapy, laser therapy, interferon therapy, 5-fluorouracil (5-FU), doxorubicin, bleomycin, verapamil, retinoic acid, imiquimod 5% cream, tamoxifen, tacrolimus, botulinum toxin, and other promising therapies such as transforming growth factor (TGF)–beta3, and recombinant human (rh) interleukin (IL)–10 (rhIL-10), which are directed at decreasing collagen synthesis.

• Prevention: This is the first rule in keloid therapy.
• • Avoid performing nonessential cosmetic surgery in patients known to form keloids; however, the risk is lower among patients who have only earlobe lesions.
  • Close all surgical wounds with minimal tension.
  • Incisions should not cross joint spaces.
  • Avoid making midchest incisions, and ensure that incisions follow skin creases whenever possible.
• Standard treatments: These include occlusive dressings, compression therapy, and intralesional corticosteroid injections.
• • Occlusive dressings include silicone gel sheets and dressings, nonsilicone occlusive sheets, and Cordran tape. These measures have been used with varied success. Antikeloidal effects appear to result from a combination of occlusion and hydration, rather than from an effect of the silicone.
  • • Previous studies have shown that in patients treated with silicone occlusive sheeting with pressure worn 24 h/d for up to 12 months, 34% showed excellent improvement, 37.5% showed moderate improvement, and 28% demonstrated no or slight improvement.
    • Of patients treated with semipermeable, semiocclusive, nonsilicone-based dressings for 8 weeks, 60% experienced flattening of keloids, 71% had reduced pain, 78% had reduced tenderness, 80% had reduced pruritus, 87.5% had reduced erythema, and 90% were satisfied with the treatment.
    • Cordran tape is a clear surgical tape that contains flurandrenolide, a steroid that is uniformly distributed on each square centimeter of the tape, and it has been shown to soften and flatten keloids over time.
• • Compression therapy involves pressure, which has long been known to have thinning effects on skin. Reduction in the cohesiveness of collagen fibers in pressure-treated hypertrophic scars has been demonstrated by electron microscopy.
  • • Compression treatments include button compression, pressure earrings, ACE bandages, elastic adhesive bandages, compression wraps, spandex or elastane (Lycra) bandages, and support bandages. In one study, button compression (2 buttons sandwiching the earlobe applied after keloid excision) prevented recurrence during 8 months to 4 years of follow-up observation.
    • Other pressure devices include pressure earrings and pressure-gradient garments made of lightweight porous Dacron, spandex (also known as elastane), or bobbinet fabric (usually worn 12-24 h/d) and zinc oxide adhesive plaster. Overall, 60% of patients treated with these devices showed 75-100% improvement.
  • Corticosteroids, specifically intralesional corticosteroid injections, have been the mainstay of treatment. Corticosteroids reduce excessive scarring by reducing collagen synthesis, altering glucosaminoglycan synthesis, and reducing production of inflammatory mediators and fibroblast proliferation during wound healing. The most commonly used corticosteroid is triamcinolone acetonide (TAC) in concentrations of 10-40 mg/mL administered intralesionally with a 25- to 27-gauge needle at 4- to 6-week intervals.
  • • Intralesional steroid therapy as a single modality and as an adjunct to excision has been shown to be efficacious in various studies. Response rates varied from 50-100%, with recurrence rates of 9-50% in completely resolved scars.
    • When combined with excision, postoperative intralesional TAC injections yielded a recurrence rate of 0-100%, with most studies citing a rate of less than 50%.
    • Complications of repeated corticosteroid injections include atrophy, telangiectasia formation, and pigmentary alteration.
• Recent innovations: New treatments for keloids and hypertrophic scars include intralesional interferon, 5-FU, doxorubicin, bleomycin, verapamil, retinoic acid, imiquimod 5% cream, tacrolimus, tamoxifen, botulinum toxin, TGF-beta3, and rhIL-10.
• • Interferon therapy, including interferon alfa, interferon beta, and interferon gamma, has been demonstrated in in vitro studies to reduce keloidal fibroblast production of collagen types I, III, and VI mRNA.
  • • Interferon alfa and interferon beta also reduce fibroblast production of glycosaminoglycans (GAGs), which form the scaffolding for the deposition of dermal collagen. Interferon gamma enhances GAG production.
    • Interferon alfa, interferon beta, and interferon gamma have been shown to increase collagenase activity. Studies have shown that interferon gamma modulates a p53 apoptotic pathway by inducing apoptosis-related genes. p53 is a protein synthesized following DNA damage. Once damage is repaired, p53 is degraded. Mutations of this protein are believed to predispose cells to hyperproliferation, possibly resulting in keloid formation. In addition, p53 is a potent suppressor of IL-6, a cytokine implicated in hyperproliferative and fibrotic conditions.
    • Interferon injected into the suture line of keloid excision sites may be prophylactic for reducing recurrences. Berman and Flores reported statistically significant fewer keloid recurrences in a study of 124 keloid lesions after postoperative interferon alfa-2b injection treatment (5 million U, 1 million U injected per cm of scar) into keloid excision sites (18%) versus excision alone (51.1%) and TAC treatment (58.4%).
  • 5-FU, a pyrimidine analogue with antimetabolite activity, inhibits fibroblastic proliferation in tissue culture and is believed to reduce postoperative scarring by decreasing fibroblast proliferation. Some data suggest that 5-FU is effective in the treatment of hypertrophic scars and is somewhat effective in small keloids. Two studies have shown the effectiveness of 5-FU.
  • • In one prospective, randomized, uncontrolled trial, 28 patients were treated with weekly injections of 0.5-2 mL at a 50-mg/mL concentration of 5-FU for 12 weeks. At the 24-week follow-up, 70% of the patients had more than 50% improvement in keloid size.
    • In the other retrospective study of 1000 patients with hypertrophic scars and keloids over a 9-year period, the most effective regimen was found to be 0.1 mL of TAC (10 mg/mL) and 0.9 mL of 5-FU (50 mg/mL) up to 3 times a week.
  • Doxorubicin (Adriamycin) is a commonly used chemotherapeutic agent that irreversibly inactivates prolyl 4-hydroxylase in human skin fibroblasts and has been shown to inhibit collagen alpha-chain assembly.
  • • Sasaki et al showed through sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis that doxorubicin, at a clinically therapeutic concentration of 12.5 µm, inhibits the assembly of collagen triple-helical molecules. SDS-PAGE analysis of control cultures showed a large fraction of [3H]proline-labeled procollagen polypeptides in triple-helical conformation; however, after the addition of doxorubicin at 12.5 µm, a very small amount of intact alpha-chains were found.
    • These results suggest that the impaired wound healing observed in cancer patients who receive doxorubicin may result from the inhibition of prolyl 4-hydroxylase.
    • Further studies are warranted to determine if doxorubicin can be useful to treat patients with excessive scarring.
  • Bleomycin injections cause necrosis of keratinocytes with a mixed inflammatory infiltrate. In 2 studies, bleomycin was used to treat keloids and hypertrophic scars.
  • • In one study, bleomycin was given at a concentration of 1.5 IU/mL to 13 patients using the multiple-puncture method. Bleomycin was dripped onto the lesion, and then multiple punctures were made on the lesions using a syringe. Seven patients had complete flattening, 5 patients had highly significant flattening, and 1 patient had significant flattening.
    • In another study of 31 keloids, patients were treated with 3-5 infiltrates of bleomycin within a 1-month period. Total regression occurred in 84% of the keloids, and both keloid volume and functional impairment were reduced.
  • Verapamil is a calcium channel blocker that blocks the synthesis and secretion of extracellular matrix molecules (eg, collagen, GAGs, fibronectin) and increases fibrinase. In a study of 22 patients with keloids, patients were treated with surgical excision and 5 treatments of verapamil at 2.5 mg/mL (varying doses from 0.5-5 mL, depending on keloid size) over a 2-month period and were evaluated at 2-year follow-up. Two patients had keloids that decreased in size from the original lesion, 2 patients had hypertrophic scars, 4 patients had pruritus, and 1 patient had a keloid on the donor site.
  • Retinoic acid decreases normal tonofilament and keratohyalin synthesis, increases the production of mucoid substances and the epidermal cell growth rate, and inhibits DNA synthesis in vitro. In a clinical trial involving 21 patients with 28 keloids and hypertrophic scars, topical retinoic acid was applied for at least 3 months twice daily and showed favorable results in 77-79% of the lesions. This includes a decrease in the size and symptoms of the scar.
  • Imiquimod (1-[2-methylpropyl]-1H-imidazo[4,5-c]quinolin-4-amin) belongs to the family of imidazoquinolines. Imiquimod induces tumor necrosis factor-alpha (TNF-alpha), interferon-alpha and interferon-gamma, IL-1, IL-4, IL-5, IL-6, IL-8, and IL-12 and alters the expression of markers for apoptosis. In one study, 13 keloids were treated with excision in combination with nightly applications of imiquimod 5% cream for 8 weeks. Ten patients with 11 keloids completed the 6-month study, and no keloids recurred after 6 months. Mild irritation was experienced with the application of imiquimod, and some patients needed a vacation period from the medication. Hyperpigmentation was experienced by more than half of the patients in the study.
  • Tacrolimus is an immunomodulator that inhibits TNF-alpha. gli-1, an oncogene, has been found to be overexpressed in fibroblasts of keloids. Rapamycin, a close analogue of tacrolimus, was used in an in vitro study and was found to inhibit the gli-1 oncogene, thus giving a rationale to initiate clinical trials of topical tacrolimus and rapamycin. In an open-label pilot study, 11 patients used tacrolimus 0.1% ointment twice daily for 12 weeks on their keloids. Although the results were not statistically significant, the study showed a decrease in induration, tenderness, erythema, and pruritus for most patients.
  • Tamoxifen, a synthetic nonsteroidal antiestrogen used to treat breast cancer, has been shown to inhibit proliferation of keloid fibroblasts and their collagen synthesis in monolayer cultures. Hu et al demonstrated that tamoxifen exhibits a dose-dependent and reversible inhibition of contraction of adult human dermal fibroblast in vitro. Tamoxifen has also been shown to reduce TGF-alpha, and its isoform TGF-alpha1, production by keloid fibroblasts in vitro. Mikulec et al have shown that keloid fibroblasts have a significantly lower TGF-alpha1 production when exposed to 16 µmol/L of tamoxifen at day 2 of culture when compared with control keloid fibroblasts (P = .05).
  • TGF-beta and its isomers have been shown to play a central role in fibrotic disorders characterized by excessive accumulation of interstitial matrix material in the lungs, kidneys, liver, and other organs. TGF-beta1 and TGF-beta2 have been shown to stimulate fibroblasts to produce collagen and have a direct and independent effect on the contraction of fibroblasts in vitro. However, TGF-beta3 may prevent scarring.
  • • A study by Shah et al demonstrated that exogenous addition of TGF-beta3 reduces fibronectin and collagen types I and III deposition in the early stages of cutaneous rat wound healing and in overall wound scarring.
    • A new antifibrotic product, Justiva, will be released by Renovo in the near future. Justiva is derived from human recombinant TGF-beta3. This new medication has shown promise in a phase 1 trial and 2 phase 2 trials completed in the United Kingdom. In these studies, wounds treated with Justiva showed a statistically significant improvement in scar appearance, with a response rate of greater than 70%. After analyzing safety data on more than 1000 human subjects, Justiva does not seem to have safety or tolerability issues for use in the prevention or reduction of scarring.
  • ILs also regulate fibroblast differentiation and proliferation, and IL-10 has been shown to induce scarless healing when overexpressed in adult mouse wounds. Renovo has also developed Prevascar, a human recombinant IL-10 formulation. Preclinical experiments have demonstrated that application of Prevascar to the margins of acute incisional wounds by intradermal injection decreases subsequent scarring. Renovo is also currently involved in a phase 2, single-center, double-blinded, placebo-controlled, randomized clinical trial to evaluate the antiscarring efficacy of varying doses of Prevascar in 175 subjects (1400 wounds). This trial is expected to report in 2007 whether Prevascar is effective in preventing and/or reducing scarring of the skin.
• Radiation therapy
• • Using radiotherapy to treat keloids remains controversial. Although many studies have demonstrated efficacy and decreased recurrence rates, the safety of radiotherapy has been questioned.
  • In one retrospective study of superficial x-ray therapy of 24 excised keloids, the author reported a recurrence rate of 53%. Use of iridium Ir 192 interstitial irradiation after excisional surgery resulted in a 21% recurrence rate after 1 year. Excisional surgery and preoperative hyaluronidase solution (150 U/mL sodium chloride) followed by external radiation (7.2-10.8 Gy) had a 0% recurrence rate. Adjunctive high dose rate brachytherapy (¹⁹²Ir) used after excision and closure resulted in a 12% reoccurrence rate after 26 months.
  • When excisional surgery is followed by postoperative radiation therapy, the total fractionated dose should be a minimum of 12 Gy, according to a comparative study showing a higher recurrence rate for patients treated with total doses less than 12 Gy.
• Other potential therapies
• • Additional potential therapeutic options for treating hypertrophic and keloidal scarring that have been shown in vitro to affect collagen synthesis include the use of proline-cis-hydroxyproline and azetidine carboxylic acid, tranilast (antiallergic drug shown to decrease collagen and GAG synthesis), and pentoxifylline (inhibits DNA replication).
  • In addition, wounds treated with anti-TGF healed with minimal scar tissue formation and without affecting wound tensile strength. A possible candidate for affecting wounds via the neutralizing effect of TGF is the proteoglycan termed decorin.

Surgical Care

• Cryotherapy
• • Cryosurgical media (eg, liquid nitrogen) affects the microvasculature and causes cell damage via intracellular crystals, leading to tissue anoxia.
  • Generally, 1, 2, or 3 freeze-thaw cycles lasting 10-30 seconds each are used for the desired effect. Treatment may need to be repeated every 20-30 days. Take care to administer liquid nitrogen in short application periods because of the possibility of reversible hypopigmentation. Cryotherapy can cause pain and permanent depigmentation in selected patients.
  • As a single modality, cryosurgery led to total resolution with no recurrences in 51-74% of patients after 30 months of follow-up observation.
• Excision
• • Apply basic soft tissue handling techniques at primary wound repair sites.
  • Carefully plan closure with minimal tension, paralleling the relaxed skin tension lines.
  • Use buried sutures when necessary for layered closure and to reduce tension.
  • Whenever feasible, apply pressure dressings and garments during the immediate postoperative period to wounds of patients in whom hypertrophic scars and keloid formation occur.
  • Decreased recurrence rates have been reported with excision in combination with other postoperative modalities, such as radiotherapy, injected interferon, or corticosteroid therapy.
  • Excisional surgery alone has been shown to yield a 45-100% recurrence rate and should very rarely be used as a solitary modality, although excision in combination with adjunct measures can be curative. Most studies in which excisional surgery was combined with injected steroids indicated less than 50% recurrence.
  • The authors have studied the effects of topically applied imiquimod 5% cream (Aldara) on the postexcision recurrence rates of 13 keloids excised surgically from 12 patients.
  • • Starting the night of surgery, imiquimod 5% cream was applied for 8 weeks. Patients were examined at weeks 4, 8, 16, and 24 for local erythema, edema, erosions, pigment alteration, and/or recurrence of the keloid.
    • Of the 11 keloids evaluated at 24 weeks, none (0%) recurred. The rate of hyperpigmentation was 63.6%. Two cases of mild irritation and superficial erosion cleared with temporary discontinuation of imiquimod. Both patients completed the 8 weeks of topical therapy and the final 24-week assessment.
    • At 24 weeks, the recurrence rate of excised keloids treated with postoperative imiquimod 5% cream was lower than recurrence rates previously reported in the literature.
• Laser therapy
• • Ablation of keloids and hypertrophic scars using a carbon dioxide laser (10,600 nm) can cut and cauterize the lesion, creating a dry surgical environment with minimal tissue trauma. When used as a single modality, the carbon dioxide laser was associated with recurrence rates of 39-92%, and when the carbon dioxide laser was combined with postoperative injected steroids, it was associated with recurrence rates of 25-74%.
  • The argon laser (488 nm), similar to the carbon dioxide laser, can induce collagen shrinkage via generation of excessive localized heat. The argon laser has demonstrated recurrence rates of 45-93%.
  • The pulsed dye laser (585 nm) provides photothermolysis, resulting in microvascular thrombosis. Beginning in the 1980s, authors noted that scars became less erythematous, more pliable, and less hypertrophic after treatment with the 585-nm pulsed dye laser. The findings were later confirmed using objective measurements of erythema by reflectance spectrometry readings, scar height, and pliability measurements. Because of its efficacy, safety, and relatively low cost, the pulsed dye laser remains the laser treatment of choice for hypertrophic scars.
  • The Nd:YAG laser (1064 nm) has demonstrated recurrence rates of 53-100%.

MEDICATION

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Drug Category: Corticosteroids

Most commonly used corticosteroid is TAC.

Drug Category: Interferons

Family of glycoproteins produced mainly by eukaryotic cells when induced by viral and nonviral triggers. Antiviral properties include induction of 2'-5' A synthetase, ribonuclease L, and protein kinase P1. Antiproliferative properties include induction of 2'-5' A synthetase, inhibition of growth factors, enhancement of p53, and down-regulation of c-myc, c-fos, and certain c-ras. Immunoregulatory properties include induction of class I and II MHC antigens, increase of natural killer cells, and inhibition of the production of TH-2 cytokines.

Drug Category: Calcium channel blockers

Drug Category: Antineoplastics

Drug Category: Retinoid acid derivatives

Decrease normal tonofilament and keratohyalin synthesis, increase production of mucoid substances and epidermal cell growth rate, and inhibit DNA synthesis in vitro.

Drug Category: Immunosuppressants

Drug Category: Immune response modifiers

FOLLOW-UP

Section 8 of 11  

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• Medication
• Follow-up
• Miscellaneous
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Further Outpatient Care

• Because of the high rate of recurrence, a follow-up period of at least 1 year is necessary to fully evaluate the effectiveness of therapy.
• Close follow-up monitoring is vital during immediate and aggressive treatment of subsequent keloid formation. Noncompliant patients who are lost to follow-up care for months often return for further evaluation long after further adjunct treatment would have been most beneficial.
• Preoperative evaluation is critical to assess a patient's motivation for treatment and to assess the patient's ability to participate in long-term care and follow-up visits.

Deterrence/Prevention

• Advise patients to avoid sharp trauma to the skin.
• Minimize inflammation resulting from acne or surgery.

Complications

• Trauma to the keloid may predispose the lesion to erosion and localized bacterial infection.

Prognosis

• Keloids rarely resolve spontaneously; however, with treatment, they may become softer, less tender, less painful, and less pruritic.
• Following excision treatment alone, keloids frequently recur (>50%).

Patient Education

• Advise patients to avoid local skin trauma (eg, skin piercing, tattoos) and to control inflammatory acne. Initially, focus is placed on the alleviation of symptoms.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to keep accurate documentation, because the high risk of recurrence and potential for poor cosmetic outcome may be independent of the skill and experience of the treating physician
• Failure to obtain witnessed and informed consent following candid discussion with the patient regarding risks, benefits, and alternatives
• Failure to obtain photodocumentation, which should be considered for all patients

Special Concerns

• The patient should guide the focus to the scar-associated symptoms (eg, pruritus, pain, tenderness) or the cosmesis of the scar. A conservative approach should be considered for a patient who is concerned only with the scar-associated symptoms.
• Prevention is always the best advice that can be given to a patient who is prone to abnormal scarring, no matter how efficacious and safe scar treatments may become.

MULTIMEDIA

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Media file 1:  Clawlike outline of a keloid. Courtesy of Dirk M. Elston, MD.
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Media file 2:  Keloid. Courtesy of Dirk M. Elston, MD.
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Media file 3:  Keloid. Courtesy of Dirk M. Elston, MD.
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Media file 4:  Keloid. Courtesy of Dirk M. Elston, MD.
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Media file 5:  Histology of keloid demonstrating central zone of hyalinized collagen (hematoxylin and eosin stain). Courtesy of Dirk M. Elston, MD.
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Media file 6:  Histology of keloid demonstrating thick hyalinized collagen bundles (hematoxylin and eosin stain). Courtesy of Dirk M. Elston, MD.
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REFERENCES

Section 11 of 11

• Authors and Editors
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• References

• Al-Attar A, Mess S, Thomassen JM, et al. Keloid pathogenesis and treatment. Plast Reconstr Surg. Jan 2006;117(1):286-300. [Medline].
• Alhady SM, Sivanantharajah K. Keloids in various races. A review of 175 cases. Plast Reconstr Surg. Dec 1969;44(6):564-6. [Medline].
• Beckenstein MS, Kuniaki T, Matarasso A. The effect of Scarguard on collagenase levels using a full-thickness epidermal model. Aesth Surg J. 2004;24(6):1-5.
• Berman B, Bieley HC. Keloids. J Am Acad Dermatol. Jul 1995;33(1):117-23. [Medline].
• Berman B, Flores F. Interferons. In: Wolverton SE, ed. Comprehensive Dermatologic Drug Therapy. Philadelphia, Pa: WB Saunders; 2001:339-57.
• Berman B, Romagosa R, Zell D. Keloid Scarring. In: Lebwohl MG, Heymann WR, Berth-Jones J, Coulson I, eds. Treatment of Skin Disease: Comprehensive Therapeutic Strategies. 2nd ed. New York, NY: Elsevier Health; 2006:. Chapter 108.
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Article Last Updated: Feb 1, 2007