Report

Lichenoid and granulomatous dermatitis

Cynthia M. Magro, MD, and A. Neil Crowson, MD

From the Department of Pathology, Abstract

Cell Biology, and Anatomy, Medical Background The prototypic lichenoid eruptions, lichen planus (LP), lichenoid drug
College of Thomas Jefferson
eruptions, secondary syphilis, and collagen vascular disease, are defined histologically by a
University, Philadelphia,
Pennsylvania, Central Medical
band-like lymphocytic infiltrate in close apposition to the epidermis. We describe a novel form
Laboratories, Winnipeg, Manitoba, of lichenoid dermatitis with a granulomatous component.
Canada, and Regional Medical Design Skin biopsies from 40 patients demonstrating a band-like lymphocytic infiltrate with
Laboratories, St John Medical Center, concomitant granulomatous inflammation were encountered over 4 years. Clinicians were
Tulsa, Oklahoma
contacted to elucidate underlying triggers and medical illnesses.
Results A lichenoid dermatitis, a linear eruption, vasculitis, annular erythema, and
Correspondence
A. Neil Crowson, MD erythroderma were among the clinical presentations. A drug-based etiology was implicated
Regional Medical Laboratories in 14 cases: the drugs included antibiotics, lipid-lowering agents, anti-inflammatory drugs,
St John Medical Center antihistamines, hydroxychloroquine sulfate, and angiotensin-converting enzyme inhibitors.
1923 S. Utica Avenue
Over one-third of patients with drug-related eruptions had other medical illnesses associated
Tulsa, OK 74114⫺4109
with cutaneous granulomatous inflammation, namely rheumatoid arthritis (RA), Crohn’s
Presented at the US–Canadian disease, hepatitis C, diabetes mellitus, and thyroiditis. A microbial trigger was implicated in
Academy of Pathology Meeting, San 12 patients in the context of infective id reactions to herpes zoster, Epstein–Barr virus (EBV),
Francisco, CA, March 20–26, 1999 or streptococci, or active infections by Mycobacterium tuberculosis, M. leprae, fungi, and
spirochetes. The remainder had hepatobiliary disease and RA without obvious exogenous
Drug names
atenolol: Tenormin
triggers, cutaneous T-cell lymphoma (CTCL), and idiopathic lichenoid eruptions (i.e. LP,
captropril: Capoten lichen nitidus, and lichen striatus). One patient with LP had underlying multicentric
diclofenac: Voltaren reticulohistiocytosis. The histiocytic infiltrate assumed one or more of five light microscopic
enalapril: Vasotec patterns: (i) superficially disposed loose histiocytic aggregates; (ii) cohesive granulomata
hydroxychloroquine sulfate: Plaquenil
within zones of band-like lymphocytic infiltration with or without deeper dermal extension; (iii)
lovastatin: Mevacor
simvastatin: Zocor
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 erythematosus (SCLE).6 Light microscopic clues help to

Lichenoid eruptions represent a heterogeneous clinical
group which have in common the light microscopic pattern
of a superficial band-like lymphocytic infiltrate accom-
panied by degenerative epithelial alterations. The clinical
associations include lichen planus (LP),1,2 lichenoid drug
reactions,3 secondary syphilis,4 mixed connective tissue
126 disease (MCTD),5 and subacute cutaneous lupus
discriminate one lichenoid syndrome from another. For
example, tissue eosinophilia in concert with parakeratosis
is characteristic of lichenoid drug eruptions, while plasma-
cellular 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.

International Journal of Dermatology 2000, 39, 126–133 © 2000 Blackwell Science Ltd
Magro and Crowson Lichenoid and granulomatous dermatitis Report 127

Table 1 Idiopathic group

Age/sex Clinical impression Location of lesions Diagnosis/medical illnesses

54/F Lichen planus vs. flat warts Forearm Lichen nitidus

78/F Lichen planus Scalp Lichen planopilaris
27/F Warts Neck Lichen nitidus
7/M Yellow papules in a linear array Forehead Lichen striatus
29/M Lichen nitidus Arms Lichen nitidus
10/F Lichen planus Abdomen and vulva Lichen planus
51/F Lichen planus Generalized Lichen 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 eosin-
stained 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),
Figure 1 A post-herpetic zosteriform eruption in a patient
pityriasis lichenoides (1), secondary syphilis (1), tuberculoid
with acute myelogenous leukemia (infectious idiopathic
leprosy (1), and guttate psoriasis (1). Lesions involved the
group). Illustration courtesy of Sandy Tsao, MD, Boston, MA
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 and nasal herpes, while another developed annular truncal
idiopathic lichenoid eruptions, namely LP (three patients), plaques in association with acute Epstein–Barr virus (EBV)
LN (three patients), and LS (one patient). One patient had infection. Three patients had a zosteriform lichenoid erup-
underlying multicentric reticulohistiocytosis (Table 1). tion at sites of antecedent varicella (Fig. 1). Two patients’
Twelve patients had antecedent or concurrent infections. eruptions occurred in concert with streptococcal tonsillitis.
An LS-like eruption developed in a 32-year-old woman Lesions represented active infection in four patients, namely
seropositive for hepatitis C. One patient seropositive for tinea capitis, infections with Mycobacterium marinum and
human immunodeficiency virus developed a generalized M. leprae, and syphilis (Table 2).
lichenoid eruption in the setting of cytomegalovirus retinitis In 14 patients, the eruption was temporally associated

© 2000 Blackwell Science Ltd International Journal of Dermatology 2000, 39, 126–133
128 Report Lichenoid and granulomatous dermatitis Magro and Crowson

Table 2 Infectious id/active infection

Age/sex Clinical impression Location of lesions Diagnosis/medical illness

46/M Lichenoid dermatitis Extremities/scalp/trunk CMV, retinitis/nasal herpes in the setting of HIV
34/M Zosteriform plaque Back Herpes zoster
5/F Zosteriform eruption Arm Herpes
39/F Linear eruption Leg Hepatitis C
22/F Zosteriform eruption Leg Herpes in the setting of acute myelogenous leukemia
6/F Pityriasis lichenoides Generalized Recurrent streptococcal tonsillitis
61/F Erythematous papules Axilla Infectious mononucleosis
51/M Guttate psoriasis Generalized Recurrent streptococcal tonsillitis
39/F Majocchi’s granuloma vs. GA Arm Mycobacterium marinum
17/M Tinea capitis Scalp Tinea capitis
36/F Secondary syphilis Generalized Serologically proven secondary syphilis
62/M Tuberculoid leprosy Leg Tuberculoid leprosy

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

Table 3 Drug related

Age/sex Clinical impression Location of lesions Underlying medical illnesses Implicated drug

43/F NLD Forearm Crohn’s disease Sulfamethoxazole/

trimethoprim
54/M Erythroderma Generalized Hepatitis C Sulfonumile
17/F Lichenoid eruption Extremities None Tetracycline
86/F LCV vs. psoriasis Foot Crohn’s disease Captopril
38/M Eruption Left arm Antecedent otitis media Oxacillin
64/F Drug reaction Back Hypercholesterolemias Simvastatin
50/M Drug reaction Back Hypertension Lovastatin, β-blocker
50/F Photodistributed reaction Arms, chest, upper back Negative Quinine tonic water
54/F NLD vs. pretibial myxedema Lower extremities Thyroiditis and diabetes Antibiotic
79/F Schamberg’s disease Leg None Cimetidine
74/F Drug reaction Leg Hypothyroidism Diclofenac
61/F Eczema vs. subacute LE Photodistributed Rheumatoid arthritis Hydroxychloroquine
47/M Lichen planus vs. lichenoid drug Generalized Negative Atenolol
69/F Erythroderma Generalized Negative 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 Vasculitis Face/upper extremities Variegate porphyria

30/F Papular eruption Generalized PBC/autoimmune cholangitis
40/M Granulomatous eruption Axillae Alcoholic hepatitis
46/M Erythroderma Generalized CTCL
59/M NLD Mid back CTCL
60/M Dermatitis ?CTCL Leg 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 tors, lipid-lowering agents, β-blockers, H2 antagonists,
following drug withdrawal. The implicated drugs included nonsteroidal anti-inflammatory drugs (NSAIDs), hydroxy-
antibiotics, angiotensin-converting enzyme (ACE) inhibi- chloroquine, and quinine-containing tonic water. In two

International Journal of Dermatology 2000, 39, 126–133 © 2000 Blackwell Science Ltd
Magro and Crowson Lichenoid and granulomatous dermatitis Report 129

cases, the clinical impression was one of pigmentary pur-

pura. Five of these patients had underlying systemic condi-
tions 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 afore-
mentioned 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 Figure 2 (A) Nodular proliferation of large multinucleated
a folliculocentric infiltrate with destruction of the outer histiocytic forms consistent with reticulohistiocytoma.
root sheath epithelium and scattered plasma cells. (B) Band-like lymphocytic infiltrate with interposed sheets of
paler histiocytes. There is obliteration of the basal layer of
Biopsies held clinically to represent LN revealed a focal
the epidermis with resultant subepidermal cleft formation
lichenoid infiltrate which, in one case, involved two
(idiopathic group: lichen planus in the setting of multicentric
dermal papillae and, in another, assumed a broader pattern reticulohistiocytosis)
(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 mid-dermal diffuse interstitial mononuclear cell infiltrate
apposition to the epidermis. Two cases showed subepithelial was noted in one case.
fibrin deposition and erythrocytic extravasation. A subtle The case held to represent LS showed a broad band of

© 2000 Blackwell Science Ltd International Journal of Dermatology 2000, 39, 126–133
130 Report Lichenoid and granulomatous dermatitis Magro and Crowson

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 lymph-
ocytosis to necrotic keratinocytes, basilar vacuolo-
pathy, 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 vascul-
itis. One biopsy showed concomitant lymphoid atypia. Most
commonly, the extravascular granulomatous component
comprised occasional giant cells or loose histiocytic aggreg-
ates 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 Figure 4 Band-like lymphocytic infiltrate with interposed
syphilis showed tissue eosinophilia without discernible histiocytic foci in a sclerotic background with higher power
plasma cells. The case of tinea capitis showed a dense band- magnification of the histiocytic component (drug-related
like infiltrate of lymphocytes and histiocytes in apposition to group: lichenoid hypersensitivity to captopril in the setting
the follicular epithelium (Fig. 5). of Crohn’s disease)

International Journal of Dermatology 2000, 39, 126–133 © 2000 Blackwell Science Ltd
Magro and Crowson
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 charac-
terized 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.
© 2000 Blackwell Science Ltd
Lichenoid and granulomatous dermatitis Report 131
Discussion
We have described 40 patients whose biopsies showed a
lichenoid and granulomatous dermatitis associated clinic-
ally 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 granulomat-
ous component, the histology in the cases presented in this
series was typical of idiopathic LP, comprising orthohyper-
keratosis and hypergranulosis without discernible mid-
dermal perivascular extension of the infiltrate. The pre-
sentation 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 accom-
panied by granulomatous inflammation, a finding conven-
tionally 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 drug-
associated cases included parakeratosis, keratinocyte
necrosis, acrosyringeal accentuation, a lichenoid pigment-
ary 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 infilt-
rates, such as thyroiditis, diabetes mellitus, hepatitis C,
RA, and Crohn’s disease,7 suggesting granulomatous koeb-
nerization 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
International Journal of Dermatology 2000, 39, 126–133
132 Report Lichenoid and granulomatous dermatitis
therapy in a patient with underlying systemic lupus eryth-
ematosus was reported, whereby lymphoid atypia produced
a morphology reminiscent of granulomatous CTCL;13 ACE
inhibitors are implicated in pseudolymphomatous CTCL-
like infiltrates.14
Lichenoid and granulomatous infiltrates are a manifesta-
tion 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 stimu-
lating 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 immun-
ologic 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 erup-
tions 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 cerebri-
form lymphocytes were helpful clues.14 Granulomatous
International Journal of Dermatology 2000, 39, 126–133
Magro and Crowson
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 con-
fined to dermal papillae capillaries. This and a similar
reported case32 beg the question as to whether granulomat-
ous 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.
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Occupational marks: scars II

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.

© 2000 Blackwell Science Ltd International Journal of Dermatology 2000, 39, 126–133