Report

Lichenoid and granulomatous dermatitis
Cynthia M. Magro, MD, and A. Neil Crowson, MD

From the Department of Pathology, Cell Biology, and Anatomy, Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania, Central Medical Laboratories, Winnipeg, Manitoba, Canada, and Regional Medical Laboratories, St John Medical Center, Tulsa, Oklahoma Correspondence A. Neil Crowson, MD Regional Medical Laboratories St John Medical Center 1923 S. Utica Avenue Tulsa, OK 74114 4109 Presented at the US–Canadian Academy of Pathology Meeting, San Francisco, CA, March 20–26, 1999 Drug names atenolol: Tenormin captropril: Capoten diclofenac: Voltaren enalapril: Vasotec hydroxychloroquine sulfate: Plaquenil lovastatin: Mevacor simvastatin: Zocor

Abstract
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.

Introduction Lichenoid eruptions represent a heterogeneous clinical group which have in common the light microscopic pattern of a superficial band-like lymphocytic infiltrate accompanied by degenerative epithelial alterations. The clinical associations include lichen planus (LP),1,2 lichenoid drug reactions,3 secondary syphilis,4 mixed connective tissue disease (MCTD),5 and subacute cutaneous lupus
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erythematosus (SCLE).6 Light microscopic clues help to discriminate one lichenoid syndrome from another. For example, tissue eosinophilia in concert with parakeratosis is characteristic of lichenoid drug eruptions, while plasmacellular infiltrates are conspicuous in secondary syphilis, and epithelial attenuation with suprabasilar dyskeratosis and mesenchymal mucinosis typify SCLE. We encountered 40 cases of lichenoid inflammation with a granulomatous component.
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Table 1 Idiopathic group
Age/sex 54/F 78/F 27/F 7/M 29/M 10/F 51/F Clinical impression Lichen planus vs. flat warts Lichen planus Warts Yellow papules in a linear array Lichen nitidus Lichen planus Lichen planus Location of lesions Forearm Scalp Neck Forehead Arms Abdomen and vulva Generalized Diagnosis/medical illnesses Lichen Lichen Lichen Lichen Lichen Lichen Lichen nitidus planopilaris nitidus striatus nitidus planus planus/multicentric reticulohistiocytosis

Materials and methods
Skin biopsies from 40 patients showing a lichenoid and granulomatous dermatitis were retrieved from two outpatient dermatopathology data bases by computerized natural language search of 350,000 cases accessioned over 4 years. On each requisition, the clinical impression and lesion distribution were indicated by the referring clinician, who was then contacted to establish the spectrum of potential triggers and medical illnesses associated with the eruption. All biopsies were reviewed to ascertain light microscopic features which might discriminate between potential triggers and etiologies. The material examined comprised hematoxylin and eosinstained 5-µm sections of formalin-fixed, paraffin-embedded tissue. Where an infectious etiology was considered, special stains for organisms were performed.

Clinical summary There were 21 women, 15 men, 3 girls, and 1 boy (aged 5–86 years) who presented in most cases with an eruption of acute or recent onset. Clinical impressions included lichenoid dermatitis (5), a linear eruption (5), such as lichen striatus (LS) or a zosteriform process, lichen nitidus (LN) (3), drug eruption (3), erythroderma (3), necrobiosis lipoidica (2), granulomatous dermatitis (2), psoriasis (1), cutaneous T-cell lymphoma (CTCL) (1), tinea capitis (1), pityriasis lichenoides (1), secondary syphilis (1), tuberculoid leprosy (1), and guttate psoriasis (1). Lesions involved the arms (13), legs (9), trunk (8), and head and neck (4). In six cases, the eruption was generalized. Follow-up at 6–24 months subsequent to the biopsy was obtained. In seven patients, the lesions were held to represent idiopathic lichenoid eruptions, namely LP (three patients), LN (three patients), and LS (one patient). One patient had underlying multicentric reticulohistiocytosis (Table 1). Twelve patients had antecedent or concurrent infections. An LS-like eruption developed in a 32-year-old woman seropositive for hepatitis C. One patient seropositive for human immunodeficiency virus developed a generalized lichenoid eruption in the setting of cytomegalovirus retinitis
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Figure 1 A post-herpetic zosteriform eruption in a patient

with acute myelogenous leukemia (infectious idiopathic group). Illustration courtesy of Sandy Tsao, MD, Boston, MA

and nasal herpes, while another developed annular truncal plaques in association with acute Epstein–Barr virus (EBV) infection. Three patients had a zosteriform lichenoid eruption at sites of antecedent varicella (Fig. 1). Two patients’ eruptions occurred in concert with streptococcal tonsillitis. Lesions represented active infection in four patients, namely tinea capitis, infections with Mycobacterium marinum and M. leprae, and syphilis (Table 2). In 14 patients, the eruption was temporally associated
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Table 2 Infectious id/active infection
Age/sex 46/M 34/M 5/F 39/F 22/F 6/F 61/F 51/M 39/F 17/M 36/F 62/M Clinical impression Lichenoid dermatitis Zosteriform plaque Zosteriform eruption Linear eruption Zosteriform eruption Pityriasis lichenoides Erythematous papules Guttate psoriasis Majocchi’s granuloma vs. GA Tinea capitis Secondary syphilis Tuberculoid leprosy Location of lesions Extremities/scalp/trunk Back Arm Leg Leg Generalized Axilla Generalized Arm Scalp Generalized Leg Diagnosis/medical illness CMV, retinitis/nasal herpes in the setting of HIV Herpes zoster Herpes Hepatitis C Herpes in the setting of acute myelogenous leukemia Recurrent streptococcal tonsillitis Infectious mononucleosis Recurrent streptococcal tonsillitis Mycobacterium marinum Tinea capitis Serologically proven secondary syphilis Tuberculoid leprosy

CMV, cytomegalovirus; HIV, human immunodeficiency virus; GA, granuloma annulare.

Table 3 Drug related
Age/sex 43/F 54/M 17/F 86/F 38/M 64/F 50/M 50/F 54/F 79/F 74/F 61/F 47/M 69/F Clinical impression NLD Erythroderma Lichenoid eruption LCV vs. psoriasis Eruption Drug reaction Drug reaction Photodistributed reaction NLD vs. pretibial myxedema Schamberg’s disease Drug reaction Eczema vs. subacute LE Lichen planus vs. lichenoid drug Erythroderma Location of lesions Forearm Generalized Extremities Foot Left arm Back Back Arms, chest, upper back Lower extremities Leg Leg Photodistributed Generalized Generalized Underlying medical illnesses Crohn’s disease Hepatitis C None Crohn’s disease Antecedent otitis media Hypercholesterolemias Hypertension Negative Thyroiditis and diabetes None Hypothyroidism Rheumatoid arthritis Negative Negative Implicated drug Sulfamethoxazole/ trimethoprim Sulfonumile Tetracycline Captopril Oxacillin Simvastatin Lovastatin, β-blocker Quinine tonic water Antibiotic Cimetidine Diclofenac Hydroxychloroquine Atenolol Enalapril

LCV, leucocytoclastic vasculitis; LE, lupus erythematosus; NLD, necrobiosis lipoidica diabeticorum.

Table 4 Hepatobiliary disease and CTCL
Age/sex Clinical impression Location of lesion Diagnosis and/or medical illness

54/F 30/F 40/M 46/M 59/M 60/M

Vasculitis Papular eruption Granulomatous eruption Erythroderma NLD Dermatitis ?CTCL

Face/upper extremities Generalized Axillae Generalized Mid back Leg

Variegate porphyria PBC/autoimmune cholangitis Alcoholic hepatitis CTCL CTCL Large plaque parapsoriasis

CTCL, cutaneous T-cell lymphoma; NLD, necrobiosis lipoidica diabeticorum; PBC, primary biliary cirrhosis.

with the commencement of a drug and/or lesional resolution following drug withdrawal. The implicated drugs included antibiotics, angiotensin-converting enzyme (ACE) inhibiInternational Journal of Dermatology 2000, 39, 126–133

tors, lipid-lowering agents, β-blockers, H2 antagonists, nonsteroidal anti-inflammatory drugs (NSAIDs), hydroxychloroquine, and quinine-containing tonic water. In two
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cases, the clinical impression was one of pigmentary purpura. Five of these patients had underlying systemic conditions associated with cutaneous granulomatous infiltrates, namely Crohn’s disease,7 hepatitis C,7 diabetes mellitus,7 antecedent bacterial infection,7 and thyroid disease7 (Table 3). One patient with rheumatoid arthritis (RA) developed a pigmented purpura-like eruption on the left leg in the absence of a specific trigger. In addition to the two aforementioned patients with hepatitis C, three had underlying hepatobiliary disease: primary biliary cirrhosis (PBC) in one, alcoholic hepatopathy in one, and idiopathic variegate porphyria in one (Table 4). In three, a diagnosis of CTCL was eventually made (Table 4). Histopathology All cases shared a band-like infiltrate of lymphocytes admixed with histiocytes obscuring the dermoepidermal junction, accompanied by variable degenerative epithelial alterations: vacuolopathy, dyskeratosis, and colloid body formation. The histiocytic component was disposed in one of five patterns: (i) superficially disposed loose small histiocytic aggregates amidst a band-like lymphocytic infiltrate; (ii) small epithelioid granulomata within and subjacent to the areas of band-like lymphocytic infiltration; (iii) an interstitial array between collagen fibers reminiscent of interstitial granuloma annulare (GA); (iv) scattered singly disposed Langhans and/or foreign body type giant cells; and (v) granulomatous vasculitis. Additional light microscopic features were observed depending upon the specific systemic disease or trigger. Two cases were held to represent LP. The first case had the characteristic light microscopic alterations, namely hypergranulosis and orthohyperkeratosis without mid or deep dermal perivascular extension in the setting of multicentric reticulohistiocytosis (Figs. 2a,b). The second case was without the characteristic alterations of the granular cell layer and stratum corneum and also showed rare eosinophils; the histiocytes were arranged as poorly defined small aggregates within a superficially confined lymphoid infiltrate. The case of lichen planopilaris showed a folliculocentric infiltrate with destruction of the outer root sheath epithelium and scattered plasma cells. Biopsies held clinically to represent LN revealed a focal lichenoid infiltrate which, in one case, involved two dermal papillae and, in another, assumed a broader pattern (Fig. 3). The attenuated epidermis showed parakeratosis with slight suprabasilar exocytosis. The granulomatous component comprised histiocytes and scattered giant cells in loose aggregates amidst a lymphocytic infiltrate in direct apposition to the epidermis. Two cases showed subepithelial fibrin deposition and erythrocytic extravasation. A subtle
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Figure 2 (A) Nodular proliferation of large multinucleated

histiocytic forms consistent with reticulohistiocytoma. (B) Band-like lymphocytic infiltrate with interposed sheets of paler histiocytes. There is obliteration of the basal layer of the epidermis with resultant subepidermal cleft formation (idiopathic group: lichen planus in the setting of multicentric reticulohistiocytosis)

mid-dermal diffuse interstitial mononuclear cell infiltrate was noted in one case. The case held to represent LS showed a broad band of
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Figure 3 A discrete focus of lymphocytic and histiocytic infiltration distends a dermal papilla resulting in ‘‘claw-like’’ deformity of the epidermis (idiopathic group: lichen nitidus)

lymphocytes apposed to a flattened epidermis with loose aggregates of admixed histiocytes, focal suprabasilar lymphocytosis to necrotic keratinocytes, basilar vacuolopathy, neutrophil-imbued parakeratosis, and focal hemorrhage. Drug-associated cases showed tissue eosinophilia and plasmacellular infiltrates with interface inflammation accentuated in eccrine, acrosyringeal, and straight ducts. Suprabasilar lymphocytosis with dyskeratosis was present. A superficial vasculopathy comprising endothelial swelling with hemorrhage was observed in six cases. In two cases, the angiocentric histiocytic infiltrates were associated with fibrin deposition warranting designation as granulomatous vasculitis. One biopsy showed concomitant lymphoid atypia. Most commonly, the extravascular granulomatous component comprised occasional giant cells or loose histiocytic aggregates amidst the lymphoid populace (Fig. 4). In cases with antecedent infection, additional histologic features included infiltration of hair follicles, perineurium, and eccrine structures, sometimes with lymphocytic and granulomatous vasculitis and/or focal cell-poor vacuolar interface dermatitis. The case of atypical mycobacterial infection showed interstitial histiocytic infiltration mimicking GA, a lymphocytic eccrine hidradenitis, follicular inflammation, and granulomatous vasculitis. Similar changes were seen in the lesion of tuberculoid leprosy, but were accompanied by deep-seated elongated granulomata, likely representing the residua of destroyed nerves, and neutrophilic debris. The case of secondary syphilis showed tissue eosinophilia without discernible plasma cells. The case of tinea capitis showed a dense bandlike infiltrate of lymphocytes and histiocytes in apposition to the follicular epithelium (Fig. 5).
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Figure 4 Band-like lymphocytic infiltrate with interposed

histiocytic foci in a sclerotic background with higher power magnification of the histiocytic component (drug-related group: lichenoid hypersensitivity to captopril in the setting of Crohn’s disease)
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Discussion We have described 40 patients whose biopsies showed a lichenoid and granulomatous dermatitis associated clinically with a variety of disorders. The individual lesions presented most frequently as lichenoid papules which, in roughly 20% of cases, ultimately were held to be idiopathic lichenoid eruptions: LN, LP, or LS. LN classically presents clinically as miliary papules involving the arms, trunk, and penis,8 and histologically as a superficial lymphocytic and granulomatous infiltrate which imparts a ‘‘ball in claw’’ appearance to the epidermis and subjacent dermal papillae. Although standard descriptions of LP do not emphasize granulomatous inflammation, other than the granulomatous component, the histology in the cases presented in this series was typical of idiopathic LP, comprising orthohyperkeratosis and hypergranulosis without discernible middermal perivascular extension of the infiltrate. The presentation of LS is classically as a linear eruption involving an extremity,9–11 biopsies of which show a hybrid lichenoid and ezcematous dermatitis with suprabasilar dyskeratosis. Similar alterations were seen in our cases, but were accompanied by granulomatous inflammation, a finding conventionally used as a discriminator to favor dermatoses such as LN over LS. A characteristic feature of LS seen in this series is lymphocytic eccrine hidradenitis; seemingly novel was the finding of erythrocyte extravasation. Lymphocytic eccrine hidradenitis, interface dermatitis, and hemorrhage are seen in viral id reactions and may implicate a viral trigger in the propagation of LS. One patient in this series in fact had hepatitis C associated with an LS-like pattern (Table 4). Additional light microscopic features in the drugassociated cases included parakeratosis, keratinocyte necrosis, acrosyringeal accentuation, a lichenoid pigmentary purpura-like reaction pattern, granulomatous vasculitis, tissue eosinophilia, plasmacellular infiltrates, and sparing of the deep dermis. One case manifested lymphoid atypia. Among the clinical presentations were erythroderma, lichenoid eruptions, and vasculitis. Implicated drug classes included lipid-lowering agents, β-blockers, ACE inhibitors, H2 antagonists, hydroxychloroquine, and antimicrobials, several of which are associated with lichenoid reactions.12 Some patients had underlying medical illnesses having known associations with cutaneous granulomatous infiltrates, such as thyroiditis, diabetes mellitus, hepatitis C, RA, and Crohn’s disease,7 suggesting granulomatous koebnerization of a lichenoid drug reaction. A similar argument might be proposed for the patient with multicentric reticulohistiocytosis who developed an eruption resembling LP clinically (i.e. ‘‘histiocytic’’ koebnerization of idiopathic LP). A case of lichenoid and granulomatous dermatitis associated with Aldomet, chlorothiazide, and ACE inhibitor
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Figure 5 Band-like lymphocytic and histiocytic infiltrate in

apposition to the follicular outer root sheath epithelium (infectious group: patient with tinea capitis)

Among the histologic features seen in patients with underlying hepatobiliary disease were deep extension of the infiltrate, a lymphocytic eccrine hidradenitis, granulomatous vasculitis, and variable tissue eosinophilia. The extravascular granulomatous component was characterized by a diffuse interstitial GA-like pattern in one case and scattered superficially disposed histiocytic aggregates in the other two cases. Biopsies from the three cases of incipient or overt CTCL manifested conspicuous lymphoid atypia with Sezary cells in the epidermis and dermis, accompanied by course laminated papillary dermal sclerosis. Minimal degenerative epithelial alterations were observed, except in one case where prominent keratinocyte necrosis was seen, likely reflecting antecedent psoralen plus UVA (PUVA) treatment. Also present were eosinophils and plasma cells. In the patient with RA in whom a drug reaction could not be implicated, a biopsied vasculitic eruption showed a pigmentary purpura-like lichenoid dermatitis with foci of superficial granulomatous vasculitis.
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therapy in a patient with underlying systemic lupus erythematosus was reported, whereby lymphoid atypia produced a morphology reminiscent of granulomatous CTCL;13 ACE inhibitors are implicated in pseudolymphomatous CTCLlike infiltrates.14 Lichenoid and granulomatous infiltrates are a manifestation of infection, including active infection, or an idiopathic response to nonviable microbial antigen. The organisms include those with superantigen properties, namely viruses, mycobacterial and treponemal species, and streptococci. Superantigens are microbial proteins which interact with the variable region of the T-cell receptor and the conserved residues of class II antigen-presenting cells, thereby stimulating a much larger percentage of the T-cell repertoire than do traditional bacterial oligopeptides.15–22 Excessive T-helper 1 (Th1) activity would be expected to generate an infiltrate rich in lymphocytes and histiocytes, such as was seen in these cases.22 Follicular inflammation, lymphocytic eccrine hidradenitis, and perineural infiltrates are also characteristic, particularly in post-herpetic lesions. Acral lichenoid and granulomatous purpuric dermatitis in the setting of antecedent infection with Mycobacterium sp. and hepatitis C has been reported.23 Besides the patient with a drug reaction in the setting of hepatitis C, cases of hepatobiliary disease included a second patient with hepatitis C and an LS-like eruption clinically, a patient with variegate porphyria, and one with PBC. Both LP-like eruptions and sarcoidal granulomata have been described in the setting of hepatitis C and PBC,24 but not with variegate porphyria, although the latter is often associated with underlying hepatitis C.25 As regards the lymphocytic eccrine hidradenitis and granulomatous vasculopathy seen in the hepatobiliary disease cases, both hepatitis C and PBC demonstrate a T-cell-mediated immunologic response directed at bile duct epithelium. Antigenic homology between basilar epidermis and bile duct epithelia could result in a concomitant lymphocytic and granulomatous phenomenon affecting both structures.25 The eccrine involvement in our cases mirrors the changes seen in the portal tracts in PBC and hepatitis C;26,27 patients with PBC also develop lymphocytic infiltrates in their lacrimal and salivary glands.28 A common immunologic injury mechanism may exist for all epithelial duct structures in these patients, reflecting antigenic similarity between bile duct and eccrine epithelia, as both express cytokeratin 18.29 A superficial band-like infiltrate of atypical lymphocytes and granulomata with variable epitheliotropism was characteristic of patients with CTCL. Clinically, the eruptions were consistent with CTCL; none was described as ‘‘lichenoid.’’ Absent epidermal injury (except for one case where there was prior PUVA therapy), a sclerotic papillary dermis, and haphazard epidermal permeation by cerebriform lymphocytes were helpful clues.14 Granulomatous
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infiltrates may manifest in lesions of CTCL as interstitial infiltrates reminiscent of GA to which the appellations granulomatous mycosis fungoides and granulomatous slack skin are applied.30,31 One patient with RA developed a lichenoid pigmentary purpura-like reaction with granulomatous vasculitis confined to dermal papillae capillaries. This and a similar reported case32 beg the question as to whether granulomatous lichenoid pigmentary purpura should be considered a manifestation of RA. Most RA patients, however, ingest NSAIDs which provoke lichenoid eruptions;12 despite an absent temporal association between the eruption and drug intake, one might view these as lichenoid drug reactions with granulomatous koebnerization. Acknowledgments Karen Dueck made invaluable secretarial contributions and Sharon Allentuch provided library assistance. Lorraine Kapitoler assisted in the darkroom, funding for which was derived from the Misercordia Foundation, Winnipeg, Canada. References
1 Altman J, Perry HO. The variation and course of lichen planus. Arch Dermatol 1961; 84: 179–191. 2 Ellis FA. Histopathology of lichen planus based on analysis of one hundred biopsy specimens. J Invest Dermatol 1967; 48: 143–148. 3 Almeyda J, Levantine A. Drug reactions XVI. Lichenoid drug eruptions. Br J Dermatol 1971; 85: 604–607. 4 Jeerapaet P, Ackerman AB. Histologic patterns of secondary syphilis. Arch Dermatol 1973; 107: 373–377. 5 Magro CM, Crowson AN, Regauer S. Mixed connective tissue disease. A clinical, histologic, and immunofluorescence study of eight cases. Am J Dermatopathol 1997; 19: 205–212. 6 Magro CM, Crowson AN, Harrist TJ. The use of antibody to C5b-9 in the subclassification of lupus erythematosus. Br J Dermatol 1996; 134: 855–862. 7 Magro CM, Regaeur S, Crowson AN. Granuloma annulare and necrobiosis lipoidica tissue reactions in association with systemic disease. Hum Pathol 1996; 27: 50–56. 8 Ellis FA, Hill WF. Is lichen nitidus a variety of lichen planus: Arch Dermatol Syph 1938; 38: 569–573. 9 Lee H. Lichen striatus. Lancet 1951; 1: 615–617. 10 Staricco RG. Lichen striatus. A study of 15 new cases with special emphasis on the histopathological changes and review of the literature. Arch Dermatol 1959; 79: 311–324. 11 Senea FE, Caro MA. Lichen striatus. Arch Dermatol Syph 1941; 43: 116–133. 12 Crowson AN, Magro CM. Drug eruptions. In: Barnhill R, Crowson AN, Busam K, Granter S, eds. Textbook of
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Dermatopathology. New York: McGraw-Hill, 1998: 257–270. Gonzalez JG, Marcus MD, Santa Cruz DJ. Giant cell lichenoid dermatitis. J Am Acad Dermatol 1986; 15: 87–91. Magro CM, Crowson AN. Drug induced immunedysregulation as a cause of atypical lymphoid infiltrates. Hum Pathol 1996; 27: 125–132. Dellabona P, Peccoud J, Kappler J, et al. Superantigens interact with MHC class II molecules outside of the antigen groove. Cell 1990; 62: 1115–1121. Mollick JA, Miller GG, Musser JM, et al. A novel superantigen isolated from pathogenic strains of Streptococcus pyogenes with aminoterminal homology to staphylococcal enterotoxins B and C. J Clin Invest 1993; 92: 710–719. Reda KB, Kapur V, Mollick JA, et al. Molecular characterization and phylogenetic distribution of the streptococcal superantigen gene (ssa) from Streptococcus pyogenes. Infect Immun 1994; 62: 1867–1874. Drake CG, Kotzin BL. Superantigens: biology, immunology, and potential role in disease. J Clin Immunol 1992; 12: 149–162. Ohmen JD, Barnes PF, Grisso Cl, et al. The T cell receptors of human gamma delta T cells reactive to mycobacterium tuberculosis are encoded by specific V genes but diverse V–J junctions. M. tuberculosis contains a superantigen (abstract). J Immunol 1993; 150: 94A. Abe J, Takeda T, Watanabe Y, et al. Evidence for superantigen production by Yersinia pseudotuberculosis. J Immunol 1993; 151: 4183–4188. Cole BC, Atkin CL. The Mycoplasma arthritidis T-cell mitogen, MAM: a model superantigen. Immunol Today 1991; 12: 271–1276. Magro CM, Crowson AN. Interface and granulomatous dermatitis as a manifestation of antecedent microbial infection: the superantigen id reaction. J Cutan Pathol 1998; 25: 538–544. Occupational marks: scars II

23 Saito R, Matsuska Y. Granulomatous pigmented purpuric dermatosis. J Dermatol 1996; 23: 551–555. 24 Magro CM, Crowson AN. Vesiculopustular lesions in association with liver disease. Int J Dermatol 1997; 36: 837–844. 25 Herero C, Vicente A, Bruguera M, et al. Is hepatitis C virus infection a trigger of porphyria tarda? Lancet 1993; 341: 788–799. 26 Di Bisceglie AM, Goodman ZD, Ishak KG, et al. Long term clinical and histopathologic follow-up of chronic posttransfusion hepatitis. Hepatology 1991; 14: 969–974. 27 Bach N, Thung SN, Schaffner F. The histological features of chronic hepatitis C and autoimmune chronic hepatitis: a comparative analysis. Hepatology 1992; 15: 572–577. 28 Epstein O, Thomas HC, Sherlock S. Primary biliary cirrhosis in a dry gland syndrome with features of chronic graft versus host disease (GVH). Lancet 1980; 1(8179): 1166–1168. 29 Magro CM, Crowson AN. Sterile neutrophilic folliculitis with perifollicular vasculopathy: a distinctive cutaneous reaction pattern reflecting systemic disease. J Cutan Pathol 1998; 25: 215–221. 30 Leboit PE, Beckstead JH, Bond B, et al. Granulomatous slack skin: clonal rearrangement of the T-cell receptor B gene is evidence for the lymphoproliferative nature of cutaneous elastolytic disorder. J Invest Dermatol 1987; 89: 183–186. 31 Ackerman AB, Chongchitnant N, Sanchez J, et al., eds. Histologic Diagnosis of Inflammatory Skin Diseases, 2nd edn. Baltimore: Williams and Wilkins, 1997: 838– 856. 32 Jorizzo J, Gonzalez EB, Apisarnthanarax P, Daniels J. Pigmented purpuric eruption in a patient with rheumatoid arthritis. Arch Intern Med 1982; 142 2184–2185.

Scars may raise peculiar judicial controversies as in the following case. In a domestic relations court a woman was seeking to divorce her husband charging him with cruelty, because, in an attempt to win back her affections he slashed himself on the left side of his thorax with a razor, supposedly to show her his suicidal intentions. The man contended that the scars were due to scratches he suffered two years previously in the New Guinea jungle and that he never used the razor on himself. The judge asked an expert to say if the scars were the result of a razor cut or from a jungle injury; i.e. if they were result of injury six months previously or two years previously. If only six months old, that was the date the wife stated the husband slashed himself with the razor. If two years old, according to the husband’s statement, they were from the jungle and the razor story was to be discarded and, of course, divorce denied. The scars were smooth, white, linear and consistent with a cutting instrument injury, very likely a razor. With ordinary light they were hardly visible, which was consistent with scars older than six months. Under the Wood light they were darker but not as dark as if they were six months old. Consequently the verdict was that the scars were not from the jungle but from a cutting instrument most likely, self-inflicted, but they were older than six months, the time of the alleged self stabbing. Neither party was telling the truth, but the judge preferred the least damage, viz., refusing to grant a divorce. From Ronchese F. Occupational Marks and other Physical Signs: a guide to personal identification. New York: Grune & Stratton, 1948.
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