Features of particular processes20
Signs of photosensitivity20
Signs of rubbing/scratching20
Subtle clues to drug reactions20
Clues to elastic tissue alterations20
Clues to deficiency states21
Clues to fungal infections21
Subtle clues to a folliculitis21
Histological features – what do they suggest?22
Superficial and deep inflammation22
Filled papillary dermis23
Sparse perivascular neutrophils23
Thickened basement membrane23
Mid-dermal infiltrate and mucin24
Epidermotropism and exocytosis24
The epidermal/follicular ‘vacuum cleaner’24
Parakeratosis as a helpful sign25
Parakeratotic follicular lipping25
The ‘bare underbelly’ sign26
Intraluminal giant cells/histiocytes26
High apoptotic (dyskeratotic) keratinocytes26
Vertical collagen bundles27
Loose pink fibrillary collagen27
Pallor of epidermal cells27
Tumors with hemosiderin28
Clues to a particular disease29
Clues to herpes folliculitis29
Clues to Grover’s disease29
Clues to pityriasis rubra pilaris29
Clues to cicatricial pemphigoid29
Clues to epidermolysis bullosa acquisita29
Clues to mycosis fungoides29
Clues to alopecia areata30
Clues to androgenetic alopecia30
Granuloma annulare versus necrobiosis lipoidica30
Granuloma annulare versus lichen nitidus30
Clues to trichoepithelioma (over BCC)30
Clues to Kaposi’s sarcoma30
Clues to bacillary angiomatosis30
General helpful hints and cautions31
Beware of keratoacanthoma simulants31
Be cautious with amyloid stains31
‘Do serials, not deepers’31
Fungi may be missed on PAS stain31
Dermal neutrophils – often forgotten31
The demonstration of cryptococci32
The edge of Bowen’s disease32
False negative immunoperoxidase32
Some of the clues that follow are original observations; many have been around for decades. An acknowledgement should be made here of the work of Bernard Ackerman, who has contributed more ‘clues’ to diagnostic dermatopathology than anyone else.
Like all ‘short cuts’, the following ‘clues’ must be used with caution. They are not absolute criteria for diagnosis and they are not invariably present at all stages of a disease. An attempt has been made to group the clues into several sections.
FEATURES OF PARTICULAR PROCESSES
SIGNS OF PHOTOSENSITIVITY (Fig. 2.1)
• Dilated vessels in the upper dermis
• Stellate fibroblasts/dendrocytes
• Deep extension of the infiltrate
• Epidermal ‘sunburn’ cells.
|Fig. 2.1 |
Photosensitivity reaction. (A) Note the mild telangiectasia, scattered stellate cells, deep extension of the infiltrate and mild deep solar elastosis. (B) Note the stellate cells. (H & E)
Note: The duration of the process and the underlying nature of the light reaction will influence the response. Only one or two features may be present, e.g. sunburn cells (apoptotic keratinocytes) are confined to phototoxic and photosensitive drug eruptions.
SIGNS OF RUBBING/SCRATCHING (Fig. 2.2)
|Pale pink epidermis, sometimes with loss of cell borders; pin-point erosions or larger ulcers; fibrin below the epidermis.|
|Psoriasiform epidermal hyperplasia; vertical streaks of collagen in the papillary dermis; stellate fibroblasts/dendrocytes; fibroplasia of varying amounts; enlarged follicular infundibula (as prurigo nodularis commences); compact orthokeratosis.|
|Fig. 2.2 |
Chronic rubbing leading to vertical collagen in the papillary dermis and psoriasiform hyperplasia of the epidermis. (H & E)
SUBTLE CLUES TO DRUG REACTIONS
• Superficial dermal edema
• Eosinophils and/or plasma cells
• Endothelial swelling of vessels
• Exocytosis of lymphocytes
• Apoptotic keratinocytes.
The changes present will mirror the clinical types of reaction. In morbilliform reactions, lymphocytes extend into the lower epidermis and the apoptotic keratinocytes are in the basal layer.
CLUES TO ELASTIC TISSUE ALTERATIONS
• Small blue coiled/clumped fibers (pseudoxanthoma elasticum)
• Wavy epidermis (particularly in children)
• Dispersed neutrophils (early cutis laxa)
• Unusually thickened collagen (connective tissue nevus).
• Confluent parakeratosis
• Superficial epidermal necrosis and/or pallor
• Mild psoriasiform hyperplasia
• Hemorrhage (in pellagra and mixed deficiencies).
CLUES TO FUNGAL INFECTIONS (Fig. 2.3)
Basically, these features should prompt the performance of a PAS stain. Many simulants exist.
|Fig. 2.3 |
Dermatophyte. The fungal elements are present in the region with compact orthokeratosis. Note the adjacent normal ‘basket-weave’ pattern. (H & E)
• Compact orthokeratosis with no other explanation
• Layering of epidermal cornification (‘sandwich sign’)
• Neutrophils in the epidermis/stratum corneum
• Spongiosis, particularly palmoplantar
• Suppurative folliculitis.
SUBTLE CLUES TO A FOLLICULITIS (Fig. 2.4)
These signs refer to a likely folliculitis at deeper levels of the biopsy.
|Fig. 2.4 |
Folliculitis. There is deep dermal inflammation and an ‘uneven vasculitis’ more superficially. A ruptured and inflamed follicle was present on deeper levels. (H & E)
• Neutrophils on top of the stratum corneum
• Neutrophils at the edge of the tissue section
• Focal splaying of neutrophils and dust in mid dermis.
‘LAST WEEK’S SIGN’ (Fig. 2.5)
This refers to a dermatosis, no longer active, which is ‘playing itself out’. It was presumably more active some days earlier.
|Fig. 2.5 |
‘Last week’s sign’. The return to the production of normal basket-weave keratin beneath a layer of parakeratosis suggests there is little ongoing activity in this region. (H & E)
• Parakeratosis overlying basket-weave orthokeratin (the key feature)
• Mild hyperplasia of the epidermis
• Mild dermal inflammation.
This refers to several conditions in which the clinical appearances may be striking in comparison to the histology.
• Sclerodermoid GVHD may have ‘rock-hard skin’, but only subtle collagen deposition.
• Cicatricial alopecia can be similar.
• Urticaria – histology underestimates the edema because of dehydration during tissue processing.
• Prurigo nodularis – there may be clinical nodules but no histological swollen infundibula, only psoriasiform hyperplasia of lichen simplex chronicus.
• Pauci-cellular photodermatoses – there may be striking clinical changes but only telangiectasia and sparse inflammatory cells on histology.
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HISTOLOGICAL FEATURES – WHAT DO THEY SUGGEST?
SUPERFICIAL AND DEEP INFLAMMATION (Fig. 2.6)
The presence of a superficial and deep inflammatory cell infiltrate within the dermis should trigger the mnemonic ‘8Ls + DRUGS’.
|Fig. 2.6 |
A superficial and deep dermal infiltrate. This is one of the ‘L’ diseases – polymorphiclight eruption. (H & E)
• Lipoidica (necrobiosis)
• Lepidoptera (and other arthropods)
• Reticular erythematous mucinosis
• Urticarial stages (bullous pemphigoid)
• Scleroderma (localized)
• And, of course, drug reactions
A ‘BUSY’ DERMIS (Fig. 2.7)
‘Busy’ refers to a dermis that appears focally hypercellular on scanning magnification and is not usually due to the usual inflammatory infiltrates.
|Fig. 2.7 |
A ‘busy’ dermis. There is hypercellularity in this case of interstitial granulomatous drug reaction. (H & E)
• Incomplete form of granuloma annulare
• Interstitial granulomatous dermatitis
• Interstitial granulomatous drug reaction
• Resolving vasculitis (increased mucin also)
• Chronic photodermatoses
• Folliculitis – at deeper levels (cells are neutrophils and dust)
• Desmoplastic melanoma (also perivascular lymphocytes)
• Kaposi’s sarcoma (early stage).
ABSENT STRATUM CORNEUM
• Staphylococcal scalded skin syndrome
• Psoriatic erythroderma (psoriasiform hyperplasia present)
FILLED PAPILLARY DERMIS (Fig. 2.8)
The low power impression is that of a variably hypercellular papillary dermis. Excluded from consideration are nodular and diffuse infiltrates also involving the reticular dermis. The ‘LUMP’ mnemonic covers most cases: l
rticaria pigmentosa, m
ycosis fungoides, p
igmented purpuric dermatoses. Expressed differently they are:
• Most of the lichenoid tissue reactions
• Pigmented purpuric dermatoses
• Cutaneous T-cell lymphoma
• Parapsoriasis (if not included above)
• Early lichen sclerosus et atrophicus.
|Fig. 2.8 |
The papillary dermis is filled. This is mastocytosis. (H & E)
PAPILLARY MICROABSCESSES (Fig. 2.9)
• Dermatitis herpetiformis
• Localized cicatricial pemphigoid
• Bullous lupus erythematosus
• Epidermolysis bullosa acquisita
• Hypersensitivity vasculitis (rare)
• Rheumatoid neutrophilic dermatosis
• Pemphigoid gestationis (eosinophils)
• Deep lamina lucida pemphigoid
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