S5C1 - CELL-POOR LICHENOID REACTIONS (tier 1)

(LE-like lichenoid Reactions)

SECTION 5

Chapter 1

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Richard J. Reed, M.D., New Orleans, LA 70125

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Lichenoid Reactions in the Setting of Collagen-Vascular Disease, including Lupus Erythematosus and Dermatomyositis (plus miscellaneous lichenoid reactions)

This section presents a discussion of lichenoid reactions of the collagen-vascular diseases. In addition, graft vs host disease and a variety of miscellaneous lichenoid reactions are discussed.

The lichenoid reactions of the collagen-vascular diseases are relatively cell-poor at the dermal-epidermal interface. They are distinguished by this cell-poor quality and by perivenular and appendageal components. In addition, they tend to be associated with interstitial infiltrates of inflammatory cells; lymphocytes and histiocytes infiltrate among collagen bundles of the reticular dermis. They may be associated with dermal mucinosis or sclerosis (either of which might be characterized as a variant of a collagenosis [i.e., mucinous collagenosis]).

The epidermal changes of a lesion of lupus erythematosus (LE) generally are distinctive. The lichenoid reaction produces “atrophy” of the basal unit to such a degree that the rete ridges are completely effaced. In most examples, the interface between the epidermis and the dermis is straight. Vacuoles form on both sides of what often is a thickened, hyalinized basement membrane. The epidermis is composed of hypertrophied keratinocytes with prominent tonofibrils (intra-cellular keratinocytic sclerosis); the cells have a long axis that is parallel to the surface of the skin. The entire epidermis takes on the qualities of a superficial unit showing terminal differentiation. Terminal differentiation is that process which eventuates in a physiologic form of cell death; the dying cells contract to form plate-like, keratin-rich lamellae along the surface of the skin . In the LE-like lichenoid disorders, normal maturation of the superficial unit is distorted; the keratinized product along the surface often is composed of compactly aggregated lamellae (compact ortho-keratosis).

The thickened basement membrane of lupus erythematosus is rather unique. A thickened basement membrane may be encountered in lesions of radiodermatitis. It is uncommon as a feature of the cell-poor lichenoid reaction of some lesions of dermatomyositis. Lesions of scleroderma rarely are associated with hyaline thickening of the basement membrane (perhaps as an expression of “mixed connective tissue disease”). The epidermis bordering a bulla in the setting of porphyria cutanea tarda occasionally  may show hyaline thickening. A thickened basement membrane is a feature of some lesions of lichen sclerosis et atrophicus.

The vascular changes of lupus erythematosus include telangiectasia and irregular, perivascular deposits of hyalin. Similar changes may be seen in lesions of dermatomyositis.

The changes of graft vs host disease in the skin resemble those of lupus erythematosus, particularly the subacute variant of LE. In more chronic examples, the changes at the dermal-epidermal interface resemble systemic lupus erythematosus while those of the reticular dermis qualify as sclerodermoid patterns.

In lupus profundus, the changes in the lower portion of the dermis share some features with those of scleroderma, but mucinous changes often are prominent. Both disorders are characterized by perivascular infiltrates of lymphocytes and plasma cells; interstitial infiltrates of lymphocytes and histiocytes; and substitutive fibrosis in which newly formed fibrous tissue encroaches upon, and partially replaces, the domain of the neighboring subcutaneous fat. Scleroderma tends to involve septa of the subcutaneous fat. Lupus profundus, in addition to fibrosis and interstitial inflammation of fibrous septa, produces hyaline atrophy of the adipose tissue; the changes may progress to areas of hyalinization, hyaline necrosis, and calcification.

In the spectrum of patterns in the setting of lupus erythematosus, some lesions are characterized by perivenular infiltrates of lymphocytes and histiocytes to the exclusion of significant changes at the dermal-epidermal interface; they qualify as lymphocytic infiltrates of the dermis. The differential diagnosis for the general category of the lymphocytic infiltrates includes lymphocytic infiltrate of Jessner, erythema annulare centrifugum, and polymorphic light eruption, among others.