Lichenoid dermatoses and tissue reactions are some of the most diverse clinical and histologic presentations in dermatology and pathology. The term interface dermatitis is sometimes used interchangeably. The prototypical lichenoid dermatitis is lichen planus. Yet, there are numerous diseases that have similar histology. The following list describes some of them but many dermatoses have a lichenoid inflammatory cell component.
Fixed drug eruptions
Lichen planus-like keratosis
Lichenoid drug eruptions
Lichenoid tissue reactions are characterized by epidermal basal cell damage. Killer T lymphocytes (CD8) attack the basal keratinocytes probably induced by ICAM-1 (Intercellular adhesion molecule-1) expression in the keratinocytes. The result is cell death leading to Civatte bodies, a result of apoptosis. Vacuolar alteration, also known as liquefaction degeneration results form intracellular edema leading to separation. With continued damage at the dermoepidermal junction, melanin transfer from melanocytes to keratinocytes is disrupted leading to release and phagocytosis by macrophages.
Gross Appearance and Clinical Variants Histopathological Features and Variants Differential Diagnosis Commonly Used Terms Internet Links
CLINICAL VARIANTS CHARCTERIZATION ANNULAR LICHENOID DERMATATIS OF YOUTH
Annular lichenoid dermatitis of youth.
Annessi G, Paradisi M, Angelo C, Perez M, Puddu P, Girolomoni G.
Servizio di Istopatologia, Istituto Dermopatico dell'Immacolata, IRCCS, Via Monti di Creta 104, 00167 Rome, Italy.
J Am Acad Dermatol. 2003 Dec;49(6):1029-36. Abstract quote
BACKGROUND: Lichenoid dermatoses are composed of a wide spectrum of disorders with a common histopathologic interface pattern but diverse causes and pathophysiology.
OBJECTIVE: We describe a series of young patients with a peculiar annular lichenoid dermatitis, the clinical appearance of which initially suggested diagnoses of morphea, mycosis fungoides, or annular erythema.
RESULTS: The study involved 23 patients (median age 10 years; age range 5-22 years). Lesions consisted of persistent asymptomatic erythematous macules and round annular patches with a red-brownish border and central hypopigmentation, mostly distributed on the groin and flanks. Histology revealed a peculiar lichenoid dermatitis with massive necrosis/apoptosis of the keratinocytes limited to the tips of rete ridges, in the absence of dermal sclerosis and epidermotropism of atypical lymphocytes. The infiltrate was composed mainly of memory CD4(+) CD30(-) T cells with few B cells and macrophages. Analysis of T-cell receptor-gamma-chain gene rearrangement in skin biopsy specimens revealed polyclonality in all the 15 cases studied. Topical and systemic corticosteroids or phototherapy were effective in most patients with relapse after treatment withdrawal.
CONCLUSIONS: We suggest that this is a distinctive inflammatory condition, and we propose to term it "annular lichenoid dermatitis of youth."
- Lichenoid eruptions in children.
Tilly JJ, Drolet BA, Esterly NB.
New York University School of Medicine, Medical College of Wisconsin, Milwaukee, USA.
J Am Acad Dermatol. 2004 Oct;51(4):606-24. Abstract quote
Lichenoid eruptions are quite common in children and can result from many different origins. In most instances the precise mechanism of disease is not known, although it is usually believed to be immunologic in nature. Certain disorders are common in children, whereas others more often affect the adult population.
Lichen striatus, lichen nitidus, Gianotti-Crosti syndrome, and lichen spinulosus are examples of lichenoid lesions that are more common in children than adults. Distinguishing these diseases is necessary for prediction of the course of the eruption and for optimal management. In most cases, certain clinical characteristics enable the clinician to reach a diagnosis, whereas in other cases biopsy is required for a definitive answer.
Many of these lesions are self-limited and only require symptomatic treatment, although corticosteroids can hasten resolution in certain disorders. Discontinuation of the medication is often sufficient for resolution of lichenoid drug eruptions.
HISTOPATHOLOGICAL VARIANTS CHARACTERIZATION
Lichenoid and granulomatous dermatitis.
Magro CM, Crowson AN.
Department of Pathology, Cell Biology, and Anatomy, Medical College of Thomas Jefferson University, Philadelphia, PA, USA.
Int J Dermatol 2000 Feb;39(2):126-33 Abstract quote
BACKGROUND: The prototypic lichenoid eruptions, lichen planus (LP), lichenoid drug eruptions, secondary syphilis, and collagen vascular disease, are defined histologically by a band-like lymphocytic infiltrate in close apposition to the epidermis. We describe a novel form of lichenoid dermatitis with a granulomatous component.
DESIGN: Skin biopsies from 40 patients demonstrating a band-like lymphocytic infiltrate with concomitant granulomatous inflammation were encountered over 4 years. Clinicians were contacted to elucidate underlying triggers and medical illnesses.
RESULTS: A lichenoid dermatitis, a linear eruption, vasculitis, annular erythema, and erythroderma were among the clinical presentations. A drug-based etiology was implicated in 14 cases: the drugs included antibiotics, lipid-lowering agents, anti-inflammatory drugs, antihistamines, hydroxychloroquine sulfate, and angiotensin-converting enzyme inhibitors. Over one-third of patients with drug-related eruptions had other medical illnesses associated with cutaneous granulomatous inflammation, namely rheumatoid arthritis (RA), Crohn's disease, hepatitis C, diabetes mellitus, and thyroiditis. A microbial trigger was implicated in 12 patients in the context of infective id reactions to herpes zoster, Epstein-Barr virus (EBV), or streptococci, or active infections by Mycobacterium tuberculosis, M. leprae, fungi, and spirochetes. The remainder had hepatobiliary disease and RA without obvious exogenous triggers, cutaneous T-cell lymphoma (CTCL), and idiopathic lichenoid eruptions (i.e. LP, lichen nitidus, and lichen striatus). One patient with LP had underlying multicentric reticulohistiocytosis. The histiocytic infiltrate assumed one or more of five light microscopic patterns: (i) superficially disposed loose histiocytic aggregates; (ii) cohesive granulomata within zones of band-like lymphocytic infiltration with or without deeper dermal extension; (iii) a diffuse interstitial pattern; (iv) scattered singly disposed giant cells; and (v) granulomatous vasculitis. Additional features included lymphocytic eccrine hidradenitis in those patients with drug reactions, hepatobiliary disease, and antecedent viral illnesses, tissue eosinophilia and erythrocyte extravasation in drug hypersensitivity, granulomatous vasculitis in patients with microbial triggers, drug hypersensitivity or RA, and lymphoid atypia in lesions of CTCL or drug hypersensitivity.
CONCLUSIONS: The cutaneous lichenoid and granulomatous reaction may reflect hepatobiliary disease, endocrinopathy, RA, Crohn's disease, infection, or a drug reaction. One-fifth of cases represent idiopathic lichenoid disorders. Lymphoproliferative disease or pseudolymphomatous drug reactions must be considered in those cases showing lymphoid atypia.
Epidermal Changes Dermal Histologic Pattern Additional Clues Diagnosis Interface-Vacuolar Superficial Perivascular Dermatitis Lymphocytes predominate Ballooning and individual necrotic keratinocytes-normal cornified layter Erythema multiforme Ballooning and individual necrotic keratinocytes-parakeratosis Mucha-Haberamann disease (PLEVA) Ballooning and individual necrotic keratinocytes-prominent granular layer Graft vs. Host disease Ballooning and individual necrotic keratinocytes-necrotic keratinocytes in papillary dermis also Effects of nitrogen mustard on mycosis fungoides, patch/plaque No ballooning and few, if any, necrotic keratinocytes-cornified layer normal Drug eruption
No ballooning and few, if any, necrotic keratinocytes-basement membrane sometimes thickened, smudged interface, thinned epidermis Discoid lupus erythematosus
No ballooning and few, if any, necrotic keratinocytes-sclerosis in upper part of dermis LSEA (Morphea) No ballooning and few, if any, necrotic keratinocytes-melanophages in papillary dermis Postinflammatory pigmentary alteration Eosinophils and neutrophils predominate Ballooning and individual necrotic keratinocytes-cornified layer normal Fixed drug eruption, superficial Interface-Lichenoid Lymphocytes predominate Jagged epidermal hyperplasia, wedged hypergranulosis, compact orthokeratosis Lichen planus Esoinophils sometimes, focally thinned epidermis, focal parakeratosis Lichen planus-like drug eruption
Individual necrotic keratinocytes, ballooning, spongiosis, pallor in the upper part of the epidermis, and parakeratosis Mucha-Habermann disease Lymphocytes along adnexal structures in reticular dermis, individual necrotic keratinocytes Lichen striatus Thinned epidermis, prominent granular layer, parakeratosis Graft vs. host reaction Extravasated erythrocytes and/or siderophages Lichenoid purpura of Gourgerot and Blum Necrotic keratinocytes, focal parakeratosis, residuum of solar lentigo sometimes Lichen planus-like keratosis Coronoid lamellae Disseminated superficial actinic porokeratosis Lymphocytes within epidermis, scant spongiosis Mycosis fungoides, plaque Histiocytes predominate Discrete foci in papillary dermis Lichen nitidus Discrete foci and, sometimes, confluence of foci in reticular dermis Sarcoidosis Langerhans' cells predominate Large cells, crenated outlines of large pale nuclei, abundant amphophilic cytoplasm Letterer-Siwe disease Superficial and Deep Perivascular Dermatitis Interface-Vacuolar Lymphocytes predominate Basement membrane sometimes thickened, smudged interface, thinned epidermis DLE Individual necrotic keratinocytes, ballooning, parakeratosis Mucha-Habermann disease Neutrophils and eosinophils prominent Individual necrotic keratinocytes, ballooning Fixed drug eruption Interface-Lichenoid Lymphocytes predominate Eosinophils sometimes, focal parakeratosis Lichenoid drug eruption Individual necrotic keratinocytes sometimes Lichenoid photodermatitis Individual necrotic keratinocytes, ballooning, spongiosis Mucha-Habermann disease Thickened basement membrane, smudged appearance of interface, thinned epidermis focally DLE Thinned epidermis, prominent granular layer, parakeratosis Graft vs. host reaction Abnormal lymphocytes in wedge shaped infiltrate, often plasma cells, eosinophils, and neutrophils, as well as small lymphocytes Lymphomatoid papulosis Lymphocytes in epidermis, scant spongiosis Mycosis fungoides, plaque stage Neutrophils, eosinophils, and plasma cells prominent Abnormal lymphocytes in wedge shaped infiltrate Lymphomatoid papulosis Ballooning Interface Lymphocytes predominate Individual necrotic keratinocytes, normal cornified layer Erythema multiforme Individual necrotic keratinocytes, prominent granular layer, parakeratosis Graft vs. host reaction Eosinophils and neutrophils prominent Individual necrotic keratinocytes, ballooning, normal cornified layer Fixed drug eruption, superficial Individual necrotic keratinocytes, spongiosis, neutrophils as solitary units within epidermis Toxic shock syndrome
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