Lichen Sclerosus

The Scar Solution Natural Scar Removal

The Scar Solution By Sean Lowry

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LS is a lymphocyte-mediated inflammatory disease characterized by pallor and scarring. It is commoner in females and can affect any age but the majority of patients are either prepubertal or menopausal (21-26). The etiology is unknown, but there is evidence to support that LS is an autoimmune disorder, and in females it may be

Table 6 Crohn's Disease

Diagnosis

Symptoms

Clinical appearance

Differential diagnosis

Therapy

Crohn's disease

Pain and, less often, itch. Wetness if lymphatics are leaking lymph

Edema, erythema, Hidradenitis and ulceration. suppurativa Deep, wide fissures. Edematous perianal skin tags and pyoderma gangrenosum

Topical potent steroid ointments. Oral metronidazole. Treatment of GIT involvement Infliximab for fistulas Exploration of sinus tracts to exclude fistula formation

Abbreviation: GIT, gastrointestinal tract.

associated with other autoimmune disorders such as vitiligo in children and thyroid disease in older women.

The classical lesions seen on the extragenital skin are ivory white papules and plaques with follicular swelling and ecchymosis (Fig. 13A). Anogenital disease tends to be characterized by flatter lesions of atrophic, whitened epithelium, which may become confluent extending around the vulvar and perianal skin in a figure of eight configuration (the "keyhole" distribution, cigarette paper wrinkling rather than white) (Fig. 13B). There may also be bullae, erosions, and ulceration. The sites

Clitorectomy
Figure 12 (A) Hidradenitis suppurativa showing inflamed nodules, abscesses, and large linear sinus tracts. (B) Hidradenitis suppurativa—the inflammation frequently involves the sweat glands.
Table 7 Hidradenitis Suppurativa

Clinical

Differential

Diagnosis

Symptoms

appearance

diagnosis

Therapy

Hidradenitis

Painful

Pustules, nodules,

Crohn's

Long-term oral

suppurativa

discharge

and abscesses.

disease

tetracyclines

Linear sinus

Antiseptic washes

tracts

and weight

reduction; oral

retinoids

Surgical excision

to lay open

sinus tracts,

and excision

and grafting

for extensive

disease poorly

controlled with

medical

treatment

most commonly affected are the inner aspects of the labia majora, labia minora, clitoris, and clitoral hood. Less commonly lesions occur in the genitocrural folds. Vestibular involvement is rare and vaginal lesions do not occur, as LS seems to spare noncornified stratified squamous epithelia, i.e., mucosal epithelium. Perianal lesions occur in approximately 30% of female patients in contrast to men who do not seem to develop perianal involvement. Extragenital lesions occur in some women with vulvar disease. The extragenital areas may be truncal, at sites of pressure, upper back, wrists, buttocks, and thighs. The Koebner phenomenon has also been reported at sites of radiotherapy, scar tissue, and vaccination sites. Facial, scalp, and nail involvement (27) have all been reported. Lesions of LS in the oral cavity are extremely rare and many of the reports of oral involvement in the literature have often not been confirmed histologically and many have probably been examples of LP (28). It is not uncommon for patients with vulvar LS to have coexistent oral LP.

LS is a scarring dermatosis and the changes that can occur on the vulva include loss of the labia minora, and sealing over of the clitoral hood, burying the clitoris. Introital narrowing because of anterior and posterior labial fusion sometimes results in a tiny opening into the vestibule. Milia may occur.

The classical histology is a thinned epidermis with flattening of the rete pegs. The underlying dermis is hyalinized (homogenized appearance). Below the hyali-nized area is a lymphocytic mixed infiltrate (Fig. 13C). In some cases the epidermis is not thin but thickened, i.e., with squamous cell hyperplasia.

The differential diagnosis includes vitiligo, mucous membrane pemphigoid, LP, and morphea as they may present with a similar clinical appearance. There can be clinical and histological overlap between morphea, LP, and LS.

The incidence of SCC developing on LS in clinical practice is of the order of 4% or less.

The histological patterns associated with SCC arising on LS include epithelial hyperplasia and both differentiated and undifferentiated intraepithelial neoplasia.

Lichen Sclerosus Vulva

Figure 13 (A) Lichen sclerosus showing white wrinkled skin on the inner aspects with sheets of ecchymosis on the inner labia minora. (B) (See color insert) Lichen sclerosus involving the vulva and perianal skin with extension into the genitocrural folds, resulting in loss of the labia minora and sealing over of the clitoral hood. (C) (See color insert) Lichen sclerosus—there is thinning of the epidermis with loss of rete pegs and dermal homogenization. Dermal inflammation beneath the area of dermal homogenization is variable and is minimal here.

Figure 13 (A) Lichen sclerosus showing white wrinkled skin on the inner aspects with sheets of ecchymosis on the inner labia minora. (B) (See color insert) Lichen sclerosus involving the vulva and perianal skin with extension into the genitocrural folds, resulting in loss of the labia minora and sealing over of the clitoral hood. (C) (See color insert) Lichen sclerosus—there is thinning of the epidermis with loss of rete pegs and dermal homogenization. Dermal inflammation beneath the area of dermal homogenization is variable and is minimal here.

Verrucous carcinoma has also been described in association with LS. More rarely, vulvar basal cell carcinoma (29) and melanoma (30) have been reported occurring in association with LS. The validity of the case report of an association with malignant melanoma and LS was questioned but the original authors upheld their view.

Treatment: The current recommended treatment for uncomplicated LS is a potent topical corticosteroid, e.g., clobetasol propionate (31). There are no randomized controlled trials providing evidence for any particular corticosteroid or treatment regimen being more effective than any other. The regimen recommended by the author for a newly diagnosed case is initially clobetasol propionate once a night for four weeks then alternate nights for four weeks and for the final month twice a week. A 30 g tube of clobetasol propionate should last 12 weeks and the patient is then reviewed. The clobetasol propionate is then continued and used as and when required. Most patients seem to require 30 to 60 g annually. Some patients will go into complete remission requiring no further treatment. Others will continue to have flares and remissions and they are advised to use clobetasol propionate as required. A soap substitute is also recommended, and an information sheet on LS and the instructions for the use of the topical steroid. In the past topical testosterone was used with an improvement in the clinical appearance and diminution of symptoms. Clobetasol dipropionate is a more effective treatment and has now replaced testosterone in the treatment of LS. Surgical excision is not necessary in the management of most LS and it should be used exclusively for the management of functional problems because of postinflammatory scarring (32,33), premalignant lesions, and malignancy (Table 8).

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Responses

  • frank
    Can lichen sclerosus go into remission?
    2 years ago
  • sarah
    What is lichen sclerosus pictures?
    3 months ago

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