**10. Lupus erythematosus**

Lupus erythematosus is an autoimmune disease that can affect one or more internal organs as well as the skin. This disease is a clinical spectrum ranging from mildly affected patients with only localized skin disease to those at risk of dying from systemic manifestations. The skin involvement is among the most frequent symptoms; and is characterized by its natural history of relapsing and chronicity. The scalp (Fig 5) is a common area of involvement, and permanent alopecia may result with the following morphological features; sclero-atrophy, erythema, follicular hyperkeratosis, plugging and telangiectasia. The irreversible, scarring alopecia differs from the reversible non scarring alopecia that is seen in patients with systemic lupus erythematosus.

protective measures, including sunscreens, protective clothing and medical therapy includes

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Routine histologic examination of lesional skin from CLE patients is necessary, as the diagnosis of CLE generally requires clinicopathologic correlation and the distinction between different types of CLE based on histological findings without clinical correlation is difficult; all forms of CLE are similar histologically in broad terms. Histopathological features (Fig 6) include pilosebaceous atrophy, hyperkeratosis, parakeratosis, basement membrane thickening, subepidermal oedema and vasodilatation. A perivascular and peri-appendageal superficial and deep lymphoid cell infiltrate with plasma cells are other histolopathological findings.

**Figure 6.** DLE pathology. Note the hyperkeratosis, basal cell degeneration and heavy inflammatory infiltrate.

seen in other types of scarring alopecia.

Using immunohistochemistry[

Direct immunofluorescence (DIF) of lesional skin in CLE is an adjunctive test; it helps to confirm the diagnosis when the routine histological findings are equivocal. The test is positive only in some of lesional skin biopsies; so light microscopy should be carried out before DIF. For DIF, the optimal lesion of LE should be an established, erythematosus lesion, and of at least 6-8 weeks in duration. The most suggestive findings are the presence of multiple immunoreactants typically IgG and IgM, in a special pattern (bright in intensity, continuous, perifollicular, and granular) [8]. Sometimes complement components may be present includ‐ ing C3b and C1q. Scalp lesions have been reported to show the highest frequency of the DIF test (83 %), the immunoreactants deposits occur around hair follicles, an important feature not

zone (BMZ) in patients with active DLE and this explain the previous histological findings of thickened BMZ in DLE. There was an increase in the expression of the anchoring fibril and

9], there were significant alterations in the basement membrane

corticosteroids (topical or intralesional) and antimalarials.

Scarring alopecia in DLE may mimic other types of scarring alopecia seen in some dermatoses, the most common differential diagnosis of this is lichen planopilaris (LPP) and the differen‐ tiation between them is possible by early clinical and histological changes. Both LPP and DLE show perifollicular erythema and keratotic follicular papules, but the distinctive clinical features of DLE of the scalp are the presence of erythema, scaling, telangiectasia, and mottled hyperpigmentation within the areas of scarring alopecia and the presence of hyperkeratotic papules in the central part of the bald area in DLE, while in LPP it presents at the margin of the alopecia patch [7].

**Figure 5.** Discoid lupus erythematosus of the scalp. The typical scaling is evident.

DLE is a scarring disease and so early treatment is needed to control existing cutaneous lesions and limit scaring and to prevent the development of the disease. Patients with DLE lesions should have regular clinical evaluation accompanied by simple laboratory studies to evaluate the possible progression from the primary cutaneous disorder to the disorder accompanied by systemic involvement. Therapy begins with general measures such as the use of sunprotective measures, including sunscreens, protective clothing and medical therapy includes corticosteroids (topical or intralesional) and antimalarials.

**10. Lupus erythematosus**

18 Skin Biopsy - Diagnosis and Treatment

erythematosus.

the alopecia patch [7].

Lupus erythematosus is an autoimmune disease that can affect one or more internal organs as well as the skin. This disease is a clinical spectrum ranging from mildly affected patients with only localized skin disease to those at risk of dying from systemic manifestations. The skin involvement is among the most frequent symptoms; and is characterized by its natural history of relapsing and chronicity. The scalp (Fig 5) is a common area of involvement, and permanent alopecia may result with the following morphological features; sclero-atrophy, erythema, follicular hyperkeratosis, plugging and telangiectasia. The irreversible, scarring alopecia differs from the reversible non scarring alopecia that is seen in patients with systemic lupus

Scarring alopecia in DLE may mimic other types of scarring alopecia seen in some dermatoses, the most common differential diagnosis of this is lichen planopilaris (LPP) and the differen‐ tiation between them is possible by early clinical and histological changes. Both LPP and DLE show perifollicular erythema and keratotic follicular papules, but the distinctive clinical features of DLE of the scalp are the presence of erythema, scaling, telangiectasia, and mottled hyperpigmentation within the areas of scarring alopecia and the presence of hyperkeratotic papules in the central part of the bald area in DLE, while in LPP it presents at the margin of

**Figure 5.** Discoid lupus erythematosus of the scalp. The typical scaling is evident.

DLE is a scarring disease and so early treatment is needed to control existing cutaneous lesions and limit scaring and to prevent the development of the disease. Patients with DLE lesions should have regular clinical evaluation accompanied by simple laboratory studies to evaluate the possible progression from the primary cutaneous disorder to the disorder accompanied by systemic involvement. Therapy begins with general measures such as the use of sunRoutine histologic examination of lesional skin from CLE patients is necessary, as the diagnosis of CLE generally requires clinicopathologic correlation and the distinction between different types of CLE based on histological findings without clinical correlation is difficult; all forms of CLE are similar histologically in broad terms. Histopathological features (Fig 6) include pilosebaceous atrophy, hyperkeratosis, parakeratosis, basement membrane thickening, subepidermal oedema and vasodilatation. A perivascular and peri-appendageal superficial and deep lymphoid cell infiltrate with plasma cells are other histolopathological findings.

**Figure 6.** DLE pathology. Note the hyperkeratosis, basal cell degeneration and heavy inflammatory infiltrate.

Direct immunofluorescence (DIF) of lesional skin in CLE is an adjunctive test; it helps to confirm the diagnosis when the routine histological findings are equivocal. The test is positive only in some of lesional skin biopsies; so light microscopy should be carried out before DIF. For DIF, the optimal lesion of LE should be an established, erythematosus lesion, and of at least 6-8 weeks in duration. The most suggestive findings are the presence of multiple immunoreactants typically IgG and IgM, in a special pattern (bright in intensity, continuous, perifollicular, and granular) [8]. Sometimes complement components may be present includ‐ ing C3b and C1q. Scalp lesions have been reported to show the highest frequency of the DIF test (83 %), the immunoreactants deposits occur around hair follicles, an important feature not seen in other types of scarring alopecia.

Using immunohistochemistry[ 9], there were significant alterations in the basement membrane zone (BMZ) in patients with active DLE and this explain the previous histological findings of thickened BMZ in DLE. There was an increase in the expression of the anchoring fibril and collagen component antigens in the BMZ with gross thickening and protrusion into the dermis in active DLE lesions (Fig 7).

**Figure 8.** LPP of the scalp.

epidermis and the papillary dermis.

also show basal cell degeneration.

Histologically (Fig 9) has been reported to show two different patterns [11], each pattern characterized by the presence of specific histological features that reflects the specific stage of the progression of the disease. In the first pattern, hair follicles and the perifollicular dermis were mainly involved in the pathologic process, with no involvement of the interfollicular structures. In the second pattern, the pathologic changes extended to the interfollicular

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**Figure 9.** LPP pathology. The inflammation is mainly perifollicular with some involvement of the basal cell layers which

**Figure 7.** Anti-type IV collagen staining in DLE with an exaggerated expression as demonstrated by thickness of the basement membrane and protrusions.
