| Keloid |
| Classification and external resources |
Keloid on the throat |
| ICD-10 |
L91.0 |
| ICD-9 |
701.4 |
| MedlinePlus |
000849 |
| eMedicine |
article/1057599 article/1298013 |
| MeSH |
D007627 |
A keloid ( /ˈkiːlɔɪd/; also keloidal scar)[1] is a type of scar which, depending on its maturity, is composed mainly of either type III (early) or type I (late) collagen. It is a result of an overgrowth of granulation tissue (collagen type 3) at the site of a healed skin injury which is then slowly replaced by collagen type 1. Keloids are firm, rubbery lesions or shiny, fibrous nodules, and can vary from pink to flesh-coloured or red to dark brown in colour. A keloid scar is benign and not contagious, but sometimes accompanied by severe itchiness, pain,[2] and changes in texture. In severe cases, it can affect movement of skin.
Keloids should not be confused with hypertrophic scars, which are raised scars that do not grow beyond the boundaries of the original wound.
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Contents
- 1 Signs and symptoms
- 2 Cause
- 3 Pathology
- 4 Treatments
- 5 Epidemiology
- 6 History
- 7 Gallery
- 8 References
- 9 External links
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Signs and symptoms
Keloids expand in claw-like growths over normal skin.[3] They have the capability to hurt with a needle-like pain or to itch without warning, although the degree of sensation varies from patient to patient.
If the keloid becomes infected, it may ulcerate. Removing the scar is one treatment option; however, it may result in more severe consequences: the probability that the resulting surgery scar will also become a keloid is high, usually greater than 50%. Laser treatment has also been used with varying degrees of success.
Keloid from being whipped.
[4]
Keloids form within scar tissue. Collagen, used in wound repair, tends to overgrow in this area, sometimes producing a lump many times larger than that of the original scar. Although they usually occur at the site of an injury, keloids can also arise spontaneously. They can occur at the site of a piercing and even from something as simple as a pimple or scratch. They can occur as a result of severe acne or chickenpox scarring, infection at a wound site, repeated trauma to an area, excessive skin tension during wound closure or a foreign body in a wound. Keloids can sometimes be sensitive to chlorine. Keloid scars can grow, if they appear at a younger age, because the body is still growing.
Location
Keloids can develop in any place where an abrasion has occurred. They can be the result of pimples, insect bites, scratching, burns, or other skin trauma. Keloid scars can develop after surgery. They are more common in some sites such as the central chest, the back and shoulders and the ear lobes. They can also occur on body piercings. The most common spots are earlobes, arms, and over the collar bone.
Cause
Intentional
The Olmec of Mexico in pre-Columbian times used keloid scarification as a means of decoration.[citation needed] The Nuer and Nuba use lip plugs, keloid tattoos along the forehead, keloid tattoos along the chin and above the lip, and cornrows.[citation needed] As a part of a ritual, certain people groups of Papua New Guinea cut their skin and insert clay or ash into the wounds so as to develop permanent bumps (known as keloids or weals).[citation needed] This practice honors members of a tribe who are celebrated for their courage and endurance.[citation needed]
Pathology
Histologically, keloids are fibrotic tumors characterized by a collection of atypical fibroblasts with excessive deposition of extracellular matrix components, especially collagen, fibronectin, elastin, and proteoglycans. Generally, they contain relatively acellular centers and thick, abundant collagen bundles that form nodules in the deep dermal portion of the lesion. Keloids present a therapeutic challenge that must be addressed, as these lesions can cause significant pain, pruritus (itching), and physical disfigurement. They may not improve in appearance over time and can limit mobility if located over a joint.
Keloids affect both sexes equally, although the incidence in young female patients has been reported to be higher than in young males, probably reflecting the greater frequency of earlobe piercing among women. The frequency of occurrence is 15 times higher in highly pigmented people. Persons of African descent are at increased risk of keloid occurrences.[5]
Treatments
The best treatment is prevention in patients with a known predisposition. This includes preventing unnecessary trauma or surgery (including ear piercing, elective mole removal), whenever possible. Any skin problems in predisposed individuals (e.g., acne, infections) should be treated as early as possible to minimize areas of inflammation.
- Intralesional corticosteroids are first-line therapy for most keloids. A systematic review found that up to 70% of patients respond to intralesional corticosteroid injection with flattening of keloids, although the recurrence rate is high in some studies (up to 50% at five years)[6] While corticosteroids are one of the more common treatments, injections into and in close proximity to keloid tissue can be highly painful and can produce undesirable results in female patients.
- Excision by scalpel excision may be indicated if injection therapy alone is unsuccessful or unlikely to result in significant improvement. Excision should be combined with preoperative, intraoperative, or postoperative triamcinolone or interferon injections.[6] Recurrence rates from 45 to 100% have been reported in patients treated with excision alone; this falls to below 50% in patients treated with combination therapy.[7]
- Gel sheeting with both hydrogel and silicone scar sheets have been used for the treatment of symptoms (e.g., pain and itching) in patients with established keloids, as well as for the management of evolving keloids and the prevention at the sites of new injuries. While the precise mechanism of action is still poorly understood, there is evidence that application of gel sheeting may reduce the incidence of abnormal scarring. A controlled study found significant changes in growth factor levels of fibronectin and IL-8 with application of hydrogel sheeting with respect to normal skin. Silicone sheeting was associated with changing growth factor levels of only fibronectin.[8]
- Cryosurgery is most useful in combination with other treatments for keloids.[7] The major side effect is permanent hypopigmentation, which limits its use in people with darker skin.
- Radiation therapy, in most studies,[6] but not all, has been found to be highly effective in reducing keloid recurrence, with improvement rates of 70 to 90% when administered after surgical excision. A small, randomized trial of treatments after surgery found recurrences in two of 16 earlobe keloids (13%) treated with radiation therapy and in four of 12 earlobe keloids (33%) treated with steroid injections.[9] However, concern regarding the potential long-term risks (e.g., malignancy) associated with using radiation for an essentially benign disorder limits its utility in most patients. Only a few cases of malignancy that may have been associated with radiation therapy for keloids have been reported. Although causation cannot be confirmed in these cases, caution should still be used when prescribing radiation therapy for keloids, particularly when treating younger patients.It may occasionally be appropriate as treatment for keloids resistant to other therapies. In addition, radiation therapy may be indicated for lesions that are not amenable to resection.
- Interferon alpha injections may reduce recurrence rates postoperatively. However, all currently available studies of interferon therapy suffer from methodologic problems, making an evidence-based recommendation regarding its use difficult.[6]
- Pulsed dye laser treatment can be beneficial for keloids, and appears to induce keloid regression through suppression of keloid fibroblast proliferation, and induction of apoptosis and enzyme activity. Combination treatment with pulsed dye laser plus intralesional therapy with corticosteroids and/or fluorouracil may be superior to either approach alone.[10]
Epidemiology
Persons of any age can develop a keloid. Children under 11 are less likely to develop keloids, even from ear piercing. Keloids may also develop from pseudofolliculitis barbae; continued shaving when one has razor bumps will cause irritation to the bumps, infection, and over time keloids will form. Persons with razor bumps are advised to stop shaving in order for the skin to repair itself before undertaking any form of hair removal. The tendency to form keloids is speculated to be hereditary.[citation needed] Keloids can tend to appear to grow over time without even piercing the skin, almost acting out a slow tumorous growth; the reason for this is unknown. If a keloid grows too large, removal is the only solution, resulting in a scar or, in worst cases, amputation.
History
Keloids were described by Egyptian surgeons around 1700 BC. Baron Jean-Louis Alibert (1768–1837) identified the keloid as an entity in 1806. He called them cancroïde, later changing the name to chéloïde to avoid confusion with cancer. The word is derived from the Greek χηλή, chele, meaning "hoof", here in the sense of "crab pincers", and the suffix -oid, meaning "like". For many years, Alibert's clinic at Hôpital Saint-Louis was the world’s center for dermatology.
Gallery
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| Young male with bilateral keloid formation on the plantar surfaces of feet |
References
- ^ Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. pp. 1499. ISBN 1-4160-2999-0.
- ^ Ogawa R (February 2010). "The most current algorithms for the treatment and prevention of hypertrophic scars and keloids". Plast. Reconstr. Surg. 125 (2): 557–68. doi:10.1097/PRS.0b013e3181c82dd5. PMID 20124841. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0032-1052&volume=125&issue=2&spage=557.
- ^ Meenakshi J, Jayaraman V, Ramakrishnan KM, Babu M (2005). "Keloids and hypertrophic scars: a review". Indian J Plast Surg 38 (2): 175–9. doi:10.4103/0970-0358.19796. http://www.ijps.org/article.asp?issn=0970-0358;year=2005;volume=38;issue=2;spage=175;epage=179;aulast=Meenakshi.
- ^ Kathleen Collins, "The Scourged Back," History of Photography 9 (January 1985): 43-45.[1]
- ^ Wound Healing, Keloids at eMedicine
- ^ a b c d Shaffer JJ, Taylor SC, Cook-Bolden F (2002). "Keloidal scars: a review with a critical look at therapeutic options". J Am Acad Dermatol 46 (2 Suppl Understanding): 63–97. PMID 11807470.
- ^ a b Berman B, Bieley HC (1996). "Adjunct therapies to surgical management of keloids". Dermatologic Surgery 22 (2): 126–130. PMID 8608373.
- ^ Ricketts, C. H.; Martin, L.; Faria, D. T.; Saed, G. M.; Fivenson, D. P. (1996). "Cytokine mRNA changes during the treatment of hypertrophic scars with silicone and nonsilicone gel dressings". Dermatologic surgery : official publication for American Society for Dermatologic Surgery \et al.] 22 (11): 955–959. doi:10.1016/S1076-0512(96)00429-3. PMID 9063511. edit
- ^ Sclafani AP, Gordon L, Chadha M, Romo T 3rd (1996). "Prevention of earlobe keloid recurrence with postoperative corticosteroid injections versus radiation therapy: a randomized, prospective study and review of the literature". Dermatologic Surgery 22 (6): 569–574. doi:10.1016/1076-0512(96)00060-X. PMID 8646474.
- ^ Asilian A, Darougheh A, Shariati F (2006). "New combination of triamcinolone, 5-Fluorouracil, and pulsed-dye laser for treatment of keloid and hypertrophic scars". Dermatologic Surgery 32 (7): 907–915. doi:10.1111/j.1524-4725.2006.32195.x. PMID 16875473.
External links
- Keloids and hypertrophic scars, german version (Rossmann N, 2004)
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Cutaneous keratosis, ulcer, atrophy, and necrobiosis (L82–L94, 700–701.5)
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| Epidermal thickening |
- keratoderma: Keratoderma climactericum
- Paraneoplastic keratoderma
- Acrokeratosis paraneoplastica of Bazex
- Aquagenic keratoderma
- Drug-induced keratoderma
- Paraneoplastic keratoderma
- psoriasis
- Keratoderma blennorrhagica
- keratosis: Seborrheic keratosis
- Clonal seborrheic keratosis
- Common seborrheic keratosis
- Irritated seborrheic keratosis
- Seborrheic keratosis with squamous atypia
- Reticulated seborrheic keratosis
- Dermatosis papulosa nigra
- Keratosis punctata of the palmar creases
- other hyperkeratosis: Acanthosis nigricans
- Confluent and reticulated papillomatosis
- Callus
- Ichthyosis acquisita
- Arsenical keratosis
- Chronic scar keratosis
- Hyperkeratosis lenticularis perstans
- Hydrocarbon keratosis
- Hyperkeratosis of the nipple and areola
- Inverted follicular keratosis
- Lichenoid keratosis
- Multiple minute digitate hyperkeratosis
- PUVA keratosis
- Reactional keratosis
- Stucco keratosis
- Thermal keratosis
- Viral keratosis
- Warty dyskeratoma
- Waxy keratosis of childhood
- other hypertrophy: Keloid
- Hypertrophic scar
- Cutis verticis gyrata
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| Necrobiosis/granuloma |
| Necrobiotic/palisading |
- Granuloma annulare
- Perforating
- Generalized
- Subcutaneous
- Granuloma annulare in HIV disease
- Localized granuloma annulare
- Patch-type granuloma annulare
- Necrobiosis lipoidica
- Annular elastolytic giant cell granuloma
- Granuloma multiforme
- Necrobiotic xanthogranuloma
- Palisaded neutrophilic and granulomatous dermatitis
- Rheumatoid nodulosis
- Interstitial granulomatous dermatitis/Interstitial granulomatous drug reaction
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| Foreign body granuloma |
- Beryllium granuloma
- Mercury granuloma
- Silica granuloma
- Silicone granuloma
- Zirconium granuloma
- Soot tattoo
- Tattoo
- Carbon stain
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| Other/ungrouped |
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Dermis/
localized CTD |
Cutaneous lupus
erythematosus |
- chronic: Discoid
- Panniculitis
- ungrouped: Chilblain
- Lupus erythematosus–lichen planus overlap syndrome
- Tumid
- Verrucous
- Rowell's syndrome
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Scleroderma/
Morphea |
- Localized scleroderma
- Localized morphea
- Morphea–lichen sclerosus et atrophicus overlap
- Generalized morphea
- Atrophoderma of Pasini and Pierini
- Pansclerotic morphea
- Morphea profunda
- Linear scleroderma
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Atrophic/
atrophoderma |
- Lichen sclerosus
- Anetoderma
- Schweninger–Buzzi anetoderma
- Jadassohn–Pellizzari anetoderma
- Atrophoderma of Pasini and Pierini
- Acrodermatitis chronica atrophicans
- Semicircular lipoatrophy
- Follicular atrophoderma
- Linear atrophoderma of Moulin
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| Perforating |
- Kyrle disease
- Reactive perforating collagenosis
- Elastosis perforans serpiginosa
- Perforating folliculitis
- Acquired perforating dermatosis
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| Skin ulcer |
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| Other |
- Calcinosis cutis
- Sclerodactyly
- Poikiloderma vasculare atrophicans
- Ainhum/Pseudo-ainhum
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noco(i/b/d/q/u/r/p/m/k/v/f)/cong/tumr(n/e/d), sysi/epon
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proc, drug (D2/3/4/5/8/11)
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