1233

REVIEW

My approach to superficial inflammatory dermatoses

K O Alsaad, D Ghazarian
...............................................................................................................................

J Clin Pathol 2005;58:1233–1241. doi: 10.1136/jcp.2005.027151

Superficial inflammatory dermatoses are very common and diagnosis of inflammatory skin diseases, there
are limitations to this approach. The size of the
comprise a wide, complex variety of clinical conditions. skin biopsy should be adequate and representa-
Accurate histological diagnosis, although it can sometimes tive of all four compartments and should also
be difficult to establish, is essential for clinical include hair follicles. A 2 mm punch biopsy is too
small to represent all compartments, and often
management. Knowledge of the microanatomy of the skin insufficient to demonstrate a recognisable pat-
is important to recognise the variable histological patterns tern. A 4 mm punch biopsy is preferred, and
of inflammatory skin diseases. This article reviews the non- usually adequate for the histological evaluation
of most inflammatory dermatoses. However, a
vesiculobullous/pustular inflammatory superficial larger biopsy (6 mm punch biopsy), or even an
dermatoses based on the compartmental microanatomy of incisional biopsy, might be necessary in panni-
the skin. culitis or cutaneous lymphoproliferative disor-
ders. A superficial or shave biopsy should be
...........................................................................
avoided, because it might be misleading, produ-
cing an erroneous pattern and diagnosis.

T
he histological diagnosis of cutaneous
inflammatory diseases can be confusing,
PRACTICAL POINTS
even for the most experienced pathologist.
In the histological evaluation of skin for inflam-
This is because the immune system within the
matory dermatoses, a clinicopathological correla-
skin has limited ways in which it reacts and
tion is essential, and plays an important role in
responds to an antigenic stimulus, and many
achieving the diagnosis. The patient’s age and
inflammatory diseases do not show specific
relevant clinical history, in addition to the site
histological features. In view of this complexity
and commonality, histological patterns of recog- from which the skin biopsy was obtained, should
nition are beneficial for the rapid development of be provided to the pathologist. After proper
a differential diagnosis. This can be achievable by fixation and processing, three deeper haematox-
being familiar with the microanatomy of the skin ylin and eosin stained sections and one section
and its regional variations, in addition to the stained with periodic acid Schiff (PAS) for
basic structural alterations that can occur in evaluation of the epidermal basement mem-
different pathological conditions. This review is brane, blood vessels, and the presence of fungal
oriented towards the recognition of the histolo- organisms are considered sufficient for micro-
gical patterns seen in non-vesiculobullous/pust- scopic evaluation. The need for deeper sections
ular inflammatory superficial dermatoses that and special stains varies from one case to
involve the epidermis and papillary dermis, using another, and additional tasks can be ordered
a schematic approach. when necessary. Special stains that might be
beneficial in establishing a diagnosis of inflam-
matory dermatoses include Martius-Scarlet blue
THE ANATOMICAL COMPARTMENTS/ stain for fibrin, colloidal iron Hale’s for acid
UNITS OF THE SKIN mucin, Prussian blue for iron, toluidine blue for
From the practical point of view, the skin is mast cells, Fontana Masson for melanin pig-
divided into four anatomical compartments or ment, elastic stain for perforating disorders and
units: demonstration of elastic tissue, Von Kossa for
(1) The first compartment/unit includes the calcium deposits, and Congo red for amyloid.
epidermis, papillary dermis, and superficial Gram stain and Gomori methenamine silver
vascular plexus. These structures are inter- stain can be helpful in demonstrating bacterial
See end of article for and fungal microorganisms, respectively.
authors’ affiliations related and mutual.
....................... (2) The second compartment/unit consists of the
Correspondence to: reticular dermis and the deep vascular ‘‘Immunofluorescence studies have an essen-
Dr K O Alsaad, plexus. tial role in diagnosing immunologically
Department of Laboratory (3) The third compartment/unit consists of the related inflammatory skin diseases, specifi-
Medicine and
Pathobiology, University of pilosebaceous units, the eccrine glands, and cally vesiculo-bullous diseases and vasculitis’’
Toronto, University Health in certain anatomical locations, the apocrine
Network, Toronto, glands. Immunohistochemistry has a limited role,
Ontario, Canada; although it can be useful in certain clinical
[email protected] (4) The fourth compartment/unit is the subcu-
taneous tissue (panniculum).
Accepted for publication Abbreviations: GVHD, graft versus host disease; HIV,
26 April 2005 Although using a compartmental approach to human immunodeficiency virus; PAS, periodic acid Schiff;
....................... establish the reaction pattern facilitates the PVI, perivascular inflammatory infiltrate

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1234 Alsaad, Ghazarian

Table 1 Subclassification of inflammatory dermatoses

Compartment one without epidermal changes (superficial perivascular
(epidermis and superficial dermis) inflammation)
Type of inflammatory cell infiltrate

Lymphocytic (most common)

Non vesiculobullous/ Pustular Vesiculobullous Lymphoeosinophilic
pustular lesions dermatosis lesions Lymphoplasmacytic
Mast cell infiltrate
Lymphohistiocytic
Neutrophilic

Without epidermal changes With epidermal changes

Figure 1 Classification of the inflammatory dermatoses involving the Inflammatory dermatoses without epidermal changes
first compartment. The inflammatory skin dermatoses without epidermal
changes are manifested histologically by a superficial
conditions, such as characterising the neoplastic CD4+ T cell perivascular inflammatory infiltrate (PVI). This reactive
population in mycosis fungoides and the CD4+ and CD8+ T pattern is induced by many conditions. The type of
cell populations in patients with human immunodeficiency inflammatory cell infiltrate is different from one condition
disorder (HIV). It is worthwhile mentioning that the CD8+ T to another, allowing further subclassification of the PVI into
cell population is the predominant subtype in HIV derma- six groups (table 1).
toses. Immunofluorescence studies have an essential role in
diagnosing immunologically related inflammatory skin dis- PVI with a predominant lymphocytic infiltrate
eases, specifically vesiculo-bullous diseases and vasculitis. This is the most common type of PVI. Many conditions can
Electron microscopy is of limited value, but may be helpful in result in a lymphocytic PVI. Common causes are immuno-
certain vesiculo-bullous diseases, mycosis fungoides, and logical and non-immunological cutaneous drug eruption1–4—
Langerhans cell histiocytosis. particularly secondary to antibacterials5–7 (fig 3), urticarial
reactions,8 9 viral exanthema, infestation, and insect bites.
Other less common conditions are fungal infections, pig-
A PRAGMATIC APPROACH mented purpuric dermatoses,10–12 erythema annulare centri-
Most common superficial inflammatory dermatoses involve fugum,13 14 and other gyrate erythemas.
the first compartment/unit of the skin. The most common
pattern of reaction encountered is the superficial perivascular
PVI with lymphoeosinophilic infiltrate
inflammatory infiltrate. A transient inflammatory stimulus
Many conditions that cause PVI with a predominant
results in slight hyperaemia and a mild perivascular
lymphocytic infiltrate can present with a lymphoeosinophilic
lymphocytic infiltrate. If the stimulus persists, interstitial
infiltrate. These conditions include drug reactions (fig 4),
oedema and endothelial swelling develop. With further
urticarial reactions, a prevesicular early stage of bullous
stimulation, involvement of the overlying epidermis occurs. pemphigoid, insect bites (fig 5), infestations, and HIV related
Inflammatory dermatoses involving the first compartment of dermatoses.15 16 In pregnant women, pruritic urticarial
the skin are divided into three main categories (fig 1): (1) papules and plaques of pregnancy are characterised by a
non-vesiculobullous/pustular lesions, (2) pustular derma- perivascular lymphoeosinophilic inflammatory infiltrate in
toses, and (3) vesiculo-bullous lesions. The non-vesiculobul- skin biopsies.17 18
lous/pustular lesions, the focus of this review, are divided
into two categories based on the presence or absence of
PVI with lymphoplasmacytic infiltrate
epidermal changes. When epidermal changes are present, A prominent plasma cell component of the inflammatory
they are further subdivided into spongiotic dermatitis, infiltrate may be seen adjacent to an area of trauma,
interface dermatitis, and psoriasiform dermatitis (fig 2). ulceration, or scar. It is also seen in cases of rosacea,
secondary syphilis, and erythema chronicum migrans, which
is pathognomonic of Lyme’s disease.19 The patch stage
Non-vesiculobullous/pustular lesions with of Kaposi’s sarcoma may be associated with increased
epidermal changes of the first compartment

Spongiotic Interface Psoriasiform

dermatitis dermatitis dermatitis

Acute Chronic Vacuolar

change

Subacute
Lichenoid
reaction

Figure 2 Types of non-vesiculobullous/pustular lesions with epidermal Figure 3 Drug induced perivascular lymphocytic inflammatory cell
changes. infiltrate.

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My approach to superficial inflammatory dermatoses 1235

Figure 4 (A, B) Drug induced

perivascular lymphoeosinophilic
inflammatory infiltrate and interface
change.

plasmacytic cell infiltration.20 Occasionally, early cutaneous Figure 6 Lepromatous leprosy.

connective tissue diseases can be associated with an
increased plasma cell population. It is worth mentioning
that relatively larger numbers of plasma cells are usually
present in the mucosal biopsies and may be non-specific.

PVI with increased mast cells

Mastocytosis is a rare disease characterised by primary
pathological accumulation of excessive numbers of mast
cells in different tissues.21 Urticaria pigmentosa is the most
common form of cutaneous mastocytosis.22 23 The mast cells
are present in the interstium and around the superficial
vascular channels, and some of the mast cells show
degranulation. A toluidine blue stain is usually used to
demonstrate mast cells.

PVI with lymphohistiocytic infiltrate

This is the most confusing type of PVI. Conditions that are
associated with a lymphohistiocytic inflammatory cell infil- three conditions are usually associated with epidermal changes.
trate include drug reactions, viral infections and post-viral Leucocytoclastic
reactions, HIV dermatoses, and leprosy24 25 (fig 6). Ziel- vasculitis should be ruled out in all cases of neutrophilic
Neelsen, acid fast bacilli, Gomori methenamine silver, PAS, dermatosis31 (fig 7C). The examination of multiple haematox-
and Fite stains should be performed on all inflammatory ylin and eosin stained deeper sections is helpful.
dermatoses with a prominent lymphohistiocytic infiltrate to
exclude the presence of microorganisms. Inflammatory dermatoses with epidermal changes
The inflammatory dermatoses with epidermal changes are
PVI with a neutrophilic infiltrate classified histologically into spongiotic dermatitis, interface
A prominent perivascular neutrophilic inflammatory cell dermatitis, and psoriasiform dermatitis.
infiltrate can be associated with neutrophilic urticarial reactions
(fig 7A), dermatitis herpetiformis, early IgA dermatosis, early Spongiotic dermatitis
Sweet’s syndrome,26–28 early connective tissue disorders such as Spongiotic dermatitis is defined by the presence of epithelial
lupus erythematosus, early herpetic infection, and acute intercellular oedema.32 It is caused by a variety of clinical
generalised exanthematous pustulosis29 30 (fig 7 B). The last conditions. These include allergic/contact dermatitis, atopic
dermatitis,33 nummular dermatitis, dyshidrotic dermatitis,
seborrheic dermatitis, drug reactions, Id reaction, dermato-
phytosis, miliaria,34 Gianotti-Crosti syndrome,35 and pityriasis
rosea.36
Spongiotic dermatitis is further subclassified into acute,
subacute, and chronic, depending on the histological features
and the time the biopsy was performed.

Acute spongiotic dermatitis

This shows a variable degree of epidermal spongiosis and
vesicle formation; the vesicles are filled with proteinaceous
fluid containing lymphocytes and histiocytes (fig 8A).
Superficial dermal oedema with a perivascular lymphocytic
inflammatory cell infiltrate is usually present. Exocytosis of
the inflammatory cells is present, and there is no acanthosis
or parakeratosis. In allergic/contact dermatitis and atopic
dermatitis, eosinophils may be present in the dermis and
epidermis (eosinophilic spongiosis).

Figure 5 (A) Insect bite with pronounced oedema in the papillary Subacute spongiotic dermatitis
dermis. (B) Lymphoeosinophilic inflammatory infiltrate induced by spider This is the most frequently encountered type of spongiotic
bite. Nuclear debris and dermal necrosis are present. dermatitis. The degree of spongiosis and exocytosis of the

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1236 Alsaad, Ghazarian

Figure 7 (A) A neutrophilic urticarial reaction. (B)

Acute generalised exanthematous pustulosis. (C) A
neutrophilic infiltrate, nuclear debris, and fibrinoid
necrosis characteristic of leucocytoclastic vasculitis.

inflammatory cells is mild to moderate, and compared with Chronic spongiotic dermatitis
acute spongiotic dermatitis there is irregular acanthosis and The spongiosis is mild to absent but there is pronounced
parakeratosis. A superficial dermal perivascular lymphohis- irregular acanthosis, hyperkeratosis, and parakeratosis
tiocytic inflammatory infiltrate, swelling of the endothelial (fig 8D). Minimal dermal inflammation and exocytosis of
cells, and papillary dermal oedema are present (fig 8B, C). the inflammatory cells are present. Fibrosis of the papillary

Figure 8 (A) Epidermal spongiosis

and intraepidermal vesicular formation
in acute spongiotic dermatitis. (B, C)
Moderate inflammatory cell exocytosis
in subacute spongiotic dermatitis. (D)
Chronic spongiotic dermatitis showing
irregular acanthosis, hyperkeratosis,
and parakeratosis.

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My approach to superficial inflammatory dermatoses 1237

Table 2 Interface dermatitis Figure 9 Interface dermatitis

with vacuolar alteration caused by
Interface dermatitis with vacuolar alteration erythema multiforme-like drug
Viral exanthems eruption. Note the presence of
Phototoxic dermatitis single dyskeratotic cells in the
Acute radiation dermatitis epidermis.
Erythema multiform
Erythema multiforme-like drug eruption
Fixed drug eruption
Lichen sclerosis et atrophicus
Erythema dyschromicum perstans
Lupus erythematosus
Dermatomyositis
Acute graft versus host disease
Interface dermatitis with lichenoid alteration
Lichen planus
Lichen planus-like keratosis
Lichenoid actinic keratosis
Lichenoid drug eruption
Lupus erythematosus
Chronic graft versus host disease
Lichen nitidus dermatitis with lichenoid inflammation (fig 2). Each category
Pigmented purpuric dermatosis
has distinctive morphological features, and is caused by
Lichen amyloidosus
Pityriasis lichenoides chronica various clinical conditions (table 2).
HIV dermatitis
Syphilis Interface dermatitis with vacuolar alteration
Mycosis fungoides
Urticaria pigmentosa
This pattern of inflammatory dermatosis is characterised by
the presence of a mild inflammatory cell infiltrate along the
HIV, human immunodeficiency virus. dermoepidermal junction, with vacuolar change within the
basal keratinocytes. Individual necrotic, predominantly basal,
keratinocytes are frequently seen because the inflammatory
dermis may be present. The PAS stain is essential to exclude process causes injury to the basal keratinocytes (colloid or
fungal infection. Civatte bodies). Numerous clinical conditions can result in
All three histological subtypes of spongiotic dermatitis can vacuolar alteration of the basal keratinocytes, including: viral
be caused by various clinical conditions. The microscopic exanthems, phototoxic dermatitis, acute radiation dermatitis,
features of the chronicity of the lesion depend largely on the erythema dyschromicum perstans,37 lichen sclerosis et atro-
time of biopsy and the clinical course of the lesion. The role of phicus,38 erythema multiforme and Stevens-Johnson syn-
the pathologist is to recognise the histological features of drome,39 40 erythema multiforme-like drug eruption (fig 9),
spongiotic dermatitis. However, a clinical correlation is and fixed drug eruption.41 Vacuolar alteration is often present
crucial for a definitive diagnosis. in cutaneous connective tissue disorders such as lupus
erythematosus42 43 (fig 10A–D), and dermatomyositis.44
Interface dermatitis Acute cutaneous graft versus host disease (GVHD) (table 3)
This is histologically classified into two categories: (a) characteristically shows vacuolar alteration (fig 11), which
interface dermatitis with vacuolar change, and (b) interface ranges in severity from focal or diffuse vacuolation of the

Figure 10 Systemic lupus

erythematosus (SLE). (A, B) Interface
dermatitis with vacuolar alteration. (C)
Colloidal iron Hale’s stain demonstrates
abundant dermal mucin, often found in
SLE. (D) Thickened dermo–epidermal
junction basement membrane
highlighted by the periodic acid Schiff
stain.

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1238 Alsaad, Ghazarian

the hair follicles is in keeping with acute GVHD. The clinical

history is essential to distinguish between these two entities.

Interface dermatitis with lichenoid alteration

This is another pattern of cutaneous inflammatory reaction,
which is characterised by a confluent, band-like, dense
accumulation of inflammatory cells in the papillary dermis,
mainly consisting of small lymphocytes and a few histiocytes
along or hugging the dermo–epidermal junction. The
lichenoid reaction is often accompanied by vacuolar degen-
eration of the basal keratinocytes and the presence of
apoptotic bodies (colloid or Civatte bodies). Many clinical
conditions can result in the lichenoid alteration. These
include lichen planus46 (fig 12), lichen planus-like kerato-
Figure 11 Acute cutaneous graft versus host disease, grade II. The sis,46 47 lichenoid actinic keratosis, lichenoid drug eruption,
vacuolar change involves the dermo–epidermal junction basement lichenoid lupus erythematosus, lichenoid GVHD (chronic
membrane and extends to the hair follicle. Scattered necrotic
keratinocytes are present in the epidermis.
GVHD),48 lichen nitidus,49 pigmented purpuric dermatosis,10–12
lichen amyloidosus,50 pityriasis rosea,36 and pityriasis liche-
noides chronica.51 52 Other unusual conditions that can be
associated with a lichenoid inflammatory cell infiltrate are
HIV dermatitis,53 syphilis, mycosis fungoides,54 55 urticaria
pigmentosa,22 23 and post-inflammatory hyperpigmenta-
tion.56 57 In cases of post-inflammatory hyperpigmentation,
care should be taken not to miss the diagnosis of a mimic,
such as regressed melanocytic lesion or lichenoid pigmented
actinic keratosis. A detailed and appropriate clinical history is
essential for the accurate diagnosis of interface dermatitis.

Psoriasiform dermatitis (tables 4 and 5)

This type of inflammatory dermatosis is characterised by the
presence of regular epidermal hyperplasia, elongation of the
rete ridges, hyperkeratosis, and parakeratosis. Thinning of
the portion of the epidermal cell layer that overlies the tips of
Figure 12 Lichen planus.
dermal papillae (suprapapillary plates), and dilated, tortuous
blood vessels within these papillae are often present. A
superficial perivascular inflammatory cell infiltrate is usually
Table 3 Histological grades of acute graft versus host encountered. Numerous conditions can result in psoriasiform
disease dermatitis. These include psoriasis58 (fig 13), seborrheic
dermatitis, psoriasiform drug eruption, chronic fungal infec-
Grade Histological features
tions, lichen simplex chronicus, chronic spongiotic dermati-
Grade I Focal or diffuse vacuolar change of the basal tis, secondary syphilis, pellagra59 and other nutritional
keratinocytes deficiencies, and pityriasis rubra pilaris.60 61 Pityriasis liche-
Grade II Necrotic keratinocytes in the epidermis
Grade III Widespread keratinocyte necrosis; separation of the
noides chronica,51 52 acrodermatitis enteropathica,62 inflam-
dermo–epidermal junction matory linear verrucous epidermal naevus,63 and rarely
Grade IV Complete necrosis of the epidermis subacute psoriasiform cutaneous lupus erythematosus are
also associated with psoriasiform dermatitis.
A systemic approach is important for pathological diag-
nosis when evaluating skin psoriasiform dermatites.
Examining multiple deeper levels is recommended if the
basal keratinocytes (grade I), to separation at the dermoepi- histological features in the initial cuts do not correlate well
dermal junction (grade III).45 Drug reactions can be difficult with the clinical history. Recognising various histological
to differentiate from acute GVHD based on morphological alterations in the epidermal layers can help in narrowing
appearances. The presence of an eosinophilic inflammatory down the differential diagnosis of psoriasiform dermatitis.
component favours a drug reaction, whereas involvement of Agranulosis or hyporgranulosis of the epidermis is a feature

Figure 13 Psoriasis. (A) Note the lack

of the granular cell layer. (B)
Neutrophilic inflammatory infiltrate into
the acanthotic epidermis.

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My approach to superficial inflammatory dermatoses 1239

Table 4 Epidermal changes in psoriasiform dermatoses

Suprapapillary Microabscess Granular cell Spinous cell layer Basal cell layer
Hyperkeratosis Parakeratosis Acanthosis plate formation layer changes changes (table 6) changes

Psoriasis + Diffuse Regular Thin + Decreased or Increased mitoses; –

absent minimal spongiosis
Drug reaction + Focal Regular and Normal or 2 Normal Spongiosis; eosinophilic Inflammatory cell
irregular thick infiltrate exocytosis; single
keratinocyte
necrosis
Chronic allergic/ + Focal; crust may Irregular Normal or – Normal Spongiosis; eosinophilic –
contact and be present thick infiltrate
atopic dermatitis
Fungal infection Compact Focal; crust may Irregular Normal or 2 Normal Occasional neutrophilic –
be present thick exocytosis;
LSC + Focal; thick crust Regular or Thin or thick 2 Thickened; ¡minimal exocytosis –
irregular hypergranulosis
Scabies + Focal or diffuse Irregular Normal or 2 Normal Exocytosis; eosinophilic –
thick spongiosis
Seborrheic + Focal Irregular Normal or 2 Normal Spongiosis; lymphocytic –
dermatitis and thick and neutrophilic infiltrate
HIV dermatitis
PRP Compact Shoulder Regular or Normal or 2 Normal Spongiosis; lymphocytic Occasional
parakeratosis*; irregular thick exocytosis; rare vacuolar change
alternating acantholysis
orthokeratosis and
parakeratosis
PR + Focal Irregular Normal or 2 Normal Small foci of spongiosis; Occasional
thick lymphocytic exocytosis necrotic
keratinocytes
Syphilis + Focal Regular or Normal or 2 Normal Lymphocytic and Interface change
irregular thick neutrophilic exocytosis
PLC + Caps of Irregular Normal 2 Normal Mild spongiosis, Necrotic
parakeratosis lymphocytic exocytosis; keratinocytes
necrotic keratinocytes
MF + Focal Regular or Normal 2 Normal Minimal or no Atypical lymphoid
irregular spongiosis; ¡Pautrier cells lining the
microabscess dermo–epidermal
junction

*Parakeratotic mounds at the edge of follicular ostia.

BVs, blood vessels; LSC, lichen simplex chronicus; MF, mycosis fungoides; PLC, pityriasis lichenoides chronica; PR, pityriasis rosea; PRP, pityriasis rubra pilaris; +, present;
2, absent.

of psoriasis. However, in partially treated psoriasis, the dermatitis often show features of both spongiform and
granular cell layer may be present, so that clinical–patholo- psoriasiform changes. Evaluation of the dermoepidermal
gical correlation is crucial for accurate diagnosis. An increase junction and dermis is important. Psoriasiform dermatitis
in the intensity of the granular cell layer is associated with with interface changes can be seen in drug reactions,
lichen simplex chronicus. Different alterations that occur cutaneous lupus erythematosus, and syphilis. This is an
within the spinous layer are associated with various clinical
conditions (table 6). The microscopic findings of seborrheic
Table 6 Epidermal histological alteration in psoriasiform
dermatitis
Table 5 Dermal changes in psoriasiform dermatitis Alterations in stratum spinosum
layer Clinical conditions
Psoriasiform dermatosis Dermal changes
Increased mitotic figures Psoriasis
Psoriasis PVLI; mild oedema, dilated vessels Spongiosis and exocytosis of Chronic spongiotic dermatitis
Drug reaction PVLI or band-like infiltrate; ¡eosinophilic lymphocytes Fungal infection
infiltrate Drug reaction
Chronic allergic/contact PVLI; ¡eosinophilic infiltrate Seborrheic dermatitis
and atopic dermatitis Spongiosis and exocytosis of Atopic dermatitis
Fungal infection PVLI; +neutrophilic infiltrate eosinophils Allergic contact dermatitis
LSC PVLI; reactive fibroblasts; papillary fibrosis Nummular dermatitis
Scabies Moderate PVLI; numerous eosinophils in Drug reaction
deep dermis Arthropod bite
Seborrheic dermatitis and Mild PVLI Scabies
HIV dermatitis Prebullous bullous pemphigoid
PRP Mild PVLI Spongiosis and exocytosis of Psoriasis
PR PVLI; focal extravasated RBCs neutrophils Fungal infection
Syphilis Band-like lymphocytic infiltrate; numerous Secondary syphilis (uncommon)
plasma cells; vascular endothelial Atypical mononuclear cells Mycosis fungoides
proliferation; thick BVs; histiocytes, rare Langerhans cell histocytosis
eosinophils Cutaneous CD30 lymphoproliferative
PLC PVLI disorders
MF PVLI; atypical lymphoid cells Single keratinocytes apoptosis Drug reaction
Psoriasiform subacute lupus
BVs, blood vessels; LSC, lichen sclerosis chronicus; MF, mycosis erythematosus
fungoides; PLC, pityriasis lichenoides chronica; PR; pityriasis rosacea; Pale keratinocytes Nutritional dermopathies
PRP, pityriasis rubra pilaris; PVLI, perivascular lymphocytic infiltrate;
RBCs, red blood cells; +, present;2, absent.

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1240 Alsaad, Ghazarian

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Clinical Evidence—Call for contributors

Clinical Evidence is a regularly updated evidence-based journal available worldwide both as

a paper version and on the internet. Clinical Evidence needs to recruit a number of new
contributors. Contributors are healthcare professionals or epidemiologists with experience in
evidence-based medicine and the ability to write in a concise and structured way.
Areas for which we are currently seeking contributors:
N Pregnancy and childbirth
N Endocrine disorders
N Palliative care
N Tropical diseases
We are also looking for contributors for existing topics. For full details on what these topics
are please visit www.clinicalevidence.com/ceweb/contribute/index.jsp
However, we are always looking for others, so do not let this list discourage you.
Being a contributor involves:
N Selecting from a validated, screened search (performed by in-house Information
Specialists) epidemiologically sound studies for inclusion.
N Documenting your decisions about which studies to include on an inclusion and exclusion
form, which we keep on file.
N Writing the text to a highly structured template (about 1500-3000 words), using evidence
from the final studies chosen, within 8-10 weeks of receiving the literature search.
N Working with Clinical Evidence editors to ensure that the final text meets epidemiological
and style standards.
N Updating the text every 12 months using any new, sound evidence that becomes available.
The Clinical Evidence in-house team will conduct the searches for contributors; your task is
simply to filter out high quality studies and incorporate them in the existing text.
If you would like to become a contributor for Clinical Evidence or require more information
about what this involves please send your contact details and a copy of your CV, clearly
stating the clinical area you are interested in, to [email protected].

Call for peer reviewers

Clinical Evidence also needs to recruit a number of new peer reviewers specifically with an
interest in the clinical areas stated above, and also others related to general practice. Peer
reviewers are healthcare professionals or epidemiologists with experience in evidence-based
medicine. As a peer reviewer you would be asked for your views on the clinical relevance,
validity, and accessibility of specific topics within the journal, and their usefulness to the
intended audience (international generalists and healthcare professionals, possibly with
limited statistical knowledge). Topics are usually 1500-3000 words in length and we would
ask you to review between 2-5 topics per year. The peer review process takes place
throughout the year, and out turnaround time for each review is ideally 10-14 days.
If you are interested in becoming a peer reviewer for Clinical Evidence, please complete the
peer review questionnaire at www.clinicalevidence.com/ceweb/contribute/peerreviewer.jsp

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