Atlas and Synopsis of Lever’s Histopathology of the Skin

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Noninflammatory, fish-like scales are clinically evident on the thigh in a middle-aged man with a strong family history of ichthyosis vulgaris. At this power, the epidermis appears normal, except for uniform thickening of the stratum corneum. The stratum corneum contains no parakeratotic nuclei, constituting orthokeratosis.

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The granular layer is diminished or, as here, completely absent. Hyperkeratosis with Normal or Hypergranulosis The stratum corneum is thickened, the granular cell layer is normal or thickened, and the dermis shows only sparse perivascular lymphocytes. There is no epidermal spongiosis or exocytosis. No Inflammation There is hyperkeratosis and the upper dermis contains only sparse perivascular lymphocytes.

It is only rarely present at birth. Although female heterozygotes are frequently affected, male gender has a more severe form of the disorder. The thickness of the adherent scales increases during childhood. In contrast to ichthyosis vulgaris, the flexural creases may be involved.

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Histopathology There is hyperkeratosis. The granular layer is normal or slightly thickened but not thinned as in dominant ichthyosis vulgaris. The epidermis may be slightly thickened. Epidermolytic Hyperkeratosis Clinical Summary This rather striking histologic reaction pattern is also known as granular degeneration of the epidermis. It is seen in some linear epidermal nevi and in bullous congenital ichthyosiform erythroderma. The disease results from mutations in the K1 and K10 keratin genes chromosomes 12 and 17, respectively , which encode the keratins in the suprabasal epidermis.

These mutations cause faulty assembly of keratin tonofilaments and impair their insertion into desmosomes. These flaws prevent normal development of the cytoskeleton, resulting in epidermal lysis and a tendency to form vesicles 4. Similar changes are also seen as one of the reaction patterns in Grover's disease, and the same pattern is commonly observed as P. Histopathology The salient histologic features are a perinuclear vacuolization of the cells in the stratum spinosum and the stratum granulosum; b irregular cellular boundaries peripheral to the vacuolization; 3 an increased number of irregularly shaped, large keratohyalin granules; and 4 compact hyperkeratosis in the stratum corneum.

Large dirty scales on the ankle are characteristic.

At scanning power, the epidermis appears normal, except for uniform thickening of the stratum corneum. The thickened stratum corneum contains no parakeratotic nuclei, constituting orthokeratosis. A normal granular layer is present. Epidermodysplasia Verruciformis Clinical Summary Epidermodysplasia verruciformis EV is a genetic disease characterized by human papillomavirus HPV infection with types not seen in otherwise healthy individuals 6. It usually begins in childhood and is characterized by a generalized infection by HPV, frequent association with cutaneous carcinomas, and abnormalities of cell- mediated immunity.

Two forms of EV are recognized. Popliteal flexures are involved with keratotic, almost verrucous, malodorous scale. Erosions appear in sites of bullae. The sole of the same patient's foot shows characteristic symptomatic yellow keratoderma. The patient's son shares this autosomal dominant condition.

The epidermis is thickened and there is papillomatosis these changes are not usually seen in focal acantholytic dyskeratoses. There is compact hyperkeratosis in the stratum corneum. The epidermis shows vacuolated keratinocytes with large keratohyalin granules. There is orthokeratotic hyperkeratosis. The keratohyalin granules are irregular and cell borders are ill defined. Sections show hyperkeratosis, vacuolar change of superficial keratinocytes, and hypergranulosis. The superficially located affected keratinocytes are swollen and irregularly shaped.

There are a few lymphocytes in the upper dermis. The nuclei are enlarged, with open chromatin, and there are prominent basophilic keratohyalin granules. Some of the cases are familial.

There is no tendency for malignant transformation in this form. The second form is primarily related to HPV- 5. There is often a familial history with an autosomal recessive or X-linked recessive inheritance. In addition to the plane warts, irregularly outlined, slightly scaling macules of various shades of brown, red, and white; tinea versicolor-like lesions; and seborrheic keratosis-like lesions have been noted. Development of Bowen's disease squamous cell carcinoma in situ within lesions in exposed areas is a common occurrence, and invasive lesions of squamous cell carcinoma are occasionally found.

EV-like lesions can develop in renal transplantation patients and human immunodeficiency virus HIV -infected persons. The underlying defect in EV is not clear but may involve oncogene or immunologic dysfunction.


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Histopathology The epidermal changes, although similar to those observed in verruca plana, often differ by being more pronounced and more extensive. The affected keratinocytes are swollen and irregularly shaped. They show abundant, slightly basophilic cytoplasm and contain numerous round, basophilic keratohyalin granules.

A few dyskeratotic cells may be seen in the lower part of the epidermis. Although some nuclei appear pyknotic, others appear large, round, and empty owing to marginal distribution of the chromatin. In immunocompromised patients, EV often lacks the histologic features of verruca plana, a focally thickened granular layer is a marker for viral detection, and the risk for dysplasia in such lesions is much higher than that in cases of EV not associated with acquired immunosuppression.

Conditions to consider in the differential diagnosis: lamellar ichthyosis X-linked ichthyosis epidermolytic hyperkeratosis epidermolytic acanthoma oculocutaneous tyrosinosis tyrosinemia acanthosis nigricans large cell acanthoma EV hyperkeratosis lenticularis perstans Flegel's disease IB2. Scant Inflammation There is hyperkeratosis and lymphocytes are minimally increased around the superficial plexus. There may be a few neutrophils in the stratum corneum.

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At scanning magnification, there is slight hyperkeratosis with minimal inflammation. At this power, the epidermis appears normal, except for slight uniform acanthosis. Subtle deposits of pink amorphous material amyloid are seen in dermal papillae.

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The granular layer is normal. There are deposits of amyloid filling the papillary dermis. Patient presented with pruritic papules on the pretibial areas. Pigmented discrete papules resulting from deposition of amyloid derived from keratinocytes. In contrast to macular amyloidosis, lichen amyloidosis reveals irregular acanthosis, papillomatosis, and hyperkeratosis. The papillary dermis is expanded and there is a mild perivascular inflammatory infiltrate.

At higher magnification, the amorphous deposits of amyloid are seen in the papillary dermis associated with pigment-laden macrophages. Lichen amyloidosis is characterized by closely set, discrete, brown-red pruritic, often somewhat scaly papules and plaques that are most commonly located on the legs, especially the shins. The plaques often have verrucous surfaces and then resemble hypertrophic lichen planus or lichen simplex chronicus. It is assumed by some that the pruritus leads to damage of keratinocytes by scratching and to subsequent production of amyloid.

Histopathology Lichen and macular amyloides show deposits of amyloid that are limited to the papillary dermis. Most of the amyloid is situated within the dermal papillae. Although the deposits are usually smaller in macular amyloidosis than in lichen amyloidosis, differentiation of the two on the basis of the amount of amyloid is not possible.

The two conditions actually differ only in the appearance of the epidermis, which is hyperplastic and hyperkeratotic in lichen amyloidosis.

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Occasionally, the amount of amyloid in macular amyloidosis is so small that it is missed, even when special stains are used on frozen sections. In such instances, more than one biopsy may be necessary to confirm the diagnosis. Conditions to consider in the differential diagnosis of this category: dermatophytosis lichen amyloidosis and macular amyloidosis IC.

Hyperkeratosis with Parakeratosis The stratum corneum is thickened, the granular cell layer is reduced, and there is parakeratosis. The dermis may show only sparse perivascular lymphocytes, although some of the conditions listed here may in other instances show more substantial inflammation. Some neoplastic disorders e. Scant or No Inflammation IC1. Scant or No Inflammation Lymphocytes are minimally increased around the superficial plexus. Dermatophytosis is prototypic 8. Dermatophytosis Clinical Summary Fungal infections of seven anatomical regions are commonly recognized: tinea capitis including tinea favosa or favus of the scalp , tinea barbae, tinea faciei, tinea corporis including tinea imbricata , tinea cruris, tinea of the hands and feet, and tinea unguium.

Tinea corporis may be caused by any dermatophyte, but by far the most common cause in the United States is Trichophyton rubrum, followed by Microsporum canis and Trichophyton mentagrophytes. IC1 Tinea pedis. A leading edge of scale and erythema in a moccasin distribution characterizes this infection, most commonly caused by the dermatophyte Trichophyton rubrum.

There is slight uniform thickening of the stratum corneum. At high magnification, there is mixed orthokeratotic hyperkeratosis often sandwiched above a layer of parakeratosis and with focal collections of neutrophils.