Benign Skin Tumours

7.6 BENIGN SKIN TUMOURSSummary:

1. The Epidermis → Epithelial Tumours Seborrhoeic Keratosis, Digital Fibrokeratoma, Keratoacanthoma, Actinic Keratosis Others - Squamous papilloma, viral wart, , keratin horn, Bowens

2. The Dermis Hair follicles → Trichilemmal cyst, Trichofolliculoma, Tricholemmoma,

Tricho-epithelioma, Pilomatrixoma (Benign Calcifying Epithelioma of Malherbe)

Sebaceous Glands → Sebaceous Adenoma, Sebaceous Hyperplasia, Sebaceous Naevus of Jadassohn

Sweat Gland - Eccrine Gland → Syringoma, Acrospiroma (Eccrine poroma), Cylindroma

Neural Tissue → Neurofibroma

3. Cysts Epidermoid cysts Pilar Cysts Milia Xanthelasma

4. Pigmented Lesions

Naevus cell naevi Melanocytic naevi

1. The Epidermis - Epithelial Tumours

a. Seborrhoeic Keratosis (Seborrhoeic Wart, Senile Wart, Basal Cell Papilloma)

Greasy plaques on torso of elderly pt.Incidence

M=F, Over 50 White Stucco Keratosis – non pig SK on limbs Dermatosis papulosa nigra – multiple facial SK, dark skin, early onset

Aetiology Familial – autosomal dominant Inflammatory dermatosis Visceral malignancy manifestation Oestrogen administration

Pathology Accumulated immature keratinocytes b/n basal and keratinizing layers Acanthosis – thickening of epidermis Elongated dermal papillae Rarely malignant transformation (SCC)

Clinical Verrucous plaque Face hands and upper trunk May be pig Multiple lesions lined up with skin folds May bleed, get inflamed, itch May shed but reform

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Treatment Curettage or excision Cryotherapy Topical trichloroacetic acid (TCA – used for peels)

b. Digital Fibrokeratoma Papillary or keratotic outgrowth in finger near joint Adults M>F After trauma Hyperkeratosis and acanthosis (thick epithelium esp. stratum spinosum) Distinguish from accessory digit Treat by excision

c. Keratoacanthoma (Molluscum Sebaceum) Rapidly evolving tumour → resolves Keratinizing squamous cells originating in pilosebaceous follicles

Incidence White, M>F 3:1, 1/3 freq of SCC, Middle age+

Aetiology Sun, Coal, Tar, carcinogenic hydrocarbons (multiple), Injury and infection

inc SSG donors, Assoc with Ca larynx, internal ca and leukaemia, Assoc with deficient cell-mediated immunity.

Pathology Keratin-filled crypt, Rapidly dividing squamous cells from skin appendages,

Atypical mitosis and loss of polarityClinical

Globular tumour Keratin plug or horn Radial symmetry Resolution after 6 weeks takes 3 months, leave a depressed scar Face, dorsum hand Ferguson-Smith syndrome (single gene mutation on West Scotland) → AD

+ multiple self healing epitheliomas which look and behave as KA. Torre’s syndrome = multiple internal malignancies, KA’s and sebaceous

adenomas Distinguish from SCC

Treatment Excise to get good specimen Spontaneous resolution leaves unsightly scar 5 FU and radiotherapy shorten time to resolution

d. Actinic Keratosis Scaly crusted areas in sun exposed areas of elderly pts 20-25% develop into SCC Treatment with Efudix (5FU) or Solaraze (Diclofenac) gel.

e. OthersSquamous papilloma - Skin tag or acrochordons → exciseViral Warts - HPV → cryotherapy or curettageKeratin Horn - Hard protruding lump of cornified material, Likely to have an AK or SCC in the base Bowens - Red scaly lesion on the legs of elderly patients, Histology resembles SCC, limited to epidermis → in situ, can progress to SCC so worth removing

2. The Dermis

a. Hair Follicle Tumours


Trichilemmal cyst Sebaceous cyst of hairy skin, Wall like hair follicle Scalp, F>M, middle age, Familial (AD) Rupture causes cell proliferation and occasional malignant change Ruptured cell wall may fuse with surrounding skin (marsupialization) Treat by Excision

Trichofolliculoma Multiple malformed hair rots arising from an enlarged follicle canal Keratin-filed crater, mainly face White Hairs from a central punctum Histology like BCC But contain keratin-filled macrocysts

Tricholemmoma Hair follicle tumour – clinically like BCC Small warty papules Cowden’s syndrome → Multiple facial tricholemmomas, Keratoses on palms

and soles, Oral polyps, Breast Cancer in 50% of patients Plaques of squamous cells containing glycogen Face, middle aged →elderly men

Tricho-epithelioma Epithelial tumour differentiating towards hair follicle cells Rare, at puberty, Familial (AD) Path – like BCC, rounded masses of fusiform cells, Keratin filled lacunae Tumour islands may connect with hair follicles Malignant change to BCC Clinical – pinkish nodules, cheeks and eyelids and NL folds, (around mouth) often misdiagnosed as BCC, or MM if pigmented Treatment – Excision

Pilomatrixoma (Benign Calcifying Epithelioma of Malherbe) Hamartoma of dead calcified cells which resemble hair matrix Uncommon, <20yrs, F>M assoc with myotonia atrophica Path – Well circumscribed dermal tumour, cells mature out to inner layers Similar to hair matrix cells Mature cortex → root Central calcification and ghost cells, no basophilic granules Clinical – Dermal, s/c tumour, Head/neck/upper limb. Stony Hard lesion on the face of a child. Treat by excision

b. Tumours of Sebaceous glands Sebaceous Adenoma (Sebaceous Carcinoma) Sebaceous Hyperplasia Sebaceous Naevi (of Jadassohn)(Organoid Naevus)

Sebaceous Adenoma → smooth papules on scalp of elderly Benign tumour of incompletely differentiated sebaceous cells Rare, either sex, mainly elderly Path – multilobular tumour of upper dermis, small basophilic sebaceous

matrix cells and larger cells with fat globules Clinical– Ulcers/plaques/sessile/pedunculated. Yellowish, Face/scalp,

Sudden↑ growth Treat – Excision, Recur if incomplete, Radiosensitive

Sebaceous Hyperplasia Small yellowish lesions usually found in the face → can look clinically like

BCC


Severe seb hyperplasia of nose = rhinophyma

Sebaceous Naevi (of Jadassohn)(Organoid Naevus) Normally present at birth but usually enlarges and becomes raised in

puberty, due to hyperplasia of the sebaceous glands. Usually removed as they have a 20-30% chance of mailgnant

transformation usually into BCC or less commonly mixed appendigeal tumour

c. Sweat Gland Tumours 3 Benign Eccrine sweat gland tumours:

o Syringomao Acrospiromao Cylindroma

Adenoid Cystic Carcinoma Of The Scalp Sweat gland Carcinoma Apocrine glands → lipid secretions in membrane- bound vesicles (eg

breast) Eccrine → secretions by exostosis into ducts Holocrine → discharge whole cells → disintegrate to release secretion Sweat glands = eccrine (some apocrine) Sebaceous glands = holocrine secretion of sebum

Syringoma (Papillary Eccrine Adenoma) Benign tumour of eccrine sweat gland origin Uncommon, F>M, adolescence, multiple with Downs Path –Convoluted sweat ducts in upper dermis, +tail like (tadpole)

projections of cells Small yellow dermal papules ,<3mm, Cystic, release clear fluid on injury, Chest face neck, may look like tricho-epithelioma or xanthelasma Treat – Excision, Intralesional desiccation, Laser

Eccrine Acrospiroma (Eccrine poroma) Tumour from eccrine sweat duct epithelium. Epidermal, juxta or dermal Eccrine poroma commonest (juxta-epidermal) M=F, middle age, Usually acral (palms and soles) Path – Sweat gland duct proliferation, cells with glycogen and glycolic

enzymes Overlying hyperkeratosis. Malignant change (malignant eccrine poroma)

reported Hyperkeratotic plaque on sole or palm, may ulcerate Treatment – Excision

Dermal Cylindroma (Dermal Eccrine Cylindroma, Turban Tumour, Spiegler’s Tumour) Derived from coiled part of sweat gland (part secretory and part duct) Uncommon F>M 2:1, Often Familial AD, Early adult Path – columns of cells with hyaline between large and small (peripheral)

cell types Scalp and adjacent skin. Pinkish fleshy tumours, Hairless and multiple, May

be pain. Large or multiple = Turban tumour. Malignant change very rare. Distinguish from trichilemmal cyst (which occasionally - malignant change) Treat – excision

d. Tumours of neural tissue


Neurofibroma Skin coloured nodules composed of neural tissue and keratin Neurofibromatosis (von Recklinghausen’s disease) = Multiple cutaneous

NF, 6 or more café-au-lait patches >1.5 cm, axillary freckling, Lisch nodules on the iris (ocular neurofibromatosis)

Classified into 2 types :o Type 1 → most common with features aboveo Type 2 → assoc with CNS NF’s – very rareo 3rd Type – Schwannomatosis – very painful, very rareo Plexiform neurofibromas are large infiltrative lesions found in the

head or neck region. More diffuse, may cause neurological deficit, risk of malignancy transformation- pain, rapid growth, go hard, neuro compression, rapid met spread

Wound complications common following their excision. Chromosome 17q 2 or more of-

o Axillary Frecklingo More than 6 Cafe au laito Iris Lisch noduleso Thickening (glioma) of optic n.o Bony abnormality

1/3500 prevalence 1/2500 births

3. CystsEpidermal

Implantation dermoids After Trauma → trapping of segment of epidermis in dermis

Congenital dermoids Entrapment of epidermis during facial development. Angular dermoid → most common → Usually located in submuscular plane

towards outer corner of the eye Central dermoid Centrally anywhere between forehead and nasal tip May have deep intracranial extension → preop scan needed.

Epidermoid Cyst (Sebaceous Cyst) Young and middle aged. Inflammation and obstruction of pilosebaceous follicles Path -Epidermal lining, Birefringent keratin and break down products as

well as sebum secreted by sebaceous glands, Cholesterol clefts Clinical– Dermal spherical cyst, Tethered epidermis, Enlarge, Suppurate via

punctum Gardener’s syndrome → multiple cysts + osteomas of jaw + polyposis coli Treat – complete excision to avoid recurrent cysts.

Pilar cysts Similar to epidermoid cysts but occur on scalp

Milia Small intra-epidermal cysts usually on cheeks Treat by needle enucleation

Xanthelasma Accumulation of lipid within the skin Usually around eyes


Treat by excision → vertical rather than horizontal excision to avoid ectropion.

4. Benign Pigmented Lesions

Structure and function of melanocytes Melanocytes are derived from neural crest Spindle shaped clear cells which contain a dark nucleus + dendritic

processes. Melanin is synthesized within melanocytes from the aminoacid tyrosine via

the intermediate dihydroxyphenylalanine (DOPA). Melanin accumulates in vesicles within the melanocytes called

melanosomes. Melanosomes are distributed to the surrounding cells via long dendritic

processes. The cells surrounding the melanocyte often contain more melanin than the

melanocyte. The number of melanocytes does NOT vary bn races. The ↑ pigmentation is due to ↑ production Melanin production is stimulated by sunlight and the pituitary hormone

(MSH) melanocyte-stimulating hormone.Naevus Cells

Melanocyte leaves epidermis and enters dermis = Naevus cell They are round rather than spindle shaped. DO NOT have dendritic processes Tend to congregate in nests

Pigmented lesions – Summary

Malignant melanocytic lesion = malignant melanoma

Benign → melanocyte or naevus cello Naevus cell lesion = congenital or acquiredo Melanocytic lesions arise in = epidermis or dermis

Naevus Cell naevi Congenital → Giant hairy naevus (GHN) or Non GHN. Acquired → Junctional, Compound, Intradermal Special → Spitz, Dysplastic, Halo

Melanocytic Naevi Epidermal → Ephelis, Lentigo, Café-au-lait patch, Becker’s naevus,

Albright’s syndrome. Dermal → blue naevus, Mongolian blue spot, Naevus of Ota, Naevus of Ito


1. Naevus Cell Naevi

a. Congenital Naevus cell Naevi

Giant Hairy Naevus >20cm in adult or > 5% BSA Lifetime risk → 2-4% or up to 40% in some series M Melanomas in GHN 4-14% (5%) Risk highest in 1st 10yrs of life - worse

prognosis than other MM Leptomeningeal melanosis assoc with GHN = very poor prognosis Rarely can get tumours of neural or mesenchymal origin e.g.

rhabdomyosarcoma or liposarcoma Treatment → controversial Pigment more superficial in early neonatal period then goes deeper? →

excise, dermabrade, laser, curette may work BUT ↑↑ blood loss for neonate. Superficial excision can develop residual black areas later → leopard skin type appearance.

Debatable if superficial excision prevents malignant change. Can excise later during childhood → wide undermining and direct closure,

tissue expansion, skin grafting, integra resurfacing. Some advise just to watch and excise any changing areas. Little prospective data on incidence of malignant change or impact of Rx.

Non-giant Hairy Naevi Can be excised in early childhood, reconstruct by tissue expansion, local

flaps or grafts.

b. Acquired Naevus cell naevi Rare in infancy, appear in childhood and adolescence, less arrive in early

adulthood, stable numbers in middle age.

Junctional Naevi Flat Smooth and irregularly pigmented, usually in the young. Nests of naevus cells clustered around the epidermal/dermal junction.

Compound Naevi Round well-circumscribed slightly raised lesions Nests of naevus cells clustered at the epidermal/dermal junction extending

into dermis

Intradermal Naevi Dome shaped lesions which may be non-pigmented or hairy. Tend to occur

in adults and are composed of nests of naevus cells clustered within the dermis.

c. Special Naevus Cell Naevi

Spitz Naevus (juvenile melanoma) See 7.4 Melanoma

Dysplastic Naevi Irregular outline Patchy pigmentation >5mm Atypical naevus (atypical mole) syndrome = >100 dysplastic naevi in 1 pt

– associated with high risk of MM, but risk is also related to family HxHalo Naevus

Naevus surrounded with depigmented area of skin Relatively common in older children and teenagers


Tend to regress leaving a small scar Antimelanoma antibodies have been detected in some pts with halo naevi Treatment → expectant

2. Melanocytic Naevi

a. Epidermal melanocytic naevi

Ephelis → freckle, Normal number of melanocytes but ↑ production Disappear in the absence of sunlight

Lentigo ↑ number of melanocytes Persist without sunlight 3 types lentigo simplex → young and middle aged lentigo senilis → elderly solar lentigo → after sun exposure

Café-au-lait patch Pale brown patch >6 lesions > 1.5cm = neurofibromatosis.

Becker’s Naevus Dark patch on the shoulder, normally appears during adolescence and may

become hairy.

Albright’s syndrome (see 5.4 Cleft) Pigmented skin lesions, Fibrous dysplasia, Precocious puberty.

b. Dermal melanocytic naevi Melanocytes in the dermis

Blue naevus Round areas of blue/black colouration Arrested migration of melanocytes bound for the dermal/epidermal

junction Differential diagnosis - melanoma

Mongolian blue spot Bluish grey pigmentation over the sacrum Present in 90% of Mongolian infants?

Naevus of Ota Bluish pigment of the sclera and adjacent periorbital skin Caused by intradermal melanocytes, prevalent among Japanese.

Naevus of Ito Blue-grey discolouration around the shoulder Intradermal melanocytes Rare in Caucasians but common in Japanese.


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Benign Skin Tumours