INTEPRETATION OF PATHOLOGY REPORTS IN BIOPSIES FOR

DERMATITIS

Jessica Spies, MD

Dermatopathologist

CTA Lab, Portland, OR

Lecture goals

• Biopsy techniques– how to optimize pathologic diagnosis

• Dermatitis--how DPs evaluate biopsies

• Terminology – “buzz words” in DP

• Clinicopathologic nature of diagnosing dermatitis—team effort!

Dermatopathology training

• DP fellowships--accept physicians from both pathology and dermatology residencies

• DP training is required in both residencies

• DP training refined in fellowship—50% DP + 50% clinical derm for path trainees, 50% general pathology for derm trainees

General surgical pathologists

• DP training/expertise varies widely!

• Most will not use terminology I will describe today (eg “acute” and “chronic” inflammation terminology does not always apply in DP)

• For best results, use a dermatopathologist!

When you are sent a patient from a primary care physician with a biopsy report you don’t understand

– Have your DP review the biopsy

– Remember: PCP may not have performed the appropriate bx

– Rebiopsy patient (off treatment 2 weeks)

Evaluating a skin biopsy

“Top to bottom approach” mainly: type of epidermal change + type of dermal infiltrate

Biopsy technique

• Punch not shave biopsy for dermatitis!

• Wedge or incisional bx with a scalpel biopsy if ruling out a subcutaneous process/panniculitis

• Vesicles and bullae should be removed with scalpel, to avoid shearing off the blister

Biopsy sites to avoid if possible

• Acral sites

• Elbow/knee

• Center of alopetic patch

• Excoriated lesions (delay bx if no primary lesion)

• Treated lesions

Alopecia biopsies

• 4MM PUNCH aligned parallel to hair shaft to include SQ fat

• At ANGLE in Asians and whites, 90 DEGREES in blacks

• One punch—in KEY area—i.e. perifollicularerythema, active border in scarring alopecia, positive hair pull test site

• Avoid the hairline unless only site of hair loss! (where follicles are normally miniaturized and cycle faster)

Alopecia biopsies

Include as much clinical history and description of the lesions as possible

– Shedding? If so, acute or chronic?

–Pattern of hair loss: diffuse or patchy?

– Location of bx!

–Perifollicular erythema or hyperkeratosis

– Scarring?

Alopecia biopsies

• Use lab with experience in alopecia biopsies!!

• Incorrectly processed specimen unlikely to yield a diagnosis

• Experience with alopecia varies widely between DPs (just like in dermatology) –due to critical mass factor

• New patient previously evaluated for alopecia without definitive pathology? Biopsy again!

Horizontal sections of LPP

Tangential sections ?LPP

Biopsy for DIF

• Pemphigus and pemphigoid groups: perilesional skin or mucosa

• Dermatitis herpetiformis: normal appearing skin 0.5-1.0 cm away from lesion

• Collagen vascular disease: involved areas of skin such as active/erythematous borders

• Vasculitis: active/erythematous border of a new lesion; optimally lesions between 18-24 hours old

• Porphyria cutanea tarda: involved skin.

• Avoid old lesions, ulcers and blisters (false +/-)

• Submit in Michel’s media not formalin (frozen within 5 days)

Bullous pemphigoid DIF

DIF biopsies

• Include an H&E biopsy if possible!! DIF testing has pitfalls and artifacts which can be avoided if we can correlate with H&E bx

• Clinical history important for us

• DIF another infrequently performed test

• Experience with DIF varies greatly between dermatopathologists

Dr. Bernard Ackerman

“Pattern diagnosis”

• “Pattern diagnosis”-- the examination of a slide at scanning magnification and analysis of the silhouette (or architecture) of lesion rather than of its individual cells

• Although this is used by DPs to some extent in tumor diagnoses, it is most useful in the evaluation of biopsies for dermatitis

Example of one of Ackerman’s algorithmic flow charts for pattern diagnosis

Major tissue reaction patterns

• Spongiotic (epidermal intercellular edema)• Lichenoid/interface (basal cell damage)• Psoriasiform (regular epidermal hyperplasia)• Vesiculobullous (blister within or beneath

epidermis)• Granulomatous (chronic granulomatous)

inflammation• Vasculopathic (pathologic changes in

cutaneous blood vessels)

Patterns of inflammation

• Superficial dermal

• Superficial and deep dermal

• Perivascular and/or interstitial

• Perifollicular and/or periadnexal

• Involvement of subcutis

Characterizing the inflammatory cell infiltrate

– Eosinophils

– Neutrophils

– Plasma cells

– Histiocytes

– Lymphocytes

– Mast cells

Eosinophils• In epidermis---BP, PV,

arthropod bite reactions, drug reactions

• In dermis---all of above + urticarial or “dermal” hypersensitivity

• Not all drug reactions have eosinophils!!

• Unusual for collagen vascular disease (drug induced LE exception)

Neutrophils• In dermis---

urticaria, infection, DH, bullous LE, LAD, neutrophilicdermatosis, near folliculitis/ruptured cyst

• In epidermis--infection, psoriasis, arthropod bites, AGEP, P. foliaceous, tinea, impetigo, impetiginization

,

Plasma cells

• Normal in scalp, near mucous membranes

• Dermis-syphillis, near folliculitis, lupus, rosacea

• Syphillis doesn’t always have plasma cells!

Histiocytes• AKA macrophages,

giant cells, siderophages, melanophages

• Large numbers—think infection, espif neutrophils too

• Can form granulomas--think infection, sarcoidosis (dx of exclusion)

Mast cells• Party loving!

• Mastocytosis

Lymphocytes

• Basic inflammatory cell found in all types of dermatitis

• NK cells, T cells, and B cells

• Cannot distinguish between types without immunohistochemical(IHC) staining

• Dense infiltrates—cutaneous lymphoid hyperplasia/pseudolymphoma, cutaneous and systemic lymphomas (IHC panels)

Spongiotic dermatitis

=edema between epidermal keratinocytes which may progress to vesicles/bullae

+ epidermal (“psoriasiform”) hyperplasia when chronic

Spongiotic dermatitis

When lymphocytic, major ddx is

– allergic/contact dermatitis

– atopic dermatitis

– nummular dermatitis

– id reaction (rare)

– dermatophytosis (PAS-D stain)

– seborrheic dermatitis (scalp and face)

However…you may also see spongiosisin

• Stasis

• Arthropod bites

• Spongiotic drug eruptions

• Pityriasis rosea

• Light reactions

• Neoplastic infiltrates (Mycosis fungoides)

• Many others..

How do we narrow down our ddx?

The clinical history!

• All DP is clinicopathologic!!

• The more information you give us, the more specific we can be in our diagnosis

• Some diseases have a unique, diagnostic histology while others have a large degree of overlap with other diseases

• A good dermatopathologist tries to narrow the differential diagnosis for you.

Biopsy of spongiotic/eczematous dermatitis

Stop topical and systemic immunosuppression for 2 weeks prior to the biopsy if possible

– Mutes epidermal spongiosis

– Kills lymphocytes

Mycosis fungoides

• Biopsy off steroids after 2 weeks

• Multiple bxs (one container OK)--more definitive diagnosis by histologic and molecular methods (same T cell clone > 1 bx)

• “Spongiotic dermatitis”? call your DP and/or do additional bxs if rash evolves and/or you suspect MF

• Remember: MF is a clinicopathologic diagnosis --early (patch) stage, is very indolent—better to under rather than overdiagnosis it.

More specific types of spongiosis

• Neutrophilic spongiosis

• Eosinophilic spongiosis

• Follicular spongiosis

• Miliarial spongiosis

Neutrophilicspongiosis

= neutrophils in epidermis + some degree of spongiosis(often pustular)

Neutrophilic spongiosis

• Pustular psoriasis• Palmoplantar pustulosis• Dermatophytosis• Pustular contact dermatitis• Reiter’s syndrome• IgA pemphigus• Herpetiform pemphigus• Infantile acropustulosis• Acute generalized exanthematous pustulosis (AGEP)• Impetiginized spongiotic dermatitis

Eosinophilic spongiosis

= eosinophils in epidermis with some degree of spongiosis

Eosinophilic spongiosis

• Allergic contact dermatitis

• Id reaction

• Atopic dermatitis

• Precursor lesions of bullous pemphigoid (or pemphigus)

• Arthropod bite reactions (including scabies)

• Spongiotic drug

Follicular (or folliculocentric) spongiosis

=when prominent spongiosis in the follicular epithelium

Follicular spongiosis

• Atopic dermatitis

• Eosinophilic (suppurative) folliculitis

• Apocrine miliaria (Fox-Fordyce disease)

• Disseminate and recurrent infundibulofolliculitis

Lichenoid/interface dermatitis

• Key feature = epidermal basal layer damage—cell death +/- basal layer vacuolar change

• Terminology confusing-- some use “interface dermatitis” alone when there vacuolar change predominating or “lichenoid dermatitis” when cell death and/or a band-like dermal lymphocytic infiltrate predominates

• Most often used together as most diseases with this pattern will have some of both features

Lichenoid/interface differential

• Lichen planus and it’s variants• Lichen niditus• Lichen striatus• Lichenoid and fixed drug eruptions• Erythema multiforme• Lupus and it’s variants• Pityriasis lichenoides• Viral reactions• Perniosis• Paraneoplastic pemphigus• Pigmented purpuric dermatitis• Mycosis fungoides• Secondary syphillis• Lichen sclerosus• Many other, less common diseases

Lichenoid/interface dermatitis

• Acute or “EM like”

• “LP like”

• Psoriasiform lichenoid

• Atrophic or “LE like”

Acute or “EM like” --epidermal basal cell death and little other epidermal change

“Lichen planus like” --prominent cell death, band like lymphocytic dermal infiltrate

“Psoriasiform lichenoid”-- epidermal hyperplasia + band-like inflammatory dermal infiltrate

Atrophic or “LE like”-prominent vacuolar change + epidermal atrophy

Lupus• Superficial and deep

infiltrate

• Perifollicullarlymphocytes+plasmacells

• Rare if any eosinophils

• Increased dermal mucindeposition (colloidal iron stain)

• Newly published criteria: increased numbers of CD123+ antigen presenting cells in infiltrate

• DIF studies may or may not be + (50-90%)

Psoriasiformdermatitis

Characterized by epidermal thickening (acanthosis or hyperplasia) with regular elongation of rete ridges

Psoriasiform dermatitis

• Psoriasis and its variants• Subacute spongiotic dermatitis• Lichen simplex chronicus• Chronic candidiasis and tinea• Mycosis fungoides• Norweigan scabies• Secondary syphillis• Some deficiency states (pellagra, acrodermatitis enteropathica)• Bowen’s disease (squamous cell carcinoma in situ)• Lamellar ichthyosis• Other rare diseases such as Reiter’s syndrome, AIDS associated

psoriasiform dermatitis

Thanks!

Come visit!

Jessica Spies, Curtis Thompson and Andrea Chakrapani (all Board certified dermatopathologists)

CTA Lab503-906-7300www.cta-lab.com