Non-malignant skin disease

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Non-malignant skin disease is relatively common. The pathology may or may not be specific. Some diseases require clinical information to diagnose.

An introduction to dermatopathology is in the dermatopathology article. Nevi (moles) and other melanocytic lesions are dealt with in the article melanocytic lesions. Inflammatory skin conditions are dealt with in inflammatory skin disorders.

Other

Lichen simplex chronicus

  • Abbreviated LSC.
  • AKA squamous cell hyperplasia.[1]

General

Etiology:[4]

  • Pruritus (itchness) -> mechanical trauma -> lichenification (thickened/leathery[5].

Microscopic

Features:[6]

  • Acanthosis (epithelial thickening) - irregular.
  • Hyperkeratosis.

Other features:[7]

  • Spongiosis (epidermal intercellular edema -- cells appear to have a clear halo around 'em).
  • Parakeratosis = retention of nuclei in the stratum corneum.

DDx:

Images:

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SKIN, PUNCH BIOPSY:
- LICHEN SIMPLEX CHRONICUS.
- NEGATIVE FOR MALIGNANCY.

Oral

RETROMOLAR PAD, RIGHT, PUNCH BIOPSY:
- ORAL LICHEN SIMPLEX CHRONICUS.
- NEGATIVE FOR MALIGNANCY.

Micro

The sections show a squamous mucosa with irregular psoriasiform change, parakeratosis, and focal hypergranulosis. There is no inflammation at the interface. Epidermal intercellular bridges are easily seen. There is no significant nuclear atypia. Mitoses are not evident.

Prurigo nodularis

  • Abbreviated PN.
  • AKA chronic prurigo and picker nodule.[3]

General

Gross

  • Dome-shaped/raised - papular (<1 cm) or nodular (>1 cm).[9]

Microscopic

DDx:

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SKIN LESION, LEFT CHIN, BIOPSY: 
- PRURIGO NODULARIS.

Micro

The sections show a raised lesion with compact hyperkeratosis and irregular acanthosis. Spongiosis is seen focally. There is minimal hypergranulosis.

There is no thinning of the suprapapillary plate and no dilated superficial blood vessels. There is no interface activity.

Very common

Dermatomycosis

Dermatophytosis redirects here.

General

Note:

  • Dermatophytosis (ring worm) is a type of dermatomycosis.

Microscopic

Features:

  • Microorganisms - key feature.
    • Often hyphae (candida) - like twigs of a tree... branching.
      • May be very fragmented in section ~ size of a neutrophil.
  • Perivascular inflammation, esp. neutrophils.
  • Exocytosis - blood cell infiltrate the epidermis.

Images:

Stains

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SKIN, BIOPSY:
- SKIN WITH SUPERFICIAL FUNGAL ORGANISMS CONSISTENT WITH CANDIDA.
- REACTIVE CHANGES OF THE EPITHELIUM.

Micro

The sections show skin with a neutrophilic infiltrate in the superficial epidermis. PAS-D staining demonstrates fungal organisms with a morphology suggestive of candida.

The epithelium has parakeratosis, acanthosis and spongiosis. No mitotic activity is appreciated. The keratinocytes are moderately enlarged and have evident nucleoli.

Cicatrix

  • AKA scar, dermal scar.

General

  • Previous surgery, biopsy, trauma.

Microscopic

Features:

  • Loss of dermal papilla.
  • Dense collagen - fibers run parallel to the dermal-epidermal (DE) junction[11] - key feature.
  • Loss of adnexal structures.

Other feature:

  • Thin-walled blood vessels.
    • Described as running perpendicular to the surface[11] - this may not be apparent.

Note:

  • There should not be any nuclear hyperchromasia or pleomorphism.[12]

DDx:

Image:

IHC

  • S100 focal/scattered +ve.
    • Desmoplastic melanoma strong +ve.
  • HMB-45 -ve.
    • Sclerosing blue nevus +ve.

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SKIN, LOWER MID BACK, RE-EXCISION:
- DERMAL SCAR.
- SOLAR ELASTOSIS.

Micro

The sections show skin with a dermis with dense collagen fibres that run parallel to the skin surface without adnexal structures. The overlying dermal-epidermis interface lacks the typical undulation.

Fibroepithelial polyp

  • AKA acrochordon.
  • AKA skin tag.

General

Gross

  • Raised skin-coloured lesion.

Image:

Microscopic

Features:

  • On a stalk / epithelium on three sides.
  • Benign epidermis.

DDx:

Images:

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SKIN ("SKIN TAG"), THIGH, EXCISION:
- FIBROEPITHELIAL POLYP.

Micro

The sections show a fragment of skin with epithelium on three sides. The epithelium matures and is not hypertrophic. Orthokeratosis is present. The core of the lesion has fibrous tissue. There is no significant inflammation. No melanocytic nests are identified.

Inflamed

The sections show a fragment of skin with epithelium on three sides. The epithelium matures and is acanthotic. Minimal parakeratosis is present. The core of the lesion consists of fibrous tissue with a mild lymphocyte-predominant dermal infiltrate. Rare siderophages are present.

There is mild basal nuclear enlargement. No significant nuclear atypia is apparent. The dermal-epidermal interface is well-demarcated. Rare basal mitotic activity is identified.

Actinic keratosis

Bowenoid actinic keratosis redirects to here.

General

Risk factors:[19]

  • Sun exposure.
  • Immune suppression (e.g. organ transplant recipients).

Gross

Features:

  • Yellow-brown scaly, patches.
  • Sandpaper sensation - on touching.
  • May be pigmented.[20]

Microscopic

Features:[21]

  • Epidermal nuclear atypia:
    • Variation is size, shape and staining - must involve basilar layer.
      • Nuclear enlargement - key feature.
      • Hyperchromasia.
  • Abnormal epidermal architecture:
  • +/-Parakeratosis - may alternate with orthokeratosis, esp. early lesions.[22]
  • +/-Irregular acanthosis.

Note:

  • May be full thickness - known as bowenoid actinic keratosis.[23]

DDx:

Images:

Histologic subtypes of actinic keratosis

Like most common things, there are several variants:[22]

  • Hypertrophic actinic keratosis.
    • Increased thickness of: (1) epidermis and, (2) stratum corneum.[25]
  • Acantholytic actinic keratosis.
  • Proliferative actinic keratosis - downward finger-like projections of the epidermis.
  • Pigmented actinic keratosis.
  • Lichenoid actinic keratosis.

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SKIN LESION, RIGHT THIGH, BIOPSY:
- HYPERTROPHIC ACTINIC KERATOSIS.
- SOLAR ELASTOSIS.
- NEGATIVE FOR MALIGNANCY.

Bowenoid

SKIN LESION, RIGHT DISTAL FOREARM, BIOPSY:
- BOWENOID ACTINIC KERATOSIS, COMPLETELY EXCISED IN PLANE OF SECTION.
- EXTENSIVE SOLAR ELASTOSIS.
- NEGATIVE FOR MALIGNANCY.

Micro

General

The sections show skin with basilar epidermal nuclear enlargement and hyperchromasia with irregular nuclear palisading. Hyperkeratosis and parakeratosis is present. A granular layer is present. The dermal-epidermal interface is sharply-demarcated. There is focal inflammation at the interface. Extensive solar elastosis is present.

There is no clefting of the lesion from the surrounding stroma. The surrounding stroma does not have a myxoid quality.

Bowenoid

The sections show skin with epidermal nuclear enlargement and hyperchromasia with irregular nuclear palisading. The lesion involves the full thickness of the epidermis; however, it spares adnexal and follicular epithelium. Proliferative activity is present. Hyperkeratosis and parakeratosis is present. A granular layer is present. The dermal-epidermal interface is sharply-demarcated. There is focal inflammation at the interface. Extensive solar elastosis is present.

There is no clefting of the lesion from the surrounding stroma. Intercellular bridges are identified.

Actinic cheilitis

General

Microscopic

See actinic keratosis.

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LESION, LOWER LIP, BIOPSY: 
- ACTINIC CHEILITIS.
- SOLAR ELASTOSIS.

Micro

The sections show skin with moderate basal nuclear hyperchromasia and atypia, and parakeratosis. The squamous epithelium has maturation to the surface. There is no inflammation at the dermal-epidermal interface. Solar elastosis is present.

Seborrheic keratosis

  • Abbreviated SK.

General

  • Benign.
  • Most common tumour in older people.[26]
  • "Large number" of SKs = paraneoplastic syndrome (Leser–Trélat sign).[27]

Epidemiology:

  • Old people.
  • Usually in sun exposed area.[28]

Gross

  • "Stuck-on" appearance - raised lesion.

Image(s):

Microscopic

Features:[27]

  • Raised above skin surface.
  • Border sharply demarcated.
  • Hyperkeratosis - stratum corneum extra thick.
    • May be minimal.
  • Horn cysts - intraepidermal collections of keratin - key feature.
    • Actually invaginations - not true cysts; thus, they may more accurately be called pseudohorn cysts.[29]
  • Clusters of cells with brown granular material in the superficial dermis/dermoepidermal junction - pigmented melanocytes.

DDx:[30]

Images:

Histologic subtypes

Like very common lesion, there are subtypes:[30]

  • Acanthotic seborrheic keratosis - thickened stratum spinosum; thick epidermis.
  • Reticulated seborrheic keratosis - vaguely resembles fibroepithelioma of Pinkus (BCC, fibroepitheliomatous pattern).
  • Irritated seborrheic keratosis - spongiosis (epidermal intercellular edema) and inflammation.
  • Digitated seborrheic keratosis - papillomatous projections, architecture mimics a verruca.
  • Stucco keratosis - pointed papillomatous projections.

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SKIN LESION, MID BACK, BIOPSY:
- SEBORRHEIC KERATOSIS.

Micro

The sections show skin with acanthosis, pseudohorn cysts, parakeratosis, hyperkeratosis and focal basal epidermal pigmentation. There is no basal nuclear atypia, and there are no melanocytic nests or mitoses. There is minimal dermal inflammation. There is no apparent solar elastosis.

Without horn pseudocysts

The sections show skin with acanthosis, a thin layer of compact keratin and focal basal epidermal pigmentation. Dilated blood vessels surrounded by collagen are seen in the superficial dermis. No pseudohorn cysts are identified. A granular layer is present.

There is no basal nuclear atypia. There is no mitotic activity and no melanocytic nests. There is no solar elastosis. No koilocytes are apparent.

Minimal hyperkeratosis

The sections show skin with acanthosis, pseudohorn cysts, rare parakeratosis, minimal hyperkeratosis and focal basal epidermal pigmentation. There is no basal nuclear atypia, no appreciable mitotic activity and there are no melanocytic nests. There is minimal dermal inflammation. Solar elastosis is present.

Pilomatricoma

  • AKA calcifying epithelioma of Malherbe[32], AKA pilomatrixoma.

General

  • Benign skin tumour.
  • Most common solid skin tumour of children.[33]
  • CTNNB1 gene mutation important in pathogenesis.[34]

Clinical:

  • Hard nodule - calcification.
  • +/-Painful.

Treatment:

  • Surgical excision.[33]

Microscopic

Features:[35]

  • Nodular circumscribed lower dermis/subcutaneous adipose lesion; thus, usu. surrounded by connective tissue.
    • Sharpy demarcated island of cells.
    • Calcification in 75%.
  • Cells:[36]
    • Basaloid epithelial cells - have prominent nucleoli.
    • Anucleate squamous cells ("ghost cells").
    • Giant cell foreign body type granulomas (form in reaction to keratin).

Notes:

  • Keratin a prominent feature on cytology - lots of orange stuff.
  • May ossify.

Images:

DDx:

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SKIN LESION, RIGHT ARM, EXCISION:
- PILOMATRICOMA.

Dermatofibroma

  • Abbreviated DF.

General

  • AKA fibrous histiocytoma.
  • Reactive process -- it is not a neoplasm.
  • Usually associated with previous trauma.
    • In women... usually legs.

Microscopic

Features:[38]

  • Prominent fibrous bundles, especially at the edge of the lesion.
    • Surrounded by spindle cells (fibroblasts).
      • Usually thought of as fibroblasts surrounded by fibrous material ("collagen-trapping").
  • Lack of adnexal structures, i.e. no sweat glands, no hair.
  • +/-Epidermal changes - known as "dirty fingers":[39]
    • Acanthosis (thickened epithelial layer - specifically thickened stratum spinosum).
    • Basal keratinocyte hyperpigmentation.

DDx:

Images:

Subtypes

Like all common things... there are subtypes:[40]

  • Cellular.
  • Deep penetrating.
  • Lipidized - with foamy macrophages, hemorrhage and Touton-like giant cells.
  • Epithelioid cell histiocytoma.
  • Fibrotic.
  • Aneurysmal - large blood filled + features of lipidized.
  • Granular cell dermatofibroma.
  • Dermatofibroma with monster cells.
Cellular dermatofibroma

Features:

  • High cell density in the dermis - "blue" at low power.
  • Collagen bundles - key feature.

Images:

IHC

Features:[42][43]

  • Factor XIIIa +ve.
    • Usually negative in DFSP.
  • CD34 -ve.
    • Usually positive in DFSP.

Others:

  • D2-40 +ve.[44]
    • Usually negative in DFSP.
    • There is not much literature on D2-40 in this context. Molecular work on the protein (podoplanin) the antibody is directed at has shown it is present in DFSP.[45]

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SKIN LESION, LEFT SHOULDER, EXCISION:
- DERMATOFIBROMA.

Micro

The sections show skin with bland spindle cells interspersed between fibrous bundles. The fibrous bundles are prominent at the periphery of the lesion (collagen-trapping). Focal acanthosis is present.

The lesion does not extend to the adipose tissue. No atypia is apparent. No mitotic activity is identified.

The lesion extends to the edge of the tissue.

Ezcema

General

  • A nebulous thingy.
  • Very common.

DDx:

Microscopic

Features:[46]

  • Spongiosis (epidermal edema); keratinocytes spacing increased - key feature.
  • +/-Interdermal vesicles.
  • +/-Eosinophils (may suggest Rx reaction).
  • Perivascular lymphocytes.

Acne vulgaris

General

  • Extremely common - esp. among adolescents.
  • Very rarely seen by pathologists.

Treatments:

  • Antibiotic (minocycline).
  • Isotretinoin AKA all-trans retinoic acid (ATRA).

Gross

  • Papules, pustules, nodules or cysts.
    • White, black or erythematous.

Images:

Microscopic

Features:[47]

  • Folliculitis:[48]
    • Neutrophils around hair follicle and infiltrate into it - including the follicular canal.
  • Epidermal invagination or cyst at site of a hair follicle - contains:
    • Sebum.
    • +/-Bacteria (Propionibacterium acnes) and inflammatory cells - typically neurophils.

Subtyped into:

  1. Open comedones ("blackheads") - no extension to epidermal surface.
  2. Closed comedones ("whiteheads") - to epidermal surface have wide opening.

DDx - acneiform disorder:[48]

  • Rosacea.
  • Infective folliculitis.
  • Perioral dermatitis.
  • Acne vulgaris.

Image:

Solar elastosis

General

  • Very common.
  • Caused by sun exposure - specifically UV light.[50]
    • Severity correlated with cumulative exposure to UV light..[51]
  • Often co-localized with skin cancers - as UV light is risk factor for skin cancers.[51]
  • Benign.

Microscopic

Features:

  • Grey, spaghetti-like material in the superficial dermis.

DDx:

Note:

  • The DDx above is things associated with sun damaged skin.
  • Dermal mucin (as my be seen in lupus erythematosus) is a possible mimic - but it isn't spaghetti-like and the "background" (an interface dermatitis) is different.

Images:

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SKIN, RIGHT CHEEK, RE-EXCISION:
- DERMAL SCAR.
- EXTENSIVE SOLAR ELASTOSIS.
Prominent blood vessels
SKIN LESION, LEFT CHEEK, BIOPSY:
- SKIN WITH SOLAR ELASTOSIS AND PROMINENT SMALL BLOOD VESSELS.

SUPERIOR SHOULDER, LEFT, PUNCH BIOPSY:
- BENIGN SKIN WITH MODERATE SOLAR ELASTOSIS, PROMINENT SMALL BLOOD VESSELS AND
  SCATTERED PERIVASCULAR LYMPHOCYTES AND PLASMA CELLS.
- NEGATIVE FOR BASAL CELL CARCINOMA.
- NEGATIVE FOR ACTINIC KERATOSIS.

Micro

The sections show hair bearing skin with solar elastosis and numerous small dilated blood vessels. The dermis is mildly fibrotic. Compact keratin is present.

The epidermis matures to the surface. A granular layer is present. There is no basal epidermal atypia. No melanocytic nests are identified. There is no palisading of the basal cells. Rare scattered lymphocytes are in the dermis.

Very common - viral

Verruca vulgaris

  • AKA common wart.

General

  • Etiology - HPV.
  • Very common.

Notes:

Gross

Features:

  • Papule or plaque with granular surface.
  • Classic location: hand.

Images:

Microscopic

Features:[52]

  • Hyperkeratosis (more keratin - thick stratum corneum) - in "columns"; keratin in separate towers - not a flat thick sheet.
  • Hypergranulosis (thicker stratum granulosum).
  • Papillomatous hyperplasia:
    • Rete ridge lengthening (~7-10x normal) and thickening.
    • Rete ridge curvature toward the centre of the lesion (like the roads to the Palace of Versailles) - important.
  • Large blood vessels at the dermal-epidermal junction - between the rete ridges.
  • +/-Viral changes - perinuclear halo, nucleus small and hyperchromatic[53] - virtually diagnostic when present.
    • +/-Binucleation.

Memory device: there is more of everything - more s. corneum, s. granulosum, s. spinosum, longer rete ridges, more (larger) blood vessels.

DDx:

Images:

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SKIN LESION, RIGHT LOWER LEG, SHAVE BIOPSY:
- VERRUCA VULGARIS.

Micro

The sections show skin with elongated rete ridges, acanthosis, hypergranulosis, hyperkeratosis in vertical columns, focal parakeratosis, dilated blood vessels at the dermal-epidermal junction and koilocytic change. Mild basilar nuclear atypia is present.

Without koilocytes

The sections show skin with elongated rete ridges that curve toward the centre of the lesion, acanthosis, hypergranulosis, hyperkeratosis in vertical columns, and dilated blood vessels at the dermal-epidermal junction. Minimal basilar nuclear enlargement is present. No definite koilocytic change is apparent.

No parakeratosis is identified. Mild solar elastosis is identified. No melanocytic nests are apparent. Mitotic activity is not apparent.

Verruca plana

General

  • Common.
  • Usu. hands and face.[54]

Microscopic

Features:[54]

  • Orthokeratosis with basketweave pattern.
  • Hypergranulosis.
  • Viral keratohyaline.
  • Koilocytes.
  • Acanthosis - yet flat surface and base.

Notes:

  • It differs from verruca vulgaris... (1) orthokeratosis, (2) flat surface and base.

Less common

Chronic folliculitis

Folliculitis redirect here.

General

  • Common.
  • Infrequently biopsied.

Gross

DDx gross:

Microscopic

Features:

  • Inflammation around the hair follicle - key feature.
    • Lymphocytes - usu. predominant.
  • +/-Chronic changes:
    • Acanthosis.
    • Hyperkeratosis.
    • Hypergranulosis.

DDx:

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SKIN LESION, UPPER ARM, BIOPSY:
- CHRONIC FOLLICULITIS WITH SECONDARY SURFACE CHANGES.

Micro

The sections show hair-bearing skin with abundant lymphocytes around and within the hair follicle wall.

The non-hair follicle epidermis has acanthosis, hypergranulosis and compact hyperkeratosis. There is no inflammatory cell infiltrate in the non-hair follicle epidermis or at the non-hair follicle interface.

There are no granulomas.

Clear cell acanthoma

General

  • Benign.
  • Elderly.
  • Classically on the leg.[56]
  • Rare.
  • Clinically not distinct.
    • Suspected clinically in only ~3% of cases.[57]

Microscopic

Features:[58]

  • Psoriasiform pattern - epidermal thickening (acanthosis).
  • Keratinocytes:
    • Pale or light pink cytoplasm (when compared to surrounding non-lesional keratinocytes).
    • Separated from one another (spongiosis).
  • +/-Stratum corneum neutrophils.

DDx:

Images:

Chondrodermatitis nodularis chronica helicis

  • AKA chondrodermatitis nodularis helicis.
  • Abbreviated CNCH.

General

  • Tender/painful - key clinical feature.
  • Typically right ear - people more often sleep on this one.[59]
  • Usually >40 years old.

Etiology:

  • Trauma/mechanical.

Gross

  • Papule on ear.
  • +/-Erythematous.
  • +/-Crust.

Clinical DDx:[59]

Images:

Microscopic

Features:[59]

  • Dermal inflammation.
  • Epithelial hyperlasia.
  • Fibrosis.
  • Cartilaginous pathology:
    • Perichondrial inflammation - key feature.
    • Perichondrial disruption.
    • +/-Necrosis.
    • +/-Hemorrhage.

Images:

Sign out

Superficial biopsy

SKIN LESION, LEFT ANTIHELIX OF EAR, BIOPSY:
- SUPERFICIAL SKIN WITH ACANTHOSIS, HYPERKERATOSIS, MODERATE SOLAR ELASTOSIS, 
  HYPERGRANULOSIS AND A MILD LYMPHOCYTIC PERIVASCULAR INFILTRATE.
- NO CARTILAGE IS IDENTIFIED.
- NEGATIVE FOR DYSPLASIA AND MALIGNANCY.

COMMENT:
The findings are non-specific. Chondrodermatitis cannot be excluded.

Cutaneous calcinosis

  • AKA calcinosis cutis.

General

  • Benign in itself; underlying cause may not be benign.
  • May be a scrotal lesion - known as scrotal calcinosis.[60]

Subtypes:[61]

  1. Dystrophic - due to death of cells; may be related to a tumour.
  2. Metastatic - due to chronic renal failure; hyperkalemia; paraneoplastic phenomenon.
  3. Iatrogenic - post surgical.
  4. Idiopathic.

Microscopic

Features:

  • Dermal calcification:
    • Acellular purple blobs on H&E.
      • +/-Artefactual tearing of surrounding tissue due to processing (cutting).
      • +/-Small artefactual lines ~1-2 micrometers due to processing (cutting).
    • Usu. well-circumscribed.

Images:

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SKIN AND SUBCUTANEOUS LESION, LEFT HIP, EXCISION:
- SUBCUTANEOUS CALCIFICATION SURROUNDED BY BENIGN FIBROUS TISSUE.
- DERMAL SCAR.
- NEGATIVE FOR MALIGNANCY.

Dilated pore of Winer

General

  • Benign.
  • Looks like zit.

Microscopic

Features:[62]

  • Dilated hair follicle with keratin.
  • Acanthosis.
  • Budding of epidermis (into dermis).

Lichenoid keratosis

  • AKA lichen planus-like keratosis.
  • AKA lichenoid keratosis.

General

Clinical DDx:[63]

Microscopic

Features:[64]

  • Hyperkeratosis.
  • Parakeratosis.
  • Band of inflammatory cells at DE junction (lichenoid inflammation).
  • Dead keratinocytes (Civatte bodies).
  • Dermal melanophages.

DDx:

Images:

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SKIN LESION, MID-MIDDLE BACK, PUNCH BIOPSY:
- LICHENOID KERATOSIS.

Granuloma annulare

Main article: Granuloma annulare

Necrobiosis lipoidica

General

Associated with:

Microscopic

Features:[65]

  • Dermal palisading granuloma around:
    • Necrotic collagen - key feature.
      • Nuclei "missing" - have undergone karyolysis.
  • Little mucin, no normal dermis between foci.
  • Plasma cells - common.[66]
  • May involve adipose tissue.

DDx:

Images:

Keloid

  • Hypertrophic scar redirects to this section.

General

  • Sites of previous trauma/surgery, esp. in dark skinned individuals.[38]

Microscopic

Features:[38]

  • Thick collagen bundles - surrounded by paler staining fibroblasts - key feature.
  • Lesion replaces adnexal structures, e.g. hair, sweat glands.

DDx:

  • Hypertrophic scar.[67]

NB:

  • Reported as "keloidal-type collagen"; the clinician decides between hypertrophic scar and keloid.

Images

  • Keloid - low mag. (WC/Nephron)

  • Keloid - intermed. mag. (WC/Nephron)

  • Keloid - high mag. (WC/Nephron)

www:

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SKIN LESION, LEFT SCAPULA, EXCISION:
- DERMAL SCAR WITH KELOIDAL-TYPE COLLAGEN, SEE COMMENT.

COMMENT:
The findings are consistent with a hypertrophic scar or keloid; clinical correlation is required.

Clinical provided

SKIN LESION, LEFT NIPPLE AREOLA, EXCISION:
- DERMAL SCAR WITH KELOIDAL-TYPE COLLAGEN, CONSISTENT WITH HYPERTROPHIC SCAR.

Angiofibroma

See also: nasopharyngeal angiofibroma.
Should not be confused with angiokeratoma.

General

Clinical:

  • Firm, dome-shaped, flesh coloured.

Microscopic

Features:[38]

  • Dome-shaped.
  • Fibrotic dermis.
    • Enlarged fibroblasts.
  • Dilated small vessels.

DDx:

Image:

Benign fibrous papule

  • AKA fibrous papule.

General

Gross

  • Solitary lesion of the face - important.[68]
    • Usually on the nose.[70]

Microscopic

Features:[38]

  • Dome-shaped.
  • Fibrotic dermis.
    • Enlarged fibroblasts.
  • Dilated small vessels.
  • +/-Multinucleated stromal cells.[71]
  • +/-Stellate cells.[71]

DDx:

Note:

  • Several variants exist.[70]

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SKIN LESION, CHIN, BIOPSY:
- BENIGN FIBROUS PAPULE.

Molluscum contagiosum

  • Abbreviated MC.

General

  • Etiology: caused by molluscum contagiosum virus.
  • May be abundant in immune deficient individuals, e.g. HIV/AIDS.

Gross

Features:[72]

  • Dome-shaped papules, flesh coloured or pearly.
  • Usually face or trunk.
  • +/-Central umbilication.
    • Central depression.

DDx - gross:

Image:

Microscopic

Features:[72]

  • A suprabasilar epidermal lesion consisting of "molluscum bodies" -- in other words "molluscum bodies" are found above the stratum basale +/- extension to the skin surface.
    • Molluscum bodies - key feature:
      • Large cells with (granular) eosinophilic cytoplasmic inclusions.
        • The inclusions usually fill the cytoplasm.
        • Inclusions are usually one per cell... but may be multiple.
      • Small peripheral nucleus.
  • +/-Lymphocytes.

Notes:

  • Molluscum bodies very vaguely resemble signet ring cells -- but:
    • Cytoplasm is eosinophilic and granular.
    • Nucleus usually smaller than in signet ring cells.
    • Molluscum bodies are only in the epidermis - an uncommon place to find SRCs without finding them elsewhere.
  • The granular eosinophilic cytoplasmic inclusions represents accumulated virons.
  • Molluscum bodies "grow" toward the surface

DDx:

  • Nothing really - it is very distinctive.

Images:

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SKIN LESION ("SKIN TAG"), EXCISION:
- MOLLUSCUM CONTAGIOSUM.

Micro

The section shows fragments of skin with epithelium on three sides. Large suprabasilar cells with eosinophilic intracytoplasmic inclusions (molluscum bodies) and small eccentric nuclei are present, and extend to the skin surface. The epithelium is acanthotic; however, it matures to the surface. There is no significant inflammation.

Superficial dermal infiltrates

Discussed in detail by Alsaad and Ghazarian.[73]

Dermal perivascular lymphoeosinophilic infiltration

  • Abbreviated DPLI.

Microscopic appearance is just what it is called:

  • Lymphocytes and eosinophils around the vessels in the superficial dermis.

DDx:[73]

Notes:

  • May superficially resemble cutaneous lymphoma.[74]

Images:

Congenital dermal melanocytosis

  • AKA Mongolian spots.
  • Classically seen in asian children.

Gross:

  • Brown or blue-grey patch in the lumbosacral area.

Mastocytosis

General

Classification:[75]

  1. Cutaneous (only) - usually children.
    • Urticaria pigmentosa.
    • Others.
  2. Systemic - usually adults.
    • Indolent subvariant.
    • Aggressive subvariant.
    • Leukemic subvariant.

Microscopic

Features:[76]

  • Cells in the superficial/mid dermis that are:
    • Lymphocyte-like with more cytoplasm that is granular.
      • Cells may have spindled or stellate morphology.
      • Tend to be more abundant around vessels.
  • +/-Eosinophils (common).
  • +/-Edema - often prominent; gives cells a white halo.

Notes:

  • Lymphocyte vs. mast cell:
    • Lymphocytes = round; mast cells = ovoid.

Images:

Stains

IHC

  • CD117 +ve.
  • Tryptase +ve.[77]

Ichthyosis

General

  • Comes in different flavours.
  • Usu. inherited... thus a pediatric condition.

Gross

  • Fish scale-like appearance.

Image:

Microscopic

Features:[76]

  • Thick stratum corneum without basket-weave pattern.

Palmar fibromatosis

Main article: Fibromatosis
  • AKA Dupuytren's contracture.
  • AKA Dupuytren disease.

General

Clinical:[78]

  • Usually older - 60s or 70s (years old).
  • Male > female.
  • Associated with:
  • May be familial.

Gross

  • Ring finger - classic location.[citation needed]
  • Nodular.
  • Poorly demarcated.

Image:

Microscopic

Features:[79][80]

  • Poorly demarcated, usu. multiple lesions/multiple nodules.
  • Composed of bland spindle cells in dense collagen.
    • Pale grey cytoplasm (moderate quantity).
    • Pale ovoid nuclei with small round nucleoli.
  • Giant cells - rare.

Note:

  • No nuclear atypia.
  • Mitotic figures - rarely present, none atypical.
  • May see Pacinian corpuscle (AKA lamellar corpuscle) as an incidental finding.

DDx:[80]

Images:

IHC

  • Beta-catenin +ve (cytoplasmic & nuclear).[82]

Sign out

Left

PALMAR FASCIA, LEFT, FASCIECTOMY:
- PALMAR FIBROMATOSIS.

Right

PALMAR FASCIA, RIGHT, FASCIECTOMY:
- PALMAR FIBROMATOSIS.
Micro

The sections show multiple poorly-demarcated nodules composed of bland spindle cells with moderate pale grey cytoplasm and pale ellipsoid nuclei with small round nucleoli. The poorly-demarcated nodules are completely surrounded by dense collagen. Calcification is not present. There is no nuclear atypia or necrosis. Mitotic activity is not identified. Benign fibroadipose tissue is present.

Missed fibromatosis

PALMAR FASCIA, LEFT, FASCIECTOMY:
- PALMAR FASCIA WITHIN NORMAL LIMITS AND BENIGN FIBROADIPOSE TISSUE -- IN AN
  INDIVIDUAL WITH A CLINICAL HISTORY OF PALMAR FIBROMATOSIS.
- NEGATIVE FOR MALIGNANCY.
Micro

The sections show dense collagen (tendon) without an apparent pathology. Calcification is not present. There is no nuclear atypia or necrosis. Mitotic activity is not identified. Benign fibroadipose tissue is present. Lamellar corpuscles are present. The tissue was submitted in toto and levels were cut.

Straight
PALMAR FASCIA, RIGHT, FASCIECTOMY:
- PALMAR FASCIA WITHIN NORMAL LIMITS.
- NEGATIVE FOR FIBROMATOSIS.

COMMENT:
The tissue was submitted in toto and levels were cut.
Micro

The sections show dense collagen (tendon) without an apparent pathology. Calcification is not present. There is no nuclear atypia or necrosis. Mitotic activity is not identified. Benign fibroadipose tissue is present. Lamellar corpuscles are present.

Angiomyoma

General

  • Benign.
  • Female > male.[83]

Microscopic

Features:

  • Well-circumscribed lesion with fascicular architecture.
  • Spindle cells/epithelioid cell with moderate eosinophilic (pink) cytoplasm.
  • Thick-walled blood vessels. (???)

Images:

Angiokeratoma

General

Notes:

Gross

  • Dark lesions.

Clinical DDx:

Images

  • Angiokeratoma. (WC)

Microscopic

Features:[84]

  1. Ectatic superficial dermal vessels.
  2. Overlying hyperkeratosis (thick stratum corneum).
  • Should have "epidermal collarette".[85]
    • Vascular space surrounded by epidermis on three sides.

Others features:[citation needed]

  • Irregular acanthosis.
  • Longer rete ridges.

DDx:

Images

  • Angiokeratoma - low mag. (WC/Nephron)

  • Angiokeratoma - intermed. mag. (WC/Nephron)

www:

Sign out

SKIN LESION, LEFT POPITEAL FOSSA, PUNCH BIOPSY:
- ANGIOKERATOMA.

Inverted follicular keratosis

  • Abbreviated IFK.[86]

General

  • Benign skin lesion.
  • Central face - middle age.[87]
  • Uncommon.
  • May be considered a variant of seborrheic keratosis that is predominantly endophytic.[31]

Clinical DDx:[87][88]

Microscopic

Features:[87]

  • Keratinocyte of cytologically benign proliferation.
  • "Squamous eddies" (whorls of keratin).
  • Coarse keratohyaline granules.

DDx:

Images:

Sign out

SKIN LESION, FACE, BIOPSY:
- INVERTED FOLLICULAR KERATOSIS.

Micro

The sections show skin with acanthosis, pseudohorn cysts, and focal basal epidermal pigmentation. There is no basal nuclear atypia, no mitoses and there are no melanocytic nests. There is minimal dermal inflammation. There is no apparent solar elastosis.

Focal cutaneous mucinosis

General

  • Benign.
  • May be associated with systemic disease.[89]

Microscopic

Features:

  • Light blue whispy material in the dermis - key feature.

DDx:

Panniculitis

Main article: Panniculitis

This is dealt with in the panniculitis article.

DDx for panniculitis:

Rare

Necrotizing fasciitis

Not to be confused with nodular fasciitis.
  • AKA flesh-eating disease.

General

  • High mortality.
  • May be diagnosed at frozen section.[90]
  • Classically associated with Group A streptococcus.

Treatment:

  • Operative debridement.

Microscopic

Features:

  • Necrosis of fascia - key feature.[91]
    • PMNs and necrotic debris (amorphous grey or pink material).

Note:

  • Fat lobules between septae may be normal.

DDx:

Images:

Porokeratosis

General

  • Genetic.
  • Several subtypes.

Notes:

  • Not the same as punctate porokeratotic keratoderma.[92]

Microscopic

Features:

  • Cornoid lamella (pathognomonic) - key feature:
    • Compact keratosis over a hair follicle.
  • +/-Rete ridge loss.

Images:

Nevus sebaceous

  • AKA nevus sebaceous of Jadassohn.

General

  • Congenital - considered a hamartoma.[93]
  • Usually sporadic - may be transmitted autosomal dominant.[93]
  • Malignant tumours may arise within a nevus sebaceous.

Gross

Features:[93][94]

  • Head and neck plaque or papule with:
    • Well-circumscribed borders.
    • Waxy, yellow appearance.
  • Area usu. devoid of hair.[95]

DDx - gross:

Image:

Microscopic

Features:[94]

  • Abundant sebaceous glands.
  • Immature/abortive hair follicles.
    • No normal terminal hair follicles.
  • Papillomatous epidermal hyperplasia.

Images:

Nevus lipomatosus superficialis

  • Abbreviated NLS.
  • AKA nevus lipomatosus cutaneous superficialis, abbreviated NLCS.
  • AKA nevus lipomatosus.[96]

General

Clinically separated into:[99]

  • Solitary - one lesion.
  • Multiple - more than one lesion.

Gross

Features:[97]

  • Pedunculated lesion.
  • Soft.
  • Usually lower trunk or gluteal region.[100]

Image:

Microscopic

Features:[101]

DDx:

Images:

Sign out

SKIN LESION ("SKIN TAG"), LEFT HIP, EXCISION:
- NEVUS LIPOMATOSUS SUPERFICIALIS.

Bullous disease

Main article: Bullous disease

Cysts

Main article: Dermal cysts

See also

References

  1. ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1011. ISBN 978-1416031215.
  2. ↑ Tadrous, Paul.J. Diagnostic Criteria Handbook in Histopathology: A Surgical Pathology Vade Mecum (1st ed.). Wiley. pp. 296. ISBN 978-0470519035.
  3. ↑ 3.0 3.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 26. ISBN 978-0443066542.
  4. ↑ URL: http://emedicine.medscape.com/article/1123423-overview. Accessed on: 20 August 2010.
  5. ↑ URL: http://www.medterms.com/script/main/art.asp?articlekey=10131. Accessed on: 20 August 2010.
  6. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 1065-6. ISBN 0-7216-0187-1.
  7. ↑ URL: http://emedicine.medscape.com/article/1123423-diagnosis. Accessed on: 20 August 2010.
  8. ↑ Natarajan, E.; Woo, SB. (Jan 2008). "Benign alveolar ridge keratosis (oral lichen simplex chronicus): A distinct clinicopathologic entity.". J Am Acad Dermatol 58 (1): 151-7. doi:10.1016/j.jaad.2007.07.011. PMID 18158926.
  9. ↑ URL: http://www.pediatrics.wisc.edu/education/derm/text.html. Accessed on: 23 August 2012.
  10. ↑ URL: http://missinglink.ucsf.edu/lm/DermatologyGlossary/tinea.html. Accessed on: 25 February 2013.
  11. ↑ 11.0 11.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 499. ISBN 978-0443066542.
  12. ↑ 12.0 12.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 479. ISBN 978-0443066542.
  13. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 596. ISBN 978-1416054542.
  14. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 342. ISBN 978-0443066542.
  15. ↑ URL: http://dermatlas.med.jhmi.edu/derm/result.cfm?Diagnosis=1196583692. Accessed on: 1 September 2011.
  16. ↑ URL: http://dermatology-s10.cdlib.org/143/case_presentations/skintags/allegue.html. Accessed on: 9 January 2013.
  17. ↑ Weinberg, JM. (Jan 2006). "Topical therapy for actinic keratoses: current and evolving therapies.". Rev Recent Clin Trials 1 (1): 53-60. PMID 18393780.
  18. ↑ 18.0 18.1 Roewert-Huber, J.; Stockfleth, E.; Kerl, H. (Dec 2007). "Pathology and pathobiology of actinic (solar) keratosis - an update.". Br J Dermatol 157 Suppl 2: 18-20. doi:10.1111/j.1365-2133.2007.08267.x. PMID 18067626.
  19. ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1180. ISBN 978-1416031215.
  20. ↑ URL: http://www.dermoscopy-ids.org/index.php/newest-case/79-lentigo-maligna-vs-pigmented-actinic-keratosis. Accessed on: 23 August 2012.
  21. ↑ URL: http://emedicine.medscape.com/article/1099775-workup#a0723. Accessed on: 1 September 2011.
  22. ↑ 22.0 22.1 22.2 22.3 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 353. ISBN 978-0443066542.
  23. ↑ 23.0 23.1 Bagazgoitia, L.; Cuevas, J.; Juarranz, A. (Feb 2010). "Expression of p53 and p16 in actinic keratosis, bowenoid actinic keratosis and Bowen's disease.". J Eur Acad Dermatol Venereol 24 (2): 228-30. doi:10.1111/j.1468-3083.2009.03337.x. PMID 19515076.
  24. ↑ 24.0 24.1 Picascia, DD.; Robinson, JK. (Aug 1987). "Actinic cheilitis: a review of the etiology, differential diagnosis, and treatment.". J Am Acad Dermatol 17 (2 Pt 1): 255-64. PMID 3305604.
  25. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 352. ISBN 978-0443066542.
  26. ↑ URL: http://emedicine.medscape.com/article/1059477-overview#a0199. Accessed on: 26 August 2011.
  27. ↑ 27.0 27.1 Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 595. ISBN 978-1416054542.
  28. ↑ URL: http://emedicine.medscape.com/article/1059477-overview. Accessed on: 26 August 2011.
  29. ↑ URL: http://www.healthcare.uiowa.edu/dermatology/dpt/HornCyst.htm. Accessed on: 13 September 2012.
  30. ↑ 30.0 30.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 338-9. ISBN 978-0443066542.
  31. ↑ 31.0 31.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 341. ISBN 978-0443066542.
  32. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 387. ISBN 978-0443066542.
  33. ↑ 33.0 33.1 URL: http://emedicine.medscape.com/article/1058965-overview. Accessed on: 10 September 2011. Cite error: Invalid <ref> tag; name "emed1058965" defined multiple times with different content
  34. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 597. ISBN 978-1416054542.
  35. ↑ URL: http://emedicine.medscape.com/article/1058965-diagnosis. Accessed on: 10 September 2011.
  36. ↑ http://www.bccancer.bc.ca/HPI/CE/cytotechnology/cytosleuthquiz/nongyne/ngcase02d.htm
  37. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 389. ISBN 978-0443066542.
  38. ↑ 38.0 38.1 38.2 38.3 38.4 38.5 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 492. ISBN 978-0781765275.
  39. ↑ BD. 13 April 2011.
  40. ↑ Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Reuter, Victor E; Stoler, Mark H (2009). Sternberg's Diagnostic Surgical Pathology (5th ed.). Lippincott Williams & Wilkins. pp. 51. ISBN 978-0781779425.
  41. ↑ URL: http://www.dermpedia.org/case/cellular-dermatofibroma-mimicking-dermatofibrosarcoma-protuberans#. Accessed on: 4 February 2012.
  42. ↑ Abenoza P, Lillemoe T (October 1993). "CD34 and factor XIIIa in the differential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans". Am J Dermatopathol 15 (5): 429–34. PMID 7694515.
  43. ↑ Goldblum JR, Tuthill RJ (April 1997). "CD34 and factor-XIIIa immunoreactivity in dermatofibrosarcoma protuberans and dermatofibroma". Am J Dermatopathol 19 (2): 147–53. PMID 9129699.
  44. ↑ Bandarchi B, Ma L, Marginean C, Hafezi S, Zubovits J, Rasty G (March 2010). "D2-40, a novel immunohistochemical marker in differentiating dermatofibroma from dermatofibrosarcoma protuberans". Mod. Pathol. 23 (3): 434–8. doi:10.1038/modpathol.2009.176. PMID 20062007.
  45. ↑ Xu, Y.; Ogose, A.; Kawashima, H.; Hotta, T.; Ariizumi, T.; Li, G.; Umezu, H.; Endo, N. (Mar 2011). "High-level expression of podoplanin in benign and malignant soft tissue tumors: immunohistochemical and quantitative real-time RT-PCR analysis.". Oncol Rep 25 (3): 599-607. doi:10.3892/or.2011.1141. PMID 21234520.
  46. ↑ Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1188. ISBN 978-1416031215.
  47. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 76. ISBN 978-0443066542.
  48. ↑ 48.0 48.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 77. ISBN 978-0443066542.
  49. ↑ URL: http://www.dermnetnz.org/dermal-infiltrative/solar-elastosis.html. Accessed on: 27 March 2013.
  50. ↑ Thomas, NE.; Kricker, A.; From, L.; Busam, K.; Millikan, RC.; Ritchey, ME.; Armstrong, BK.; Lee-Taylor, J. et al. (Nov 2010). "Associations of cumulative sun exposure and phenotypic characteristics with histologic solar elastosis.". Cancer Epidemiol Biomarkers Prev 19 (11): 2932-41. doi:10.1158/1055-9965.EPI-10-0686. PMID 20802019.
  51. ↑ 51.0 51.1 Karagas, MR.; Zens, MS.; Nelson, HH.; Mabuchi, K.; Perry, AE.; Stukel, TA.; Mott, LA.; Andrew, AS. et al. (Mar 2007). "Measures of cumulative exposure from a standardized sun exposure history questionnaire: a comparison with histologic assessment of solar skin damage.". Am J Epidemiol 165 (6): 719-26. doi:10.1093/aje/kwk055. PMID 17204514.
  52. ↑ URL: http://missinglink.ucsf.edu/lm/DermatologyGlossary/verruca_vulgaris.html. Accessed on: 14 July 2010.
  53. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 106-7. ISBN 978-0443066542.
  54. ↑ 54.0 54.1 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 480. ISBN 978-0781765275.
  55. ↑ URL: http://www.webmd.com/skin-problems-and-treatments/tc/folliculitis-topic-overview. Accessed on: 7 November 2012.
  56. ↑ Akin, FY.; Ertam, I.; Ceylan, C.; Kazandi, A.; Ozdemir, F.. "Clear cell acanthoma: new observations on dermatoscopy.". Indian J Dermatol Venereol Leprol 74 (3): 285-7. PMID 18583817.
  57. ↑ Morrison, LK.; Duffey, M.; Janik, M.; Shamma, HN. (Sep 2010). "Clear cell acanthoma: a rare clinical diagnosis prior to biopsy.". Int J Dermatol 49 (9): 1008-11. PMID 20931670.
  58. ↑ URL: http://www.drmihm.com/cases/case.cfm?CaseID=45. Accessed on: 7 February 2012.
  59. ↑ 59.0 59.1 59.2 Devani, A.; Barankin, B. (May 2007). "Dermacase. Chondrodermatitis nodularis chronica helicis.". Can Fam Physician 53 (5): 821, 837. PMID 17879469.
  60. ↑ Dubey, S.; Sharma, R.; Maheshwari, V. (2010). "Scrotal calcinosis: idiopathic or dystrophic?". Dermatol Online J 16 (2): 5. PMID 20178701.
  61. ↑ URL: http://emedicine.medscape.com/article/1103137-overview. Accessed on: 21 September 2011.
  62. ↑ Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 486. ISBN 978-0781765275.
  63. ↑ 63.0 63.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 346. ISBN 978-0443066542.
  64. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 347. ISBN 978-0443066542.
  65. ↑ 65.0 65.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 51. ISBN 978-0443066542.
  66. ↑ 66.0 66.1 URL: http://dermnetnz.org/pathology/necrobiosis-lipoidica-path.html. Accessed on: 24 January 2012.
  67. ↑ Gauglitz, GG.; Korting, HC.; Pavicic, T.; Ruzicka, T.; Jeschke, MG.. "Hypertrophic scarring and keloids: pathomechanisms and current and emerging treatment strategies.". Mol Med 17 (1-2): 113-25. doi:10.2119/molmed.2009.00153. PMC 3022978. PMID 20927486. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3022978/.
  68. ↑ 68.0 68.1 68.2 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 505. ISBN 978-0443066542.
  69. ↑ URL: http://www.drdittmar.lu/Services.aspx. Accessed on: 1 September 2011.
  70. ↑ 70.0 70.1 70.2 Jacyk, WK.; Rütten, A.; Requena, L. (2008). "Fibrous papule of the face with granular cells.". Dermatology 216 (1): 56-9. doi:10.1159/000109359. PMID 18032900.
  71. ↑ 71.0 71.1 Ragaz, A.; Berezowsky, V. (1979). "Fibrous papule of the face. A study of five cases by electron microscopy.". Am J Dermatopathol 1 (4): 353-6. PMID 543528.
  72. ↑ 72.0 72.1 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 115. ISBN 978-0443066542. Cite error: Invalid <ref> tag; name "Ref_Derm115" defined multiple times with different content
  73. ↑ 73.0 73.1 Alsaad, KO.; Ghazarian, D. (Dec 2005). "My approach to superficial inflammatory dermatoses.". J Clin Pathol 58 (12): 1233-41. doi:10.1136/jcp.2005.027151. PMID 16311340.
  74. ↑ 74.0 74.1 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 1269. ISBN 0-7216-0187-1.
  75. ↑ Arock, M.; Valent, P. (Aug 2010). "Pathogenesis, classification and treatment of mastocytosis: state of the art in 2010 and future perspectives.". Expert Rev Hematol 3 (4): 497-516. doi:10.1586/ehm.10.42. PMID 21083038.
  76. ↑ 76.0 76.1 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Aster, Jon (2009). Robbins and Cotran pathologic basis of disease (8th ed.). Elsevier Saunders. pp. 1185. ISBN 978-1416031215.
  77. ↑ Rudzki, Z.; Sotlar, K.; Kudela, A.; Starzak-Gwóźdź, J.; Horny, HP. (2011). "Systemic mastocytosis (SM) and associated malignant bone marrow histiocytosis - a hitherto undescribed form of SM-AHNMD.". Pol J Pathol 62 (2): 101-4. PMID 21866466.
  78. ↑ URL: http://www.humpath.com/palmar-fibromatosis. Accessed on: 6 January 2011.
  79. ↑ URL: http://surgpathcriteria.stanford.edu/softfib/plantar_fibromatosis/printable.html. Accessed on: 6 January 2011.
  80. ↑ 80.0 80.1 URL: http://surgpathcriteria.stanford.edu/softfib/palmar_fibromatosis/differentialdiagnosis.html. Accessed on: 9 November 2012.
  81. ↑ Wang L, Zhu H (2006). "Clonal analysis of palmar fibromatosis: a study whether palmar fibromatosis is a real tumor". J Transl Med 4: 21. doi:10.1186/1479-5876-4-21. PMC 1488873. PMID 16696857. http://www.biomedsearch.com/nih/Clonal-analysis-palmar-fibromatosis-study/16696857.html.
  82. ↑ Degreef, I.; De Smet, L.; Sciot, R.; Cassiman, JJ.; Tejpar, S. (Mar 2009). "Beta-catenin overexpression in Dupuytren's disease is unrelated to disease recurrence.". Clin Orthop Relat Res 467 (3): 838-45. doi:10.1007/s11999-008-0590-z. PMID 18958538.
  83. ↑ Katenkamp D, Kosmehl H, Langbein L (1988). "[Angiomyoma. A pathologo-anatomic analysis of 229 cases]" (in German). Zentralbl Allg Pathol 134 (4-5): 423–33. PMID 3201831.
  84. ↑ 84.0 84.1 Karen, JK.; Hale, EK.; Ma, L. (2005). "Angiokeratoma corporis diffusum (Fabry disease).". Dermatol Online J 11 (4): 8. PMID 16403380.
  85. ↑ Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 548. ISBN 978-0443066542.
  86. ↑ Shih, CC.; Yu, HS.; Tung, YC.; Tsai, KB.; Cheng, ST. (Jan 2001). "Inverted follicular keratosis.". Kaohsiung J Med Sci 17 (1): 50-4. PMID 11411260.
  87. ↑ 87.0 87.1 87.2 Busam, Klaus J. (2009). Dermatopathology: A Volume in the Foundations in Diagnostic Pathology Series (1st ed.). Saunders. pp. 387. ISBN 978-0443066542.
  88. ↑ URL: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC475744/. Accessed on: 11 May 2010.
  89. ↑ Gandhi, V.; Dogra, D.; Pandhi, RK.. "Cutaneous focal mucinosis.". Indian J Dermatol Venereol Leprol 62 (4): 260-1. PMID 20948074.
  90. ↑ Majeski, J.; Majeski, E. (Nov 1997). "Necrotizing fasciitis: improved survival with early recognition by tissue biopsy and aggressive surgical treatment.". South Med J 90 (11): 1065-8. PMID 9386043.
  91. ↑ Wong, CH.; Wang, YS. (Apr 2005). "The diagnosis of necrotizing fasciitis.". Curr Opin Infect Dis 18 (2): 101-6. PMID 15735411.
  92. ↑ Alikhan, A.; Burns, T.; Zargari, O. (2010). "Punctate porokeratotic keratoderma.". Dermatol Online J 16 (1): 13. PMID 20137755.
  93. ↑ 93.0 93.1 93.2 West, C.; Narahari, S.; Kwatra, S.; Feldman, S. (Nov 2012). "Autosomal dominant transmission of nevus sebaceous of Jadassohn.". Dermatol Online J 18 (11): 17. PMID 23217958.
  94. ↑ 94.0 94.1 Simi, CM.; Rajalakshmi, T.; Correa, M.. "Clinicopathologic analysis of 21 cases of nevus sebaceus: a retrospective study.". Indian J Dermatol Venereol Leprol 74 (6): 625-7. PMID 19171988.
  95. ↑ Kim, JH.; Park, HY.; Ahn, SK. (Oct 2011). "Nevus sebaceous accompanying secondary neoplasms and unique histopathologic findings.". Ann Dermatol 23 (Suppl 2): S231-4. doi:10.5021/ad.2011.23.S2.S231. PMID 22148058.
  96. ↑ Kaw, P.; Carlson, A.; Meyer, DR. (Jan 2005). "Nevus lipomatosus (pedunculated lipofibroma) of the eyelid.". Ophthal Plast Reconstr Surg 21 (1): 74-6. PMID 15677959.
  97. ↑ 97.0 97.1 97.2 97.3 Goucha, S.; Khaled, A.; Zéglaoui, F.; Rammeh, S.; Zermani, R.; Fazaa, B. (Dec 2011). "Nevus lipomatosus cutaneous superficialis: Report of eight cases.". Dermatol Ther (Heidelb) 1 (2): 25-30. doi:10.1007/s13555-011-0006-y. PMC 3437641. PMID 22984661. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437641/.
  98. ↑ URL: http://www.dermpedia.org/dermpedia-textbook/nevus-lipomatosus. Accessed on: 8 January 2013.
  99. ↑ Triki, S.; Mekni, A.; Haouet, S.; Mokni, M.; Kchir, N.; Ben Osman Dhahri, A.; Zitouna, M. (Dec 2006). "[Nevus lipomatosus cutaneous superficialis: a clinico-pathological study of 13 cases].". Tunis Med 84 (12): 800-2. PMID 17288284.
  100. ↑ Jones, EW.; Marks, R.; Pongsehirun, D. (Aug 1975). "Naevus superficialis lipomatosus. A clinicopathological report of twenty cases.". Br J Dermatol 93 (2): 121-33. PMID 1235780.
  101. ↑ Yap, FB. (May 2009). "Nevus lipomatosus superficialis.". Singapore Med J 50 (5): e161-2. PMID 19495497.
  102. ↑ Ghosh, SK.; Bandyopadhyay, D.; Jamadar, NS. (2010). "Nevus lipomatosus cutaneous superficialis: An unusual presentation.". Dermatol Online J 16 (7): 12. PMID 20673540.
  103. ↑ Eng, W.; Cohen, PR. (Nov 1998). "Nevus with fat: clinical characteristics of 100 nevi containing mature adipose cells.". J Am Acad Dermatol 39 (5 Pt 1): 704-11. PMID 9810886.
  104. ↑ URL: http://www.dermaamin.com/site/histopathology-of-the-skin/66-n/1971-nevus-lipomatosus-superficialis----.html. Accessed on: 7 March 2012.
  105. ↑ URL: http://www.humpath.com/spip.php?article8134. Accessed on: 17 December 2012.
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