Dermatology: Made Easy

DERMATOLOGY MADE EASY
Dermatology Made Easy 2e has been comprehensively updated but remains designed to
help GPs, medical students and dermatologists diagnose skin conditions with confidence: DERMATOLOGY
↳ diagnosis is simplified by providing a comprehensive set of tables which
offer differentials by symptom, morphology, or body site – including over
500 thumbnail photos
MADE EASY
↳ once you have narrowed down the diagnosis, cross-references guide you AMANDA OAKLEY
to more detailed descriptions, and another 700 photographs, covering:
● common infections
● inflammatory rashes
● non-inflammatory conditions
● skin lesions
2nd EDITION
Every section provides consistent information on the disorder:
● who gets it and what causes it?
● what are the clinical features and does it cause any complications?
● how do you diagnose it?
● how do you treat it and how long does it take to resolve?
The book concludes with a comprehensive section on further investigations and

treatment options.
Dermatology Made Easy is the ideal rapid clinical reference – guiding diagnosis,
advising on clinical features and offering the best treatment options.
Reviews of the first edition

“…takes an approach of grouping diseases by differential diagnoses first by symptom,
then by morphology, then by body site. Subsequent chapters revisit these conditions
surprisingly thoroughly while maintaining brevity. The book is easy to read and easy
to reference. It fulfills the need for a photo-intensive introductory text that leaves the
reader with relevant pearls for diagnosing and treating skin disease.”     
“I had to use it yesterday and was amazed at the logic that has gone into organising
the book. This book is truly a tour-de-force.”     
“It’s well written, the pics are great (including some of people of colour - which is 2
something that is often lacking in Dermatology teaching!) and the reference setup
with the ability to search via site, characteristics or context is invaluable.”     
OAKLEY
“One of the best quick reference derm books! Laid out well with great info crammed
into a manageable size for everyday use! Highly recommended!”     
www.scionpublishing.com
ISBN 978-1-914961-16-8
9 781914 961168
DME_2e_Cover.indd 1-3 07/09/2022 10:26

DERMATOLOGY
MADE EASY
Derm ME.indb 1 02-Sep-22 4:04:54 PM

DERMATOLOGY
MADE EASY
2 n d E D I T IO N
AMANDA OAKLEY
Dermatologist – Waikato, Te Whatu Ora Health New Zealand, Hamilton, New Zealand
Adjunct Associate Professor, Department of Medicine, Faculty of Medical
and Health Sciences, The University of Auckland, New Zealand

Second edition © Scion Publishing Ltd, 2022
ISBN 9781914961168
First edition published in 2017 (ISBN 9781907904820)
All rights reserved. No part of this book may be reproduced or transmitted, in any form or
by any means, without permission.
A CIP catalogue record for this book is available from the British Library.
Scion Publishing Limited

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Important Note from the Publisher

The information contained within this book was obtained by Scion Publishing
Ltd from sources believed by us to be reliable. However, while every effort has
been made to ensure its accuracy, no responsibility for loss or injury whatsoever
occasioned to any person acting or refraining from action as a result of information
contained herein can be accepted by the authors or publishers.
Readers are reminded that medicine is a constantly evolving science and while the
authors and publishers have ensured that all dosages, applications and practices
are based on current indications, there may be specific practices which differ
between communities. You should always follow the guidelines laid down by the
manufacturers of specific products and the relevant authorities in the country in
which you are practising.
Although every effort has been made to ensure that all owners of copyright material
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Last digit is the print number: 10 9 8 7 6 5 4 3 2 1

Contents
About the author.............................................................vii 2.2.3 Dermatophyte skin
Preface to the second edition...................................viii infections: tinea...............................102
Acknowledgements.........................................................ix 2.2.4 Fungal nail infections....................105
Abbreviations...................................................................... x 2.2.5 Malassezia..........................................107
Terminology........................................................................xi 2.2.6 Paronychia..........................................109
2.3 Viruses.................................................................111
Chapter 1 – Differential diagnosis............... 1 2.3.1 General viral infections.................111
2.3.2 Anogenital warts..............................113
1.1 Introduction..........................................................2
2.3.3 Exanthems.........................................116
1.2 By symptoms........................................................3 2.3.4 Herpes simplex.................................120
1.2.1 Fever and a rash – acute 2.3.5 Herpes zoster....................................123
presentation of an unwell 2.3.6 Infantile papular
patient......................................................3 acrodermatitis..................................126
1.2.2 Itchy skin................................................10 2.3.7 Molluscum contagiosum..............127
1.2.3 Painful skin conditions.....................16 2.3.8 Pityriasis rosea..................................129
1.3 By morphology..................................................19 2.3.9 Viral warts...........................................131
1.3.1 Introduction..........................................19 2.4 Arthropods........................................................134
1.3.2 Blistering diseases.............................19 2.4.1 Arthropod bites and stings.........134
1.3.3 Macules and patches.........................24 2.4.2 Head lice.............................................137
1.3.4 Papules and plaques.........................33 2.4.3 Scabies.................................................139
1.3.5 Purpura...................................................40
1.3.6 Pustules..................................................41
1.3.7 Scaly rashes..........................................43 Chapter 3 – Inflammatory rashes........... 143
1.4 By body site.........................................................48 3.1 Acne......................................................................144
1.4.1 Arms.........................................................48 3.2 Bullous pemphigoid.....................................147
1.4.2 Ear............................................................50 3.3 Chilblains...........................................................150
1.4.3 Eyelid.......................................................52
3.4 Cutaneous lupus erythematosus..........152
1.4.4 Face..........................................................52
1.4.5 Flexures..................................................59 3.5 Drug eruptions................................................158
1.4.6 Genitalia.................................................61 3.5.1 General................................................158
1.4.7 Hands and feet....................................64 3.5.2 Drug hypersensitivity
1.4.8 Legs..........................................................67 syndrome............................................162
1.4.9 Lips...........................................................72 3.5.3 Morbilliform drug eruption.........165
1.4.10 Nails.........................................................75 3.5.4 Stevens–Johnson syndrome/
1.4.11 Oral mucosa..........................................79 toxic epidermal necrolysis...........167
1.4.12 Scalp........................................................82 3.6 Eczema/dermatitis.......................................173
1.4.13 Trunk........................................................87 3.6.1 General................................................173
3.6.2 Asteatotic eczema...........................175
Chapter 2 – Infections.......................................91 3.6.3 Atopic eczema...................................177
3.6.4 Contact eczema................................182
2.1 Bacteria..................................................................92 3.6.5 Discoid eczema.................................185
2.1.1 Common bacterial skin 3.6.6 Disseminated secondary
infections...............................................92 eczema.................................................186
2.1.2 Erysipelas and cellulitis...................93 3.6.7 Hand dermatitis...............................188
2.1.3 Folliculitis and furunculosis – 3.6.8 Lichen simplex..................................192
bacterial.................................................95 3.6.9 Nappy rash.........................................193
2.1.4 Impetigo.................................................96 3.6.10 Pityriasis alba....................................195
2.2 Fungi.....................................................................100 3.6.11 Pompholyx.........................................197
2.2.1 Fungal infections.............................100 3.6.12 Seborrhoeic eczema.......................198
2.2.2 Candida infections..........................100 3.6.13 Venous eczema.................................200
v

vi Contents
3.7 Erythema multiforme.................................203 5.4 Basal cell carcinoma.....................................320

3.8 Erythroderma..................................................206 5.5 Cysts.....................................................................325
3.9 Granuloma annulare....................................211 5.6 Dermatofibroma............................................330
3.10 Hidradenitis suppurativa..........................214 5.7 Intraepidermal squamous cell
3.11 Lichen planus...................................................217 carcinoma..........................................................332
3.12 Lichen sclerosus.............................................222 5.8 Lentigo................................................................335
3.13 Mouth ulcers.....................................................226 5.9 Melanoma..........................................................338
3.14 Panniculitis.......................................................231 5.10 Moles....................................................................344
3.15 Periorificial dermatitis...............................234 5.11 Seborrhoeic keratoses................................351
3.16 Photosensitivity.............................................236 5.12 Squamous cell carcinoma –
cutaneous..........................................................355
3.17 Polymorphic light eruption.....................241
5.13 Vascular lesions..............................................358
3.18 Pruritus vulvae/vulval itch......................244
3.19 Psoriasis.............................................................249
3.19.1 Psoriasis – general..........................249 Chapter 6 – Investigations and
3.19.2 Nail psoriasis.....................................253 treatments................................. 363
3.20 Rosacea...............................................................257 6.1 Dermatological investigations:
general................................................................364
3.21 Transient acantholytic dermatosis......260
6.2 Skin biopsy........................................................366
3.22 Urticaria.............................................................262
6.3 Interpreting dermatopathology
3.23 Vasculitis: cutaneous...................................267 reports.................................................................368
6.4 Treatments: introduction..........................376
Chapter 4 – Non-inflammatory 6.5 Topical formulations....................................377
conditions................................... 273
6.6 Emollients and moisturisers...................379
4.1 Alopecia areata...............................................274
6.7 Topical steroids..............................................380
4.2 Dry skin...............................................................278
6.8 Other topical drugs......................................383
4.3 Excessive hair..................................................281
6.9 Tetracyclines....................................................386
4.4 Hair loss..............................................................284
6.10 Systemic steroids..........................................388
4.5 Hyperhidrosis..................................................292
6.11 Other oral drugs............................................392
4.6 Keratosis pilaris.............................................295
6.12 Monitoring methotrexate,
4.7 Melasma..............................................................297
azathioprine, ciclosporin
4.8 Pigmentation disorders.............................300 and biologics....................................................394
4.9 Post-inflammatory pigmentation........303 6.13 Isotretinoin.......................................................397
4.10 Vitiligo.................................................................305 6.14 Physical treatments.....................................402
6.15 Role of surgery in skin disease..............407
Chapter 5 – Skin lesions............................... 309
5.1 Actinic cheilitis................................................310 Index..................................................................................409
5.2 Actinic keratosis.............................................312
5.3 Ageing skin.......................................................316

About the author
Dr Amanda Oakley is Adjunct Associate Professor for the Department of Medicine at the University of
Auckland. She lives in Hamilton, New Zealand, where she is a Dermatologist for the Waikato district.
She diagnoses for MoleMap New Zealand, writes a column for the general practice magazine, New
Zealand Doctor Rata Aotearoa, and is frequently called upon to speak at conferences and deliver
workshops on dermatological matters. Professor Oakley is actively engaged in clinical research
with many publications in peer-reviewed medical journals in print and online. Her main areas
of professional interest are vulval diseases, dermoscopy and the early diagnosis of melanoma,
teledermatology, artificial intelligence in dermatology, and education of consumers and health
professionals.
Professor Oakley is President of the International Society of Teledermatology (2020–2023) and
has been President of Waikato Postgraduate Medicine, the New Zealand Dermatological Society
Incorporated and the Australian and New Zealand Vulvovaginal Society.
Professor Oakley has received many awards for her efforts, including Companion of the New Zealand
Order of Merit, Honorary Fellowship of the Royal New Zealand College of General Practitioners, and
Honorary Memberships of the American Academy of Dermatology, the American Dermatological
Association, the Skin Cancer College of Australasia and MelNet New Zealand.
Her greatest joy is the success of DermNet New Zealand (www.dermnetnz.org).
vii

Preface to the second edition
Dermatology Made Easy, the title of this book, is an oxymoron. Dermatological diagnosis is frequently
challenging; the specialty has more than 3000 named acute and chronic diseases. The barrier function
of the skin and its interaction with the external environment and the cutaneous immune system
contribute to the complexity. Every patient presents with a unique combination of signs and is anxious
or distressed by their symptoms. Treatment may be complicated, or not required, depending on
diagnosis and individual patient factors. Specialist dermatologists are scarce and are often difficult or
expensive to access.
First learn the terminology of dermatology. Then use this book to help diagnose a skin disease or
condition. Take a history and examine your patient. Document the location or distribution of a lesion
or eruption, and the arrangement and morphology of individual lesions.
The first chapter, Differential diagnosis, helps you make a diagnosis according to symptoms,
morphology, and the affected body site(s). Don’t forget to consider patient age and sex, the onset and
behaviour of the presenting complaint, past medical history and medications.
You can review information about common infections (Chapter 2), inflammatory rashes (Chapter 3)
non-inflammatory conditions (Chapter 4), and skin lesions (Chapter 5), and formulate a plan for
further investigations and treatment (Chapter 6).
In this book I have tried to cover most common drugs used in the UK, USA and Australasia; however,
you should be aware that although the drugs detailed will all be appropriate for treatment, not all
will be available on prescription in all territories. Please refer to your local prescribing guidelines and
datasheets. In dermatology, be aware that many treatments are used off-licence.
Still stuck? Go online to www.dermnetnz.org for more information.
Enjoy!
Amanda Oakley
If you notice errors or omissions, don’t forget to tell us by emailing info@scionpublishing.com
viii

Acknowledgements
Teˉnaˉ koutou katoa (“greetings”).
I’d like to thank the Trustees of the DermNet New Zealand Trust (a New Zealand registered charity)
for permission to update Dermatology Made Easy for the second edition.
The pages in this book are adapted from the material on www.dermnetnz.org. They are derived from
and link to online pages that were originally written by dermatologists, dermatology registrars,
other medical practitioners, students and professional science writers – many of whom volunteered
their time and effort to improve the largest online resource All about the skin. These authors live in
New Zealand, Australia, the United Kingdom, the United States of America and elsewhere.
I would like to thank Anne Maloney (GP in Berkshire, UK, with a special interest in dermatology) and
Karen McKoy (dermatologist based at the Lahey Clinic in Burlington, USA) for their advice on the
different treatment options used in the UK and USA.
The list of DermNet New Zealand authors is long, and rather than inadvertently leave anyone out,
I offer sincere thanks to you all.
The book includes more than 1000 clinical images. I would like to express my gratitude to the
dermatologists, pathologists and their patients that willingly consented to having their skin conditions
used for education and publication purposes – in print and online. I am particularly grateful to
The Medical Photography team at Waikato Hospital, and for the generous support of Te Whatu Ora
Health New Zealand (Waikato), who granted permission for the inclusion of many of their images in
the book. Thank you.
Ngaˉ mihi nui (“thanks very much”).
ix

Abbreviations
AC alternating current INR international normalised ratio
ACE angiotensin-converting enzyme IPL intense pulsed light
ACTH adrenocorticotrophic hormone IUD intrauterine device
AGEP acute generalised exanthematous IV intravenous
pustulosis LDH lactic acid dehydrogenase
AIDS acquired immune deficiency LE lupus erythematosus
syndrome LFT liver function test
ALT alanine aminotransferase LH luteinising hormone
ANA antinuclear antibody LS lichen sclerosus
ANCA anti-neutrophil cytoplasmic MASI Melasma Area and Severity Index
antibodies MDM multidisciplinary meeting
BCC basal cell carcinoma MMP matrix metalloproteinase
BMI body mass index MMR measles, mumps, rubella
BP blood pressure MRI magnetic resonance imaging
BSA body surface area MSH melanocyte-stimulating hormone
CBC complete blood count NSAID non-steroidal anti-inflammatory
CCCA central centrifugal cicatricial drug
alopecia PCR polymerase chain reaction
CNS central nervous system PDT photodynamic therapy
CPC clinicopathological correlation PET positron emission tomography
CRP C-reactive protein PLE/PMLE polymorphic light eruption
CT computerised tomography PUVA photochemotherapy
DC direct current RAST radioallergosorbent test
DEET diethyltoluamide RNA ribonucleic acid
DEXA dual-energy X-ray absorptiometry SC subcutaneous
DIHS drug-induced hypersensitivity SCAR severe cutaneous adverse reaction
syndrome SCC squamous cell carcinoma
DNA deoxyribonucleic acid SDRIFE symmetrical drug-related
DRESS drug reaction with eosinophilia intertriginous and flexural
and systemic symptoms exanthema
EBV Epstein–Barr virus SIL squamous intraepithelial lesion
ECG electrocardiograph SJS Stevens–Johnson syndrome
ED exfoliative dermatitis SK seborrhoeic keratosis
ENA extractable nuclear antigen SLE systemic lupus erythematosus
FBC full blood count SPF sun protection factor
FDA Food and Drug Administration SSSS staphylococcal scalded skin
FSH follicle-stimulating hormone syndrome
GA granuloma annulare Staph. Staphylococcus
H&E haematoxylin and eosin Strep. Streptococcus
HFM hand, foot and mouth TB tuberculosis
HHV human herpes virus TEN toxic epidermal necrolysis
HIV human immunodeficiency virus TIA transient ischaemic attack
HLA human leucocyte antigen TNF tumour necrosis factor
HPA hypothalamic–pituitary–adrenal UV ultraviolet
HPV human papillomavirus UVR ultraviolet radiation
HSV herpes simplex virus VIN vulval intraepithelial neoplasia
IEC intraepidermal carcinoma VZV varicella-zoster virus

Chapter 5
Skin lesions
5.1 Actinic cheilitis.......................................... 310 5.8 Lentigo.......................................................... 335
5.2 Actinic keratosis....................................... 312 5.9 Melanoma.................................................... 338
5.3 Ageing skin................................................. 316 5.10 Moles.............................................................. 344
5.4 Basal cell carcinoma............................... 320 5.11 Seborrhoeic keratoses.......................... 351
5.5 Cysts............................................................... 325 5.12 Squamous cell carcinoma –
cutaneous.................................................... 355
5.6 Dermatofibroma...................................... 330
5.13 Vascular lesions........................................ 358
5.7 Intraepidermal squamous cell
carcinoma.................................................... 332
309

310 Chapter 5 Skin lesions
5.1 Actinic cheilitis

What is actinic cheilitis? What are the complications of actinic
Actinic cheilitis presents as diffuse or patchy cheilitis?
dryness and variable thickening of the vermilion Actinic cheilitis is a pre-malignant condition. It
of the lower lip (see Figs 5.1–5.3). The common predisposes to:
form of actinic cheilitis is due to chronic sun a intraepidermal carcinoma (Bowen disease or
exposure. It is also called actinic cheilosis, solar squamous cell carcinoma in situ).
cheilitis, and sometimes, actinic cheilitis with a invasive squamous cell carcinoma.
histological atypia.
Actinic cheilitis also describes lip Cancer of the lip is more common in smokers
involvement in actinic prurigo, a rare form of than in non-smokers. Other factors include
photosensitive dermatitis (see photosensitivity, human papillomavirus, alcohol abuse and
Section 3.16). immune suppression.
Squamous cell carcinoma should be
Who gets actinic cheilitis? suspected if the lip is focally tender, or a
Actinic cheilitis mainly affects adults with fair persistent ulcer or enlarging nodule develops.
skin who live in tropical or subtropical areas,
especially outdoor workers. They often recall
How is actinic cheilitis diagnosed?
having sunburned lips in earlier years. They may Actinic cheilitis is usually diagnosed clinically.
also have actinic keratoses on other sun-exposed A skin biopsy may be taken if skin cancer or an
sites of the scalp, ears, face and hands. inflammatory cause of cheilitis is suspected.
Actinic cheilitis is three times more common The pathological features of actinic cheilitis
in males than in females. are variable thickening or atrophy of the lip,
partial thickness epidermal dysplasia, solar
What causes actinic cheilitis? elastosis and inflammation in the dermis.
Actinic cheilitis results from chronic exposure
of the lower lip to solar ultraviolet radiation.
What is the treatment for actinic cheilitis?
It is more vulnerable than surrounding skin Smoking cessation and lifelong, year-round,
because mucosal epithelium is thinner and less daily sun protection are essential.
pigmented than the epidermis. a Limit sun exposure.
a Wear a hat with a wide brim.
What are the clinical features of actinic a Apply lip balm containing sunscreen
cheilitis? frequently.
Actinic cheilitis most commonly affects the Men can consider growing a moustache.
lower lip (90%), and causes: Topical therapies for actinic cheilitis are
a dry lips. unapproved and should be prescribed with
a thinned, fragile, skin.
a scaly patches (see Fig. 5.1).
Less common features of actinic cheilitis
include:
a swelling.
a redness.
a fissuring, focal ulceration and crusting
(see Figs 5.2 and 5.3).
a loss of demarcation between the vermilion
border of the lip and adjacent skin.
a white thickened patches (called
leukokeratosis or leukoplakia).
a discoloured skin with pale or yellow areas.
a prominent folds and lip lines.
a difficulty applying lipstick, which tends to
“bleed” into the surrounding lines. Figure 5.1. Actinic cheilitis: white scaly plaque.

5.1 Actinic cheilitis 311
Figure 5.2. Actinic cheilitis: eroded and dry. Ulceration suggests squamous cell carcinoma.
Physical treatments for actinic cheilitis include:

a cryotherapy.
a electrocautery.
a vermilionectomy (surgical removal of the lip).
a laser ablation, e.g. with Er:YAG laser.
How can actinic cheilitis be prevented?
Actinic cheilitis can be prevented by protecting
the lips from sun exposure.
What is the outlook for actinic cheilitis?

Actinic cheilitis can improve with effective
sun protection and treatment. Continued sun
exposure and lack of treatment increase the risk
Figure 5.3. Actinic cheilitis: crusted erosions. of squamous cell carcinoma, which is potentially
life-threatening.
caution, as their destructive properties may
induce erosions. They include:
a topical retinoids.
a fluorouracil cream.
a imiquimod cream.
a photodynamic therapy.

5.2 Actinic keratosis

What is an actinic keratosis? a fair skin with a history of sunburn.
An actinic keratosis is a scaly spot found on sun-
a history of long hours spent outdoors for work
or recreation.
damaged skin (see Figs 5.4–5.8). It is also known
as solar keratosis. It is considered precancerous
a immune dysfunction.
or an early form of cutaneous squamous cell What causes actinic keratoses?
carcinoma.
Actinic keratoses are a reflection of abnormal
Actinic keratoses should be distinguished
skin cell development due to DNA damage by
from other scaly spots, such as seborrhoeic
short wavelength UVB. They are more likely
keratosis (“stuck on” appearance), porokeratosis
to appear if the immune function is poor, due
(scaly rim) and keratosis pilaris (scaly follicular
to ageing, recent sun exposure, predisposing
prominence of upper arms and thighs).
disease or certain drugs.
Who gets actinic keratoses?
What are the clinical features of actinic
Actinic keratoses often affect people who have
keratosis?
lived in the tropics or subtropics, and have
predisposing factors such as: Actinic keratosis may be solitary but there are
a other signs of photoageing skin. often multiple keratoses. The appearance varies.
Figure 5.4. Actinic keratosis: indurated scaly papule on Figure 5.6. Actinic keratosis: diffuse scale crusted
dorsum hand. papules and plaques on temple.
Figure 5.5. Actinic keratosis: diffuse scaly plaques on Figure 5.7. Actinic keratosis: scaly papules and plaques
dorsum hand. on bald scalp.

5.2 Actinic keratosis 313
a A flat or thickened papule or plaque. evolve to SCC, but the risk of SCC occurring
a White or yellow; scaly, warty or horny at some stage in a patient with more than ten
surface. actinic keratoses is thought to be about 10–15%.
a Skin-coloured, red or pigmented. A tender, thickened, ulcerated or enlarging
a Tender or asymptomatic. actinic keratosis is suspicious of SCC.
Cutaneous horn may arise from an underlying
Actinic keratoses are very common on sites
actinic keratosis or SCC.
repeatedly exposed to the sun, especially the
Because they are sun damaged, people with
backs of the hands and the face, most often
actinic keratoses are also at risk of developing
affecting the ears, nose, cheeks, upper lip,
actinic cheilitis, basal cell carcinoma (which
vermilion of the lower lip, temples, forehead
is more common than SCC), melanoma and
and balding scalp. In severely chronically sun-
rare forms of skin cancer such as Merkel cell
damaged individuals, they may also be found
carcinoma.
on the upper trunk, upper and lower limbs, and
dorsum of feet. How is actinic keratosis diagnosed?
Complications of actinic keratoses Actinic keratosis is usually easy to diagnose
clinically, by location on habitually sun-exposed
The main concern is that actinic keratoses
sites, and adherent scale. Dermoscopic features
predispose to squamous cell carcinoma (SCC).
of actinic keratoses are described as “strawberry
It is rare for a solitary actinic keratosis to
pattern” on facial skin (Fig. 5.9) and as white
rosettes on the backs of the hands (Fig. 5.10).
Occasionally, biopsy is necessary, for example
to exclude SCC, or if treatment fails.
What is the treatment for actinic

keratoses?
Actinic keratoses are usually removed because
they are unsightly or uncomfortable, or because
of the risk that skin cancer may develop in them.
Treatment of an actinic keratosis requires
removal of the defective skin cells. Epidermis
regenerates from surrounding or follicular
keratinocytes that have escaped sun damage.
Tender, thickened, ulcerated or enlarging
actinic keratoses should be treated aggressively.
Figure 5.8. Actinic keratosis: tender dry patches on Asymptomatic flat keratoses may not require
dorsum hand.
Figure 5.9. “Strawberry pattern” on dermoscopy of facial Figure 5.10. White rosettes on dermoscopy of actinic
actinic keratosis. keratosis on back of hand.

active treatment but should be kept under concurrently applying calcipotriol ointment
observation. (off label).
a Imiquimod cream is an immune response
Physical treatments modifier. 5% imiquimod cream is applied
Physical treatments are used to destroy individual 2 or 3 times weekly for 4–16 weeks; 3.75%
keratoses that are symptomatic or have a thick imiquimod cream is applied daily for
hard surface scale. The lesions may recur in time, 2 weeks. Treatment can be repeated after a
in which case they may be retreated by the same break of 2–4 weeks (see Fig. 5.12).
or a different method. a Photodynamic therapy (PDT) involves
Cryotherapy using liquid nitrogen: applying a photosensitiser (a porphyrin
Cryospray is required to ensure adequate depth chemical) to the affected area prior to
and duration of freeze. This varies according to exposing it to daylight or an artificial source
lesion location, width and thickness. Healing of visible light (Figs 5.13 and 5.14).
varies from 5–10 days on face, 3–4 weeks on the
hands, and 6 weeks or longer on the legs. A light
freeze for a superficial actinic keratosis usually
leaves no mark, but longer freeze times result in
hypopigmentation or scar.
Shave, curettage and electrocautery: Shave,
curettage (scraping with a sharp instrument)
and electrocautery (burning) may be necessary
to remove a cutaneous horn or hypertrophic
actinic keratosis. Healing of the wound takes
several weeks or longer, depending on body site.
A specimen is sent for pathological examination.
Excision: Excision ensures the actinic keratosis
has been completely removed, which should be
confirmed by pathology. The surgical wound is
sutured. The sutures are removed after a few days,
the time depending on the size and location of the
lesion. The procedure leaves a permanent scar.
Field treatments
Creams are used to treat areas of sun damage
and flat actinic keratoses, sometimes after
physical treatments have been carried out. Figure 5.11. Day 12 of treatment with 5-fluorouracil
Field treatments are most effective on facial cream.
skin. Pretreatment with keratolytics (such as
urea cream, salicylic acid ointment or topical
retinoid) and thorough skin cleansing improve
response rates. Results are variable and the
course of treatment may need repeating from
time to time. With the exception of diclofenac
gel, field treatments result in local inflammatory
reactions such as redness, blistering and
discomfort for a varying length of time.
a Diclofenac is more often used as an anti-
inflammatory drug. Applied as a gel twice
daily for 3 months, it is well tolerated but less
effective than the other options listed here.
a Fluorouracil cream is a cytotoxic agent. This
is applied once or twice daily for 2–8 weeks
(see Fig. 5.11). Its efficacy is improved and Figure 5.12. Treatment with imiquimod (after 10
duration of therapy reduced by half by applications).

5.2 Actinic keratosis 315
(a)
Figure 5.13. The day of treatment with photodynamic

therapy. (b)
Prevention of actinic keratoses

Actinic keratoses are prevented by strict sun
protection. If already present, keratoses may
improve with very high sun protection factor
(50+) broad-spectrum sunscreen applied at least
daily to affected areas, year-round.
The number and severity of actinic keratoses
can also be reduced by taking low-dose acitretin,
or possibly by nicotinamide (vitamin B3) 500 mg
twice daily.
What is the outlook for actinic keratoses? Figure 5.14. (a) The day following treatment with
photodynamic therapy; (b) Two months after treatment.
Actinic keratoses may recur months or years
after treatment. The same treatment can be
repeated or another method used. Patients
who have been treated for actinic keratoses
are at risk of developing new keratoses. They
are also at increased risk of other skin cancers,
especially intraepidermal squamous cell
carcinoma, invasive cutaneous squamous cell
carcinoma, basal cell carcinoma and melanoma.
Derm ME_CH05_S1-7.indd 315 02-Sep-22 4:50:52 PM

5.3 Ageing skin

What is ageing skin? a Volume of subcutaneous fat diminishes,
especially on face, hands and feet—whereas
Ageing skin describes the changes in the
it increases on thighs, waist and abdomen.
appearance and characteristics of the skin that
occur as people get older. Ageing changes are
a Ageing is immune suppressing, leading to
increased risk of skin cancer.
particularly pronounced on the skin of the face
and hands (see Figs 5.15–5.21).
Menopause in females
Who gets prematurely aged skin? In women, loss of oestrogen levels at menopause
contribute to premature ageing, as compared
Skin appears prematurely aged in people who
with similarly aged men.
are chronically exposed to sunlight, a process
known as sun damage or photoageing.
Premature ageing of the skin also affects tobacco Photoageing
smokers and those chronically exposed to other Photoageing is due to damage caused by solar
environmental pollutants. radiation. Cell damage occurs because of the
Photoageing is pronounced in people with the formation of reactive oxygen species.
following characteristics. a High energy, short wavelength UVB
a They live in the tropics or subtropics. damages DNA and other components
a They live at high altitude. of the epidermis.
a They work outdoors or spend long periods a Longer wavelength UVA is 100 times more
outdoors for recreation. prevalent than UVB at the earth’s surface, but
a They are exposed to artificial sources of is of lower energy so is less damaging to DNA.
ultraviolet radiation (UV), such as indoor UVA penetrates more deeply into the dermis,
tanning. so also has effects on elastic tissue, collagen,
a They have fair skin (skin phototype I and II), blood vessels and immune cells.
often with blond hair and blue eyes. a Infrared radiation penetrates to the deeper
a They have genetic predisposition to dermis and subcutaneous tissue, where it
premature ageing (most marked in progeria). may also contribute to sun damage.
What causes the skin to age? Smoking

Smoking exposes the skin to several damaging
Intrinsic ageing factors.
Intrinsic ageing of the skin is inevitable, and a Nicotine narrows blood vessels, reducing
genetically predetermined. It occurs because blood flow, and thus impairs oxygen and
of accumulation of reactive oxygen species, important nutrients reaching the cells.
biological ageing of cells, and reduced cellular a Many of the other numerous chemicals
supply of nutrients and oxygen. in tobacco smoke increase dermal matrix
a The rate of epidermal cell proliferation metalloproteinases, degrading collagen and
reduces, affecting structure and function of elastin.
the skin. The skin thins and flattens, with less a The heat from burning cigarettes, and facial
resistance to shearing forces and injury. muscle movements associated with smoking,
a Water content in the stratum corneum contribute to wrinkles.
reduces, with less transepidermal water loss. a Nitrosamines and tar are carcinogens.
a Hair thins and greys.
a The numbers of melanocytes reduce. Immune dysfunction
a Sebum production reduces. Immune dysfunction also affects skin ageing.
a The dermis has reduced vascularity. Examples include:
a There are fewer dermal mast cells and a immune deficiency diseases.
fibroblasts, and reduced glycosaminoglycans, a immune suppressing treatments.
hyaluronic acid and ground substance. a chronic psychological stress.
a There is reduced collagen and elastin
turnover, and increased glycation.

5.3 Ageing skin 317
What are the clinical features of ageing of intraepidermal carcinoma, squamous cell
skin? carcinoma, lentiginous forms of melanoma
and rare skin cancers such as Merkel cell
Intrinsic ageing carcinoma.
a Ageing skin is thin, and less elastic, tearing
easily.
a It recovers more slowly from mechanical
depression than younger skin.
a Women have thinner skin than men.
a Skin is dry, especially after frequent washing
with soap and water.
a Dry skin increases the risk of asteatotic
dermatitis.
a The barrier function of the skin is less effective.
a Pigmentation is uneven due to melanocyte
activation and guttate hypopigmentation.
Genetically predisposed ageing skin may be also
prone to:
a telangiectases and cherry angiomas.
a seborrhoeic keratosis. Figure 5.15. Photoaged skin is easily torn or grazed.
Photoageing
Photoageing results in:
a fine lines and wrinkles.
a discoloration.
a textural changes.
a thin skin that easily blisters, tears and grazes
(Fig. 5.15).
a solar elastosis/heliosis (Fig. 5.16).
a solar lentigines (Fig. 5.17).
a solar comedones (Fig. 5.18) and, rarely,
colloid milia (Fig. 5.19).
a senile/solar purpura (Fig. 5.20).
a scarring.
a actinic keratosis (tender dry spots), see Fig. 5.8.
a skin cancer (destructive growths), see Fig. 5.21. Figure 5.16. Solar elastosis.
Smoking
Compared to non-smokers of the same age, long-
term smokers have:
a more facial lines.
a baggy eyelids and jawline.
a yellowish sallow complexion.
a open and closed comedones and cysts
(Favre–Racouchot syndrome).
a greater risk of skin cancer.
Complications of ageing skin
Ageing skin is prone to keratinocytic skin
cancer and melanoma. The most common form
of skin cancer is basal cell carcinoma. However,
excessively photoaged skin increases the risk Figure 5.17. Solar lentigines.

How are signs of ageing skin diagnosed?

The features of ageing skin are diagnosed
clinically. Lesions suspicious of skin cancer may
be growing lumps or sores that fail to heal. They
often undergo diagnostic biopsy before or as part
of treatment.
Classification of photoageing
Glogau classified the degree of sun damage by its
clinical signs.
a Type I, mild, “no wrinkles”.
A Mild pigment changes
A Minimal wrinkles
A No keratoses
a Type II, moderate, “wrinkles in motion”.
A Appearance of lines only when face moves
A Early lentigines
A Skin pores more prominent
A Early changes in skin texture
a Type III, advanced, “wrinkles at rest”.
Figure 5.18. Solar comedones. A Prominent pigmentation
A Noticeable solar lentigines
A Prominent small blood vessels
A Wrinkles present when face at rest
a Type IV, severe, “only wrinkles.”
A Wrinkles at rest or moving
A Yellow–grey skin colour
A Prior skin cancers
A Actinic keratoses
How are the signs of ageing treated?
Cancer and precancerous lesions
a Actinic keratoses and intraepidermal
carcinomas are most often removed by
cryotherapy or treated topically.
Figure 5.19. Colloid milia.
Figure 5.20. Senile/solar purpura. Figure 5.21. Skin cancer (squamous cell carcinoma).

5.3 Ageing skin 319
a Basal cell carcinomas (BCC) are most How can the signs of ageing skin
often removed by minor surgery, but some be prevented?
superficial BCCs can be treated topically
or by cryotherapy. Intrinsic ageing is inevitable. In perimenopausal
a Squamous cell carcinomas (SCC) and women, systemic hormone replacement may
melanoma are nearly always removed delay skin thinning; the skin is less dry, with
surgically. fewer wrinkles, and wound healing is faster than
prior to treatment. Replacement is less effective
at improving skin ageing in the postmenopausal
Dry and discoloured skin
decades. The effects of topical oestrogens,
Moisturisers will help improve dry and flaky
phyto-oestrogens and progestins are under
skin.
investigation.
Alpha-hydroxy acids, vitamin C, lipoic acid,
Protection from solar UV is essential at all
soy isoflavones or retinoid creams applied
ages.
regularly long term reduce dryness. They may
also reduce the number of fine wrinkles and
a Be aware of daily UV index levels.
even out pigmentation. Many other products
a Avoid outdoor activities during the middle
of the day and when UV index levels are high.
are under investigation but their benefits are
unclear.
a Wear sun protective clothing: broad-
brimmed hat, long sleeves and trousers/
skirts.
Facial rejuvenation
Procedures that aim to rejuvenate photoaged
a Apply very high sun-protection factor, broad-
spectrum sunscreens to exposed skin.
skin include:
a fillers (hyaluronic acid, Do not smoke and where possible, avoid
polytetrafluoroethylene implants, fat grafts) exposure to pollutants. Take plenty of exercise –
to disguise facial expression lines. active people appear younger. Eat fruit and
a botulinum toxin injections to reduce vegetables daily to provide natural antioxidants.
frowning and lessen deep furrows. Many oral supplements with antioxidant
a vascular laser and sclerotherapy to remove and anti-inflammatory properties have
facial veins and angiomas. been advocated to retard skin ageing and to
a resurfacing procedures (dermabrasion, improve skin health. They include carotenoids,
peels, and laser resurfacing). polyphenols, chlorophyll, aloe vera, vitamins B,
a cosmetic surgery to remove redundant C and E, red ginseng, squalene, and omega-3
sagging skin, e.g. blepharoplasty for baggy fatty acids. Their role is unclear.
eyelids, meloplasty (face lift) to tighten jowls.

5.4 Basal cell carcinoma

What is basal cell carcinoma? BCC is very rarely a threat to life. A small
number of BCCs grow rapidly, invade deeply, or
Basal cell carcinoma (BCC) is a common, locally
metastasise to local lymph nodes.
invasive, keratinocytic, or non-melanoma,
skin cancer. It is also known as rodent ulcer Types of basal cell carcinoma
and basalioma. Multiple tumours are often
There are several distinct clinical types of BCC,
diagnosed on a single occasion and over time.
and over 20 histological growth patterns of BCC.
Who gets basal cell carcinoma?
Nodular BCC
Risk factors for BCC include:
a age and gender – BCCs are particularly a Most common type of facial BCC
(see Fig. 5.24).
prevalent in older males; however, they also
affect females and younger adults.
a Shiny or pearly nodule with a smooth
surface.
a previous BCC or other form of skin cancer
(squamous cell carcinoma, melanoma).
a May have central depression or ulceration,
so its edges appear rolled.
a sun damage (photoageing, actinic keratoses).
a repeated prior episodes of sunburn. a Blood vessels cross its surface.
a fair skin, blue eyes and blond or red hair; a Cystic variant is soft, with jelly-like contents.
however, BCC can also affect darker skin types.
a Micronodular, microcystic and infiltrative
types are potentially aggressive subtypes.
a previous cutaneous injury, thermal burn,
disease (e.g. cutaneous lupus, sebaceous
naevus).
a inherited syndromes – BCC is a particular
problem for families with basal cell naevus
syndrome (also called Gorlin syndrome, see
Fig. 5.22), Bazex–Dupré–Christol syndrome,
Rombo syndrome, Oley syndrome and
xeroderma pigmentosum.
a other risk factors include ionising radiation,
exposure to arsenic, and immune
suppression.
What causes basal cell carcinoma?

The cause of BCC is multifactorial.
a Most often, there are DNA mutations in the
patched (PTCH) tumour suppressor gene, Figure 5.22. Multiple BCCs arising in patient with basal cell
part of hedgehog signalling pathway. naevus syndrome (Gorlin syndrome).
a These may be triggered by exposure to
ultraviolet radiation.
a Various inherited gene defects predispose
to BCC.
What are the clinical features of basal cell

carcinoma?
BCC is a locally invasive skin tumour. The main
characteristics are:
a slowly growing plaque or nodule.
a skin-coloured, pink or pigmented.
a varies in size from a few millimetres to
several centimetres in diameter.
a spontaneous bleeding or ulceration (Fig. 5.23).
Figure 5.23. Ulcerated BCC.

5.4 Basal cell carcinoma 321
Superficial BCC a Potentially more aggressive than other forms

a Most common type in younger adults of BCC.
(see Fig. 5.25).
a Most common type on upper trunk and Fibroepithelial tumour of Pinkus
shoulders. a Warty plaque.
a Slightly scaly, irregular plaque. a Usually on trunk.
a Thin, translucent rolled border, best seen on
stretching lesion. Pigmented BCC
a Multiple microerosions. a Any histological subtype.
a More common in darker skin (see Fig. 5.27).
Morphoeic BCC
a Also known as morphoeiform or sclerosing BCC. Complications of basal cell carcinoma
a Usually found in mid-facial sites (Fig. 5.26).
Recurrent BCC
a Waxy, scar-like plaque with indistinct borders.
Recurrence of BCC after initial treatment is not
a Wide and deep subclinical extension.
uncommon. Characteristics of recurrent BCC
a May infiltrate cutaneous nerves (perineural
often include:
spread).
a incomplete excision or narrow margins at
primary excision.
Basisquamous BCC
a Mixed or metatypical basal cell carcinoma
a morphoeic, micronodular, and infiltrative
subtypes.
(BCC) and squamous cell carcinoma (SCC).
a Infiltrative growth pattern.
a location on head and neck.
Figure 5.24. Nodular BCC. Figure 5.26. Morphoeic BCC.
Figure 5.25. Superficial BCC. Figure 5.27. Pigmented BCC.

Advanced BCC Mohs micrographically controlled excision

Advanced BCCs are large, often neglected Mohs micrographically controlled surgery
tumours (see Fig. 5.28). involves examining carefully marked excised
a They may be several centimetres tissue under the microscope, layer by layer, to
in diameter. ensure complete excision (see Fig. 5.30).
a They may be deeply infiltrating into tissues a Very high cure rates achieved by trained
below the skin. Mohs surgeons.
a They are difficult or impossible to treat a Used in high-risk areas of the face around
surgically. eyes, lips and nose.
a Suitable for ill-defined, morphoeic,
Metastatic BCC infiltrative and recurrent subtypes.
a Very rare. a Large defects are repaired by flap or graft.
a Primary tumour is often large, neglected or
recurrent, located on head and neck, with Superficial skin surgery
aggressive subtype. Superficial skin surgery comprises shave,
a May have had multiple prior treatments. curettage, and electrocautery. It is a rapid
a May arise in site exposed to ionising technique using local anaesthesia and does
radiation. not require sutures.
a Can be fatal. a Suitable for small, well-defined nodular or
superficial BCCs.
How is basal cell carcinoma diagnosed? a Lesions are usually located on trunk or limbs.
BCC is diagnosed clinically by the presence
of a slowly enlarging skin lesion with typical
appearance. The diagnosis and histological
subtype is usually confirmed pathologically by
a diagnostic biopsy or following excision.
Some typical superficial BCCs on trunk and
limbs are clinically diagnosed and have non-
surgical treatment without histology.
What is the treatment for primary

basal cell carcinoma?
The treatment for a BCC depends on its type,
size and location, the number to be treated,
patient factors, and the preference or expertise
of the doctor. Most BCCs are treated surgically.
Long-term follow-up is recommended to check Figure 5.28. Advanced BCC.
for new lesions and recurrence; the latter may be
unnecessary if histology has reported wide clear
margins.
Excision biopsy
Excision means the lesion is cut out and the skin
stitched up (Fig. 5.29).
a Most appropriate treatment for nodular,
infiltrative and morphoeic BCCs.
a Should include 3–5 mm margin of normal
skin around the tumour.
a Large lesions may require flap or skin graft to
repair the defect.
a Pathologist will report deep and lateral margins.
a Further surgery is recommended for lesions
that are incompletely excised. Figure 5.29. Excision biopsy.

5.4 Basal cell carcinoma 323
a Wound is left open to heal by secondary photosensitising chemical, and exposed to light
intention. several hours later (Fig. 5.32).
a Moist wound dressings lead to healing within a Topical photosensitisers include
a few weeks. aminolevulinic acid lotion and methyl
a Eventual scar quality variable. aminolevulinate cream.
a Suitable for low-risk small, superficial BCCs.
Cryotherapy a Best avoided if tumour in site of high
Cryotherapy is the treatment of a superficial skin recurrence.
lesion by freezing it, usually with liquid nitrogen. a Results in inflammatory reaction, maximal
a Suitable for small superficial BCCs on 3–4 days after procedure.
covered areas of trunk and limbs. a Treatment repeated 7 days after initial
a Best avoided for BCCs on head and neck, and treatment.
distal to knees. a Excellent cosmetic results.
a Double freeze-thaw technique.
a Results in a blister that crusts over and heals Imiquimod cream
within several weeks (see Fig. 5.31). Imiquimod is an immune response modifier.
a Leaves permanent white mark (see Fig. 5.22). a 5% imiquimod cream is best used for
superficial BCCs less than 2 cm diameter
Photodynamic therapy (see Fig. 5.33).
Photodynamic therapy (PDT) refers to a a Applied three to five times each week, for
technique in which BCC is treated with a 6–16 weeks.
a Results in a variable inflammatory reaction,
maximal at three weeks.
a Minimal scarring is usual.
Fluorouracil cream
Fluorouracil cream is a topical cytotoxic agent.
a Used to treat small superficial basal cell
carcinomas.
a Requires prolonged course, e.g. twice daily
for 6–12 weeks.
a Causes inflammatory reaction.
a Has high recurrence rates.
Radiotherapy
Radiotherapy or X-ray treatment can be used to
treat primary BCCs or as adjunctive treatment if
Figure 5.30. Mohs micrographically controlled excision.
margins are incomplete.
Figure 5.31. Ice-ball formation during cryotherapy. Figure 5.32. Reaction 24 hours after photodynamic
therapy.

Targeted therapy refers to the hedgehog

signalling pathway inhibitors, vismodegib and
sonedegib. These drugs have some important
risks and side-effects.
How can basal cell carcinoma

be prevented?
The most important way to prevent BCC is to
avoid sunburn. This is especially important
in childhood and early life. Fair-skinned
individuals and those with a personal or family
history of BCC should protect their skin from sun
exposure daily, year-round and lifelong.
a Stay indoors or in the shade in the middle of
Figure 5.33. Effect of imiquimod cream on BCC after the day.
3 weeks. a Wear covering clothing.
a Apply broad-spectrum sunscreens
a Mainly used if surgery is not suitable. generously to exposed skin if outdoors.
a Best avoided in young patients and in genetic a Avoid indoor tanning (sun beds and solaria).
conditions predisposing to skin cancer.
a Best cosmetic results achieved using multiple Oral nicotinamide (vitamin B3) in a dose of
fractions. 500 mg twice daily may reduce by 20% the
a Typically, patient attends once weekly for number and severity of BCCs in people at
several weeks. high risk.
a Causes inflammatory reaction followed
What is the outlook for basal cell
by scar.
a Risk of radiodermatitis, late recurrence, carcinoma?
and new tumours. Most BCCs are cured by treatment. Cure is most
likely if treatment is undertaken when the lesion
What is the treatment for advanced or is small.
metastatic basal cell carcinoma? About 50% of people with BCC develop a
Locally advanced primary, recurrent or second one within 3 years of the first. They are
metastatic BCC requires multidisciplinary also at increased risk of other skin cancers,
consultation. Often a combination of treatments especially melanoma. Regular self-skin
is used. examinations and long-term annual skin checks
a Surgery. by an experienced health professional are
a Radiotherapy. recommended.
a Targeted therapy.

5.5 Cysts 325
5.5 Cysts
What is a cyst? with pachyonychia congenita. More often,
steatocysts are sporadic, when these
A cyst is a benign, round, dome-shaped
mutations are not present.
encapsulated lesion that contains fluid or semi-
fluid material. It may be firm or fluctuant and
a The origin of the eruptive vellus hair cyst is
follicular infundibulum. It may be inherited
often distends the overlying skin. There are
as an autosomal dominant disorder due to
several types of cyst.
mutations in the keratin gene.
What is a pseudocyst? a A dermoid cyst is a hamartoma.
Cysts that are not surrounded by a capsule are
a The origin of a ganglion cyst is degeneration
of the mucoid connective tissue of a joint (see
better known as pseudocysts.
Fig. 5.35).
Who gets cysts? a A hidrocystoma is derived from an eccrine or
apocrine duct.
Cysts are very common, affecting at least 20% of
adults. They may be present at birth or appear
a A milium is a pseudocyst due to failure to
release keratin from an adnexal structure
later in life. They arise in all races. Most types of
(see Fig. 5.36).
cyst are more common in males than in females.
A The origin of primary milium is
What causes cysts? infundibulum of a vellus hair follicle at
the level of the sebaceous gland; a tiny
The cause of many cysts is unknown.
version of an epidermoid cyst.
a Epidermoid cysts are due to proliferation
of epidermal cells within the dermis and
originate from the follicular infundibulum.
Multiple epidermoid cysts may indicate
Gardner syndrome.
a The origin of a trichilemmal cyst is hair
root sheath (see Fig. 5.34). Inheritance is
autosomal dominant (the affected gene
is within short arm of chromosome 3) or
sporadic.
a The origin of steatocystoma is the
sebaceous duct within the hair follicle.
Steatocystoma multiplex is sometimes an
autosomal dominantly inherited disorder
due to mutations localised to the keratin
17 (K17) gene, when it may be associated
Figure 5.35. Ganglion cyst.
Figure 5.34. Trichilemmal cyst. Figure 5.36. Milia.

A The origin of secondary milium is a Trichilemmal cyst

retention cyst within a vellus hair follicle, a 90% of trichilemmal cysts (see Fig. 5.34)
sebaceous duct, sweat duct or epidermis. occur on scalp; otherwise face, neck, trunk,
A Occlusion of pilosebaceous units (hair and extremities.
follicles) or eccrine sweat ducts leads to a Most trichilemmal cysts arise in middle age.
a build-up of secretions. This can present a In 70% of cases, trichilemmal cysts are multiple.
as milia. a Adherent, round or oval, firm nodules.
a An epidermal inclusion cyst is a response a There is no punctum.
to an injury. Skin is tucked in to form a sac a The keratinous content is firm, white and
that is lined by normal epidermal cells easily enucleated.
that continue to multiply, mature and form a A trichilemmal cyst is also called pilar cyst.
keratin.
a Occlusion of the orifice of a mucous gland Steatocystoma
can lead to a fluid-filled cyst in a mucous a A solitary steatocystoma is known as
membrane (lip, vulva, vagina). steatocystoma simplex.
a Pseudocysts in acne are formed by occlusion a More often, multiple cysts occur on chest,
of the follicle by keratin and sebum. upper arms, axillae and neck (steatocystoma
multiplex, see Fig. 5.39).
What are the clinical features of cysts? a The cysts arise in the late teens and twenties
due to the effect of androgens, and persist
Epidermoid cyst
lifelong.
a Epidermoid cysts occur on face, neck, trunk
or anywhere where there is little hair
(see Fig. 5.37).
a Most epidermoid cysts arise in adult life.
a Cysts are more than twice as common in men
than in women.
a They present as one or more flesh-coloured to
yellowish, adherent, firm, round nodules of
variable size.
a A central pore or punctum may be present.
a Keratinous contents are soft, cheese-like and
malodorous.
a Scrotal and labial (see Fig. 5.38) cysts are
frequently multiple and may calcify.
a Epidermoid cyst is also called follicular
infundibular cyst, epidermal cyst and keratin
cyst. Sebaceous cyst is a misnomer.
Figure 5.38. Labial cysts.
Figure 5.37. Epidermoid cyst. Figure 5.39. Steatocystoma multiplex.

5.5 Cysts 327
a They are freely moveable, smooth flesh to A They often present as a longitudinal
yellow colour papules 3–30 mm in diameter. depression in the nail due to compression
a There is no central punctum. on the proximal matrix.
a Content of cyst is predominantly sebum.
Labial mucous cyst/mucocoele
Eruptive vellus hair cyst a A cyst in the lip may be due to occlusion of
a Eruptive vellus hair cysts are present in the salivary duct.
childhood if familial, and later if sporadic. a It is a soft to firm, 5–15 mm diameter, semi-
a Multiple 2–3 mm papules develop over the translucent nodule (Fig. 5.40).
sternum.
a The cysts contain vellus hairs. Hidrocystoma
a A hidrocystoma is a translucent jelly-like cyst
Dermoid cyst arising on an eyelid (Fig. 5.41).
a A cutaneous dermoid cyst may include a It is also known as cystadenoma, Moll
skin, skin structures and sometimes teeth, gland cyst, and sudoriferous cyst.
cartilage and bone.
a Most dermoid cysts are found on face, Milium/milia
neck, scalp; often around eyelid, forehead a They are 1–2 mm superficial (see Fig. 3.36)
and brow. white dome-shaped papules that contain
a It is a thin-walled tumour that ranges from keratin.
soft to hard in consistency. a Primary milia arise in neonates (50%),
a The cyst is formed at birth but the patient may adolescents and adults; they are rarely
not present until an adult. familial and sometimes eruptive.
a Primary milia occur on eyelids, cheeks,
Ganglion cyst nose, mucosa (Epstein pearls) and
a A ganglion cyst most often involves the palate (Bohn nodules) in babies; and
scapholunate joint of the dorsal wrist. eyelids, cheeks and nose of older children
a They arise in young to middle-aged adults. and adults.
a They are three times more common in a Transverse primary milia are sometimes
women than in men. noted across nasal groove or around areola.
a The cyst is a unilocular or multilocular a Secondary milia arise at the site of
firm swelling 2–4 cm in diameter that epidermal repair after blistering or injury,
transilluminates. e.g. epidermolysis bullosa, bullous
a Cyst contents are mainly hyaluranic acid, pemphigoid (see Fig. 5.42), porphyria cutanea
a golden-coloured goo. tarda, thermal burn, dermabrasion.
a Mucous/myxoid cysts are small lesions a Secondary milia are reported as an adverse
found in older adults on the distal phalanx. effect of topical steroids, fluorouracil cream,
A They arise from the distal interphalangeal vemurafenib and dovitinib.
joint, associated with osteoarthritis.
Figure 5.40. Labial mucous cyst/mucocoele. Figure 5.41. Hidrocystoma left medial canthus.

Figure 5.42. Milia arising after blisters have resolved in Figure 5.44. Pseudocyst of auricle.
bullous pemphigoid.
Pseudocyst of auricle
a Pseudocyst of auricle (external ear) follows
trauma (see Fig. 5.44).
Complications of cysts
Rupture of a cyst
a The contents of the cyst may penetrate the
capsular wall and irritate surrounding skin.
a The area of tender, firm inflammation spreads
beyond the encapsulated cyst (see Fig. 5.45).
a Sterile pus may be discharged.
Secondary infection
Figure 5.43. Milia en plaque.
a A ruptured cyst may infrequently become
secondarily infected by Staph. aureus, forming
a furuncle (boil), see Fig. 5.46.
a In milia en plaque, multiple milia arise on an
erythematous plaque on face, chin or ears,
Pressure effect
see Fig. 5.43.
a A dermoid cyst can cause pressure on
underlying bony tissue.
Vulval mucous cyst
a A vulval mucous cyst is due to occlusion of
a A ganglion cyst can cause joint instability,
weakness, limitation of motion and may
Bartholin or Skene duct.
compress a nerve.
a It presents as a soft swelling in the
a A digital mucous cyst may place pressure on
introitus of vagina: a posterior swelling is a
the proximal matrix and cause malformation
Bartholin cyst and a periurethral swelling is
of the nail.
a Skene cyst.
Malignancy
Comedo and acne pseudocyst
a The open comedo (whitehead) and closed
a The vast majority of cysts are benign.
comedo (blackhead) are small, superficial
a Nodulocystic basal cell carcinoma is a
common skin cancer that may initially be
uninflamed papules typical of acne vulgaris.
mistaken for a cyst, but steady enlargement,
a Solar comedones arise in sun-damaged skin
destruction of the epidermis with ulceration
and are associated with smoking.
and bleeding occur eventually.
a Large uninflamed pseudocysts accompany
a Malignant proliferative trichilemmal cyst is
inflammatory nodules in nodulocystic acne
extremely rare.
and hidradenitis suppurativa.

5.5 Cysts 329
Figure 5.45. Rupture of a cyst. Figure 5.46. Secondary infection of a cyst.
How are cysts diagnosed? a The lining of the wall of a ganglion cyst or
Cysts are usually diagnosed clinically as mucous cyst is collagen and fibrocytes.
they have typical characteristics. When a a Hidrocystoma has a thin lining wall of
cyst is surgically removed, it should undergo eosinophilic bilaminar cells.
histological examination. The type of lining of What is the treatment for cysts?
the wall of a cyst helps the pathologist classify it.
a Epidermoid cysts are lined with stratified Asymptomatic epidermoid cysts do not need to
squamous epithelium that contains a be treated. In most cases, attempt to remove only
granular layer. Laminated keratin contents the contents of a cyst is followed by recurrence.
are noted inside the cyst. An inflammatory If desired, cysts may be fully excised. Recurrence
response may be present in cysts that have even then is not uncommon, and re-excision
ruptured. may be surgically challenging.
a Trichilemmal cysts have a palisaded Inflamed cysts are sometimes treated with:
peripheral layer without granular layer. a incision and drainage.
Contents are eosinophilic hair keratin. a intralesional injection with triamcinolone.
Older cysts may exhibit calcification. The a oral antibiotics.
proliferating variety is considered a tumour. a delayed excision.
a Steatocystoma has a folded cyst wall with How can cysts be prevented?
prominent sebaceous gland lobules.
Unknown.
a Dermoid cyst contains fully mature elements
of the skin including fat, hairs, sebaceous What is the outlook for cysts?
glands, eccrine glands, and in 20%, apocrine
Cysts generally persist unless surgically
glands.
removed.

5.6 Dermatofibroma
What is a dermatofibroma? a Colour may be pink to light brown in
white skin and dark brown to black in dark
A dermatofibroma is a common benign fibrous
skin; some appear paler in the centre.
nodule that most often arises on the skin of the
lower legs.
a They do not usually cause symptoms, but
they are sometimes painful or itchy.
A dermatofibroma is also called a cutaneous
fibrous histiocytoma. Complications of dermatofibroma
Who gets dermatofibroma? Because they are often raised lesions, they may
be traumatised, for example by a razor.
Dermatofibromas occur at all ages and in people
Occasionally dozens of dermatofibromas
of every ethnicity. They are more common in
may erupt within a few months, in the setting
women than in men.
of immunosuppression (for example due
What causes dermatofibroma? to autoimmune disease, cancer or certain
medications).
It is not clear if dermatofibroma is a reactive
Dermatofibroma does not give rise to cancer.
process or if it is a neoplasm. The lesions are
However, occasionally, it may be mistaken
made up of a proliferation of fibroblasts.
They are sometimes attributed to an insect
bite or rose thorn injury, but not consistently.
They may be more numerous in patients with
altered immunity.
What are the clinical features

of dermatofibroma?
Dermatofibromas most often occur on the legs
and arms, but may also arise on trunk or any site
of the body.
a People may have one or up to 15 lesions.
a Size varies from 0.5 to 1.5 cm diameter; most
lesions are 7–10 mm diameter.
a They are firm nodules tethered to the skin
surface but mobile over subcutaneous tissue
(Fig. 5.47).
a The skin dimples on pinching the lesion Figure 5.48. A dimple on lateral compression confirms a
(Fig. 5.48). lesion to be a dermatofibroma.
Figure 5.47. Pigmented dermatofibroma. Figure 5.49. Dermoscopy of dermatofibroma often

reveals a central white zone.

5.6 Dermatofibroma 331
for dermatofibrosarcoma or desmoplastic What is the treatment for

melanoma. dermatofibroma?
How is dermatofibroma diagnosed? A dermatofibroma is harmless and seldom
Dermatofibroma is usually easy to diagnose causes any symptoms. Usually only reassurance
clinically, supported by dermoscopy. The most is needed.
common dermoscopic pattern is a central white If it is a nuisance or causing concern, the
area surrounded by faint pigment network lesion can be removed surgically.
(Fig. 5.49). Cryotherapy, shave excision and laser
Diagnostic excision or partial biopsy is treatments are rarely completely successful.
undertaken if there is an atypical feature such as How can dermatofibroma be prevented?
recent enlargement, ulceration, or asymmetrical
structures and colours on dermoscopy. The Unknown.
histology shows whirling fascicles of spindle cell What is the outlook for dermatofibroma?
proliferation with excessive collage deposition in
Unless surgically excised, a dermatofibroma
the dermis.
usually persists unchanged for years.
There are several pathological variants
of dermatofibroma. In case of doubt,
a Partial removal can lead to recurrence.
immunohistochemical staining is used to
a An enlarging or changing lesion should be
reassessed to consider another diagnosis.
confirm the diagnosis.

5.7 Intraepidermal squamous cell carcinoma

What is intraepidermal squamous cell centimetres in diameter (see Figs 5.50–5.53).
They are most often red but may also be
carcinoma?
pigmented.
Intraepidermal squamous cell carcinoma (SCC) Although intraepidermal SCC may arise
is a common superficial form of skin cancer. It on any area of skin, it is most often diagnosed
is also known as Bowen disease, intraepidermal on sun-exposed sites of the ears, face, hands
carcinoma (IEC) and carcinoma in situ of the skin. (Fig. 5.50) and lower legs (Fig. 5.52). When
Intraepidermal SCC is derived from there are multiple plaques, distribution is not
squamous cells, the flat epidermal cells that symmetrical (unlike psoriasis).
make keratin –the horny protein that makes up Rarely, intraepidermal SCC may start to
skin, hair and nails. “Intraepidermal” and “in grow under a nail, when it results in a red streak
situ” mean the malignant cells are confined to (erythronychia) that later may destroy the nail
cell of origin, i.e. the epidermis. plate (Fig. 5.53).
Who gets intraepidermal carcinoma? Complications of intraepidermal
Risk factors for intraepidermal SCC include: squamous cell carcinoma
a age – intraepidermal SCC is increasingly Invasive cutaneous SCC arises in
prevalent with age.
about 5% of intraepidermal SCC lesions.
a gender – it affects males and females, with See Section 5.12.
lesions on the lower legs being more common
in females.
a sun exposure – intraepidermal SCC is most
often found in sun-damaged individuals.
a arsenic ingestion – intraepidermal SCC is
common in populations exposed to arsenic. (a)
a ionising radiation – intraepidermal SCC
was common on unprotected hands of
radiologists early in the 20th century.
a human papillomavirus (HPV) infection – this
is implicated in intraepidermal SCC on the
fingers and fingernails.
a immune suppression due to disease
(e.g. chronic lymphocytic leukaemia) or
medicines (e.g. azathioprine, ciclosporin).
Up to 50% of patients with intraepidermal SCC
have other keratinocytic skin cancers, mainly
basal cell carcinoma.
(b)
What causes intraepidermal SCC?
Ultraviolet radiation (UV) is the main cause of
intraepidermal SCC. It damages the keratinocyte
nucleic acids (DNA), resulting in a mutant clone
of the gene p53. This sets off uncontrolled growth
of the skin cells.
UV also suppresses the immune response,
preventing recovery from damage.
What are the clinical features of

intraepidermal SCC?
Intraepidermal SCC presents as one or more
irregular scaly plaques of up to several Figure 5.50. Intraepidermal SCC on (a) finger and (b)
dorsum hand.

5.7 Intraepidermal squamous cell carcinoma 333
How is intraepidermal squamous cell in elderly patients. Keratolytic emollients,

carcinoma diagnosed? e.g. containing urea or salicylic acid, may be
sufficient to improve symptoms.
Intraepidermal SCC is often recognised
clinically because of an irregular scaly plaque
Superficial skin surgery
(Fig. 5.54a). Dermoscopy is supportive if it
Superficial skin surgery refers to shave, curettage
reveals crops of rounded or coiled blood vessels
and electrosurgery, and is a good choice for
(Fig. 5.54b).
solitary or few hyperkeratotic lesions. The lesion
Diagnosis may be confirmed by biopsy;
is sliced off or scraped out, then the base is
histology reveals full thickness dysplasia of the
cauterised. Dressings are applied to the open
epidermis.
wound to encourage moist wound healing over
What is the treatment for intraepidermal the next few weeks.
squamous cell carcinoma?
Cryotherapy
As intraepidermal SCC is confined to the surface Cryotherapy means removing a lesion by
of the skin, there are various ways to remove it. freezing it, usually with liquid nitrogen.
Recurrence rates are high, whatever method is Moderately aggressive cryotherapy is
used, particularly in immunosuppressed patients. suitable for multiple, small, flat patches of
intraepidermal SCC. It leaves a permanent white
Observation mark at the site of treatment.
As the risk of invasive SCC is low, it may not be
necessary to remove all lesions, particularly Fluorouracil cream
Fluorouracil cream contains a cytotoxic agent
and can be applied to multiple lesions. The
cream is applied twice daily for 4 weeks, and
repeated if necessary. It causes an inflammatory
reaction that may ulcerate. Results appear to be
better and quicker when calcipotriol ointment
is applied concurrently with fluorouracil cream
(off-licence).
Imiquimod cream
Imiquimod cream is an immune response
modifier used off-licence to treat intraepidermal
SCC. It is applied 3–5 times weekly for 4–16 weeks
and causes an inflammatory reaction.
Figure 5.51. Intraepidermal SCC in axilla.
Figure 5.52. Multiple intraepidermal SCCs on lower legs. Figure 5.53. Intraepidermal SCC involving distal phalanx
and nail unit.

Other
(a) Other treatments occasionally used in the
treatment of intraepidermal SCC include:
a combination treatments.
a diclofenac gel.
a topical retinoid (tazarotene, tretinoin).
a chemical peel.
a radiotherapy.
a electron beam therapy.
a carbon dioxide laser ablation.
a Erbium:YAG laser ablation.
a oral retinoid (acitretin, isotretinoin).
How can intraepidermal SCC be prevented?
(b)
Very careful sun protection at any time of life
can reduce the number of intraepidermal SCCs.
This is particularly important for ageing, sun-
damaged, white skin; and in patients who are
immunosuppressed.
a Stay indoors or in the shade in the middle of
the day.
a Wear covering clothing.
a Apply high protection SPF 50+, broad-
spectrum sunscreens generously to exposed
skin, if outdoors.
a Avoid indoor tanning (sun beds and solaria).
Figure 5.54. (a) Clinical and (b) dermoscopic images of
intraepidermal SCC. What is the outlook for intraepidermal
SCC?
Photodynamic therapy Intraepidermal SCC may recur months or years
Photodynamic therapy (PDT) refers to treatment after treatment. The same treatment can be
with a photosensitiser (a porphyrin chemical) repeated or another method used.
that is applied to the affected area prior to Patients who have been treated for
exposing it to a strong source of visible light. intraepidermal SCC are at risk of developing new
The treated area develops an inflammatory lesions of intraepidermal SCC. They are also at
reaction and then heals over a couple of weeks increased risk of other skin cancers, especially
or so. The best studied, methyl levulinate cream squamous cell carcinoma, basal cell carcinoma
PDT used off-licence, provides high cure rates and melanoma.
for intraepidermal SCC on the face or lower
legs, with excellent cosmetic results. The main
disadvantage is the pain experienced by many
patients during treatment.

5.8 Lentigo 335
5.8 Lentigo
What is a lentigo? like, where they appear on the body, causative
factors, and whether they are associated to other
A lentigo is a pigmented flat or slightly raised
diseases or conditions.
lesion with a clearly defined edge. Unlike an
Lentigines may be solitary or, more often,
ephilis (freckle), it does not fade in the winter
multiple. Most lentigines are smaller than 5 mm
months. There are several kinds of lentigo.
in diameter.
The name lentigo originally referred to its
appearance resembling a small lentil. The plural
of lentigo is lentigines, although lentigos is also
Lentigo simplex
in common use.
a A precursor to junctional naevus.
a Arises during childhood and early adult life.
Who gets lentigo? a Found on trunk and limbs.
Lentigo can affect males and females of all ages a Small brown round or oval macule or thin
plaque (Fig. 5.55).
and races. Solar lentigo is especially prevalent in
fair-skinned adults. Lentigines associated with a Jagged or smooth edge.
syndromes are present at birth or arise during a May have a dry surface.
childhood. a May disappear in time.
What causes lentigo? Solar lentigo

Common forms of lentigo are due to exposure to a A precursor to seborrhoeic keratosis.
ultraviolet radiation: a Found on chronically sun-exposed sites such
a sun damage including sunburn. as hands, face (Fig. 5.56), lower legs.
a indoor tanning. a May also follow sunburn to shoulders.
a phototherapy, especially photochemotherapy
(PUVA).
Ionising radiation, e.g. radiation therapy, can
also cause lentigo. (a)
Several familial syndromes associated with
widespread lentigo originate from mutations in
Ras-MAP kinase, mTOR signalling and PTEN
pathways.
What are the clinical features

of lentigo?
Lentigines have been classified into several
different types depending on what they look
(b)
Figure 5.55. Lentigo simplex. Figure 5.56. (a) Early seborrhoeic keratosis arising within
facial solar lentigo. (b) Dermoscopy of solar lentigo.

(a)
Figure 5.58. Melanotic macule on lower lip.

(b)
Tanning bed lentigo

a Similar to ink spot lentigo but follows indoor
tanning.
a Location anywhere exposed to tanning bed.
Radiation lentigo
a Occurs in site of irradiation (accidental or
therapeutic).
a Associated with epidermal atrophy,
subcutaneous fibrosis, keratosis,
telangiectasia.
Figure 5.57. (a) Ink spot lentigo and (b) dermoscopy of
ink spot lentigo.
Melanotic macule
a Yellow, light or dark brown regular or
a Mucosal surfaces or adjacent glabrous skin,
e.g. lip (Fig. 5.58), vulva, penis, anus.
irregular macule or thin plaque.
a May have a dry surface.
a When multiple, are also called mucosal
melanosis.
a Often has moth-eaten outline.
a Light to dark brown.
a Can slowly enlarge to several centimetres in
diameter.
Generalised lentigines
a May disappear, often through the process
known as lichenoid keratosis.
a Found on any exposed or covered site from
early childhood.
Ink spot lentigo
a Also called lentigines profusa, multiple
lentigines.
a Also known as reticulated lentigo.
a Not associated with syndromes.
a Few in number compared to solar lentigo.
a Follows sunburn in very fair-skinned
Agminated lentigines
individuals.
a Dark brown to black irregular ink spot-like
a Naevoid eruption of lentigines confined to a
single segmental area.
macule (Fig. 5.57).
a Sharp demarcation in midline.
PUVA lentigo
a May have associated neurological and
developmental abnormalities.
a Similar to ink spot lentigo but follows
photochemotherapy (PUVA).
Patterned lentigines
a Location anywhere exposed to PUVA.
a Inherited tendency to lentigines on face, lips,
buttocks, palms, soles.
a Recognised mainly in dark-skinned
individuals.

5.8 Lentigo 337
Centrofacial neurodysraphic lentiginosis In contrast, an ephilis (freckle) shows sun-

a Associated with mental retardation. induced increased melanin within the
keratinocytes, without an increase in number
Lentiginosis syndromes of cells.
a Syndromes include LEOPARD/Noonan,
Peutz–Jeghers, Laugier–Hunziker, What is the treatment for lentigo?
Moynahan, xeroderma pigmentosa, myxoma Most lentigines are left alone. Attempts to lighten
syndromes (LAMB, NAME, Carney), them may not be successful. The following
Ruvalcaba–Myhre–Smith, Bannayan–Zonana approaches are used:
syndrome, Cowden disease. a SPF 50+ broad-spectrum sunscreen.
a Inheritance is autosomal dominant. a hydroquinone bleaching cream.
a Widespread lentigines present at birth or a alpha hydroxy acids.
arising in early childhood. a vitamin C.
a Associated with neural, endocrine and a retinoids.
mesenchymal tumours. a azelaic acid.
a thiamidol.
Complications of lentigo a chemical peels.
A lentigo is harmless. The main concern is
Individual lesions can be permanently removed
cosmetic. However, it is important to identify
using:
lentiginosis syndromes, as tumours can include
a cryotherapy.
cancers.
a intense pulsed light.
How is lentigo diagnosed? a pigment laser.
Lentigines are mainly diagnosed clinically How can lentigo be prevented?
by typical appearance. Concern regarding
Lentigines associated with exposure to
possibility of melanoma may lead to:
ultraviolet radiation can be prevented by
a dermoscopy. very careful sun protection. Clothing is more
a diagnostic excision biopsy. successful at preventing new lentigines than are
Dermoscopy may reveal pigment network or sunscreens.
structureless pigmentation, depending on the
type of lentigo and its body site. Histology of What is the outlook for lentigo?
lentigo shows: Lentigines usually persist. They may increase
a thickened epidermis. in number with age and sun exposure. Some in
a an increased number of melanocytes along sun-protected sites may fade and disappear.
the basal layer of epidermis.
a unlike junctional melanocytic naevus, there
are no nests of melanocytes.
a increased melanin pigment within the
keratinocytes.
a additional features depending on type of
lentigo.

5.9 Melanoma
What is melanoma? Invasive melanomas are diagnosed slightly
more frequently in males and more males than
Melanoma is a potentially serious type of skin
females die from melanoma.
cancer, in which there is uncontrolled growth
The main risk factors for developing the
of melanocytes (pigment cells). Melanoma is
most common type of melanoma (superficial
sometimes called malignant melanoma.
spreading melanoma) include:
a increasing age (see above).
Melanocytes
a previous invasive melanoma or melanoma
Normal melanocytes are found in the basal
in situ.
layer of the epidermis (the outer layer of skin).
Melanocytes produce a protein called melanin,
a previous basal or squamous cell carcinoma.
which protects skin cells by absorbing ultraviolet
a many melanocytic naevi (moles; see Fig. 5.59).
(UV) radiation. Melanocytes are found in
a multiple (>5) atypical naevi (large or
histologically dysplastic moles).
equal numbers in black and in white skin, but
melanocytes in black skin produce much more
a strong family history of melanoma with two
or more first-degree relatives affected.
melanin. People with dark brown or black skin
are very much less likely to be damaged by UV
a white skin that burns easily.
radiation than those with white skin. These risk factors are not important for rare types
Non-cancerous growth of melanocytes results of melanoma.
in moles (properly called benign melanocytic
naevi) and freckles (ephilis and lentigo). What causes melanoma?
Cancerous growth of melanocytes results in Melanoma is thought to begin as uncontrolled
melanoma. Melanoma is described as: proliferation of melanocytic stem cells that have
a in situ, if the tumour is confined to the undergone genetic transformation.
epidermis. Superficial forms of melanoma spread out
a invasive, if the tumour has spread into the within the epidermis (in situ). A pathologist
dermis. may report this as the radial or horizontal
a metastatic, if the tumour has spread to other growth phase.
tissues.
Who gets melanoma?

The highest reported rates of melanoma in the
world are in Australia and New Zealand; about
1 in 15 white-skinned New Zealanders are
expected to develop melanoma in their lifetime,
compared with:
a 1 in 40 white-skinned Americans.
a 1 in 54 white-skinned people in the UK.
In 2012, invasive melanoma was the 3rd most
common cancer in males (after prostate and
colorectal cancers) and in females (after breast
and colorectal cancers). In the UK, melanoma is
the 7th most common cancer in males and the
5th most common cancer in females. Melanoma
is the 6th most common cancer in the USA.
Although less common in the UK and USA,
melanoma is increasing in incidence.
Melanoma can occur in adults of any age but
is very rare in children. Median age at diagnosis:
a 61 years in New Zealand.
a 63 years in the USA. Figure 5.59. Multiple moles are a risk factor for melanoma.
a 65 years in the UK.

5.9 Melanoma 339
Further genetic changes promote the tumour a Melanomas that are lacking pigment are
to invade through the basement membrane called amelanotic melanoma.
into surrounding dermis, when it becomes an a There may be areas of regression that are the
invasive melanoma. colour of normal skin, or white and scarred.
Nodular melanoma has a vertical growth
During its horizontal phase of growth, a
phase, which is potentially more dangerous
melanoma has a flat surface. As the vertical
than the horizontal growth phase. It may arise
phase develops, the melanoma becomes
within a previously healthy dermis, or within
thickened and raised.
the invasive portion of a pre-existing more
Some melanomas are itchy or tender. More
superficial kind of melanoma.
advanced lesions may bleed easily or crust over.
Once the melanoma cells have reached the
Most melanomas have characteristics
dermis, they may spread to other tissues via
described by the Glasgow 7-point checklist or
the lymphatic system to the local lymph nodes
by the ABCDEs of melanoma. Not all lesions
or via the blood stream to other organs such as
with these characteristics are malignant. Not all
the lungs or brain. This is known as metastatic
melanomas show these characteristics.
disease or secondary spread. The chance of this
happening mainly depends on how deep the
cells have penetrated into the skin. Glasgow 7-point checklist
Major features Minor features
What are the clinical features Change in size Inflammation
of melanoma? Irregular shape Oozing
Irregular colour Change in sensation
Melanoma can arise from otherwise normal- Diameter >7 mm
looking skin (in about 75% of melanomas) or
from within a mole or freckle, which starts
The ABCDEs of melanoma
to grow larger and change in appearance.
A Asymmetry
Precursor lesions include:
B Border irregularity
a melanocytic naevus (normal mole). C Colour variation
a atypical or dysplastic naevus (funny-looking D Diameter >6 mm or Different (from patient’s
mole).
other skin lesions)
a atypical lentiginous junctional naevus E Evolving (enlarging, changing)
(unstable lentigo in heavily sun-damaged
skin). Subtypes of melanoma
a large or giant-sized congenital melanocytic
naevus (brown birthmark). Conventional classification
Melanomas are described according to their
Melanomas can occur anywhere on the body, not
appearance and behaviour. Those that start off
only in areas that get a lot of sun. The most common
as a flat patch (i.e. they have a horizontal growth
site in men is the back (around 40% of melanomas
phase) include:
in men), and the most common site in women is the
a superficial spreading melanoma (Fig. 5.60).
leg (around 35% of melanomas in women).
a lentigo maligna, lentigo maligna melanoma
Although melanoma usually starts as a
and lentiginous melanoma (in sun-damaged
skin lesion, it can also rarely grow on mucous
skin, see Fig. 5.61).
membranes such as the lips or genitals.
a acral lentiginous melanoma (on soles of feet,
Occasionally primary melanoma occurs in other
palms of hands or nails, see Fig. 5.62).
parts of the body such as the eye, brain, mouth
or vagina. These superficial forms of melanoma tend to
The first sign of a melanoma is usually an grow slowly, but at any time, they may develop
unusual-looking freckle or mole. A melanoma a nodule (i.e. they progress to a vertical growth
may be detected at an early stage when it is only phase).
a few millimetres in diameter, but it may grow Melanomas that quickly involve deeper
to several centimetres in diameter before it is tissues include:
diagnosed. a nodular melanoma (Fig. 5.63).
a A melanoma may have a variety of colours a spitzoid melanoma (Fig. 5.64).
including tan, dark brown, black, blue, red a mucosal melanoma (Fig. 5.65).
and, occasionally, light grey.

a neurotropic and desmoplastic melanoma Classification by age, sun exposure

(Fig. 5.66). and number of naevi
a ocular melanoma (Fig. 5.67). Melanoma can be classified according to its
relationship with age, sun exposure, and number
Combinations may arise, e.g. nodular melanoma
of melanocytic naevi.
arising within a superficial spreading melanoma
Childhood melanomas (below 10 years of age):
or desmoplastic melanoma arising below lentigo
maligna.
a extremely rare.
Figure 5.60. Superficial spreading melanoma. Figure 5.63. Nodular melanoma.
Figure 5.61. Lentigo maligna. Figure 5.64. Spitzoid melanoma.
Figure 5.62. Acral lentiginous melanoma. Figure 5.65. Mucosal melanoma.

5.9 Melanoma 341
Figure 5.66. Neurotropic melanoma. Figure 5.68. Superficial spreading melanoma.
a infrequently associated with excessive sun Melanoma is usually epithelial in origin, i.e.
exposure. starting in the skin, or, less often, mucous
a compared to melanoma in adults, they are membranes. But very rarely, melanoma can start
more often amelanotic (flesh coloured, pink in an internal tissue such as the brain (primary
or red), nodular, bleeding and ulcerated. CNS melanoma) or the back of the eye (one type
a may arise within giant congenital of ocular melanoma).
melanocytic naevi >40 cm diameter.
How is melanoma diagnosed?
Early-onset melanomas:
Some melanomas are extremely difficult to
a more common in women than in men. recognise clinically. Melanoma may be suspected
a most common clinical subtype is superficial because of a lesion’s clinical features (see Fig. 5.68)
spreading.
or because of a history of change. The dermoscopic
a associated with many melanocytic naevi. appearance is helpful in the diagnosis of
a tend to be seen on lower extremity. featureless early melanoma (Fig. 5.69).
a tend to have BRAF V600E genetic mutation. The suspicious lesion is surgically removed
a associated with intermittent sun exposure. with a 2 mm clinical margin for pathological
Late-onset melanomas: examination (diagnostic excision). Partial biopsy
a more common in men than in women. is best avoided, but may be considered in large
a most common clinical subtype is lentigo lesions.
maligna. The pathological diagnosis of melanoma
a often occur on head and neck. can be very difficult. Histological features of
a associated with accumulated, lifelong sun superficial spreading melanoma in situ include
exposure. the presence of buckshot (pagetoid) scatter of
atypical melanocytes within the epidermis.
Figure 5.67. Ocular melanoma. Figure 5.69. Dermoscopy of melanoma from Fig. 5.68.

These cells may be enlarged with unusual nuclei. What is the treatment for melanoma?
Dermal invasion results in melanoma cells within Following confirmation of the diagnosis, wide
the dermis or deeper into subcutaneous fat. local excision is carried out at the site of the
Immunohistochemical stains may be primary melanoma. The extent of surgery
necessary to confirm melanoma. depends on the thickness of the melanoma and
its site. Margins recommended are shown below:
Pathology report Melanoma in situ: 5–10 mm
The pathologist’s report should include a Melanoma <1 mm: 10 mm
macroscopic description of the specimen Melanoma 1–2 mm: 10–20 mm
and melanoma (the naked eye view), and Melanoma >2 mm: 20 mm
a microscopic description. The following
features should be reported if there is invasive Staging
melanoma: Melanoma staging means finding out if the
a diagnosis of primary melanoma. melanoma has spread from its original site
a Breslow thickness to the nearest 0.1 mm. in the skin. Most melanoma specialists refer
a Clark level of invasion. to the American Joint Committee on Cancer
a margins of excision, i.e. the normal tissue (AJCC) cutaneous melanoma staging guidelines
around the tumour. (8th edition, 2018). In essence, the stages are:
a mitotic rate – a measure of how fast the cells
are proliferating.
Stage Characteristics
a whether or not there is ulceration. Stage 0 In situ melanoma
a pathological staging. Stage 1 Thin melanoma <2 mm in thickness
The report may also include comments Stage 2 Thick melanoma >2 mm in thickness
about the cell type and its growth pattern, Stage 3 Melanoma spread to involve local
invasion of blood vessels or nerves, inflammatory lymph nodes
response, regression and whether there is Stage 4 Distant metastases have been detected
associated in situ disease or associated naevus
(original mole). Should the lymph nodes be removed?
If the local lymph nodes are enlarged due to
What is breslow thickness? metastatic melanoma, they should be completely
Breslow thickness is reported for invasive removed. This requires a surgical procedure,
melanomas. It is measured vertically in usually under general anaesthetic. If they are
millimetres from the top of the granular layer (or not enlarged, they may be tested to see if there is
base of superficial ulceration) to the deepest point any microscopic spread of melanoma. The test is
of tumour involvement. It is a strong predictor known as a sentinel node biopsy.
of outcome; the thicker the melanoma, the more Many surgeons recommend (based on
likely it is to metastasise (spread). AJCC Guidelines) sentinel node biopsy for
melanomas thicker than 0.8 mm, especially in
What is the clark level of invasion? younger people. Although the biopsy may help in
The Clark level indicates the anatomic plane of staging the cancer, it does not offer any survival
invasion. advantage.
Level 1 In situ melanoma Lymph nodes containing metastatic
Level 2 Melanoma has invaded papillary melanoma often increase in size quickly. An
dermis involved node is usually non-tender and firm to
Level 3 Melanoma has filled papillary dermis hard in consistency.
Level 4 Melanoma has invaded reticular
dermis Treatment of advanced melanoma
Level 5 Melanoma has invaded subcutaneous If the melanoma is widespread, treatment
tissue is not always successful in eradicating the
cancer. Some patients may be offered new or
Deeper Clark levels have a greater risk of experimental treatments, such as:
metastasis. It is useful in predicting outcome a PD-1 blocking antibodies – nivolumab,
in thin tumours. It is less useful than Breslow pembrolizumab.
thickness for thick tumours. a BRAF inhibitors – dabrafenib and vemurafenib.

5.9 Melanoma 343
a MEK inhibitors – trametinib, cobimetinib. a a feel for the regional lymph nodes.
a C-KIT inhibitors – imatinib, nilotinib. a general skin examination.
a CTLA-4 antagonist – ipilimumab. a full physical examination.
a in those with many moles or atypical
What happens at follow-up? moles, baseline whole body imaging and
The main purpose of follow-up is to detect sequential macro and dermoscopic images
recurrences early but it also offers an of melanocytic lesions of concern (mole
opportunity to diagnose a new primary mapping; see Fig. 5.71).
melanoma at the first possible opportunity.
In those with more advanced primary disease,
A second invasive melanoma occurs in 5–10%
follow-up may include:
of melanoma patients, and melanoma in situ in
more than 20% of melanoma patients.
a blood tests, including LDH.
MelNet New Zealand’s Quality Statements to
a imaging – ultrasound, X-ray, CT, MRI and
PET-CT scan.
Guide Diagnosis and Treatment in New Zealand
(2021) make the following recommendations for Tests are not worthwhile for patients with
follow-up for patients with invasive melanoma. stage 1 or 2 melanoma unless there are
a Self skin examination. signs or symptoms of disease recurrence
a Regular routine skin checks by patient’s or metastasis. No tests are necessary for
preferred health professional experienced in healthy patients who have remained well for
melanoma diagnosis and management. 5 years or longer after removal of their melanoma.
a Follow-up intervals are preferably
six-monthly for two years for patients with What is the outlook for patients
stage 1 disease, three- or four-monthly with melanoma?
for three years for patients with stage 2 or Melanoma in situ is cured by excision because it
3 disease, and yearly thereafter to ten years has no potential to spread round the body.
post excision for all patients. The risk of spread and ultimate death
a Individual patients’ needs should be considered from invasive melanoma depends on several
before appropriate follow-up is offered. factors, but the main one is the Breslow
a Provide education and support to help thickness of the melanoma at the time it
patient adjust to their illness. was surgically removed.
In the UK, refer to NICE Guidelines (NG14, 2015). Metastases are rare for melanomas <0.8 mm
In the USA, refer to the American Academy of and the risk for tumours 0.8–1 mm thick is about
Dermatology Clinical Guidelines (2018). 5%. The risk steadily increases with thickness so
The follow-up appointments may be that melanomas >4 mm have a risk of metastasis
undertaken by the patient’s general practitioner of about 40%.
or specialist. Checkpoint inhibitors and targeted therapies
Follow-up appointments may include: have recently improved survival rates for
a a check of the scar where the primary patients with advanced melanoma.
melanoma was removed (see Fig. 5.70,
metastatic melanoma within the scar).
Figure 5.70. Primary melanoma removal scar Figure 5.71. Dermoscopic images of atypical naevi
(recurrent melanoma). Metastatic melanoma arising at displayed during mole mapping.
site of primary excision.

5.10 Moles
What is a mole? What are the clinical features of moles?
A mole is a common benign skin lesion Moles vary widely in clinical, dermoscopic and
due to a local proliferation of pigment cells histological appearance.
(melanocytes). It is more correctly called a a They may arise on any part of the body.
melanocytic naevus (US spelling ‘nevus’), and a Moles differ in appearance depending on the
is sometimes also called a naevocytic naevus. body site of origin.
A brown or black mole contains the pigment a They may be flat or protruding.
melanin, so may also be called a pigmented a They vary in colour from pink or flesh tones to
naevus. dark brown, steel blue, or black.
A mole can be present at birth (congenital a Light-skinned individuals tend to have
naevus) or appear later (acquired naevus). light-coloured moles and dark-skinned
There are various kinds of congenital and individuals tend to have dark brown or
acquired naevi. black moles.
a Although mostly round or oval in shape,
Who gets moles? moles are sometimes unusual shapes.
Almost everyone has at least one mole. a They range in size from a couple of millimetres
a About 1% of individuals are born with one to several centimetres in diameter.
or more congenital melanocytic naevi. This
is usually sporadic, with rare instances of Classification of melanocytic naevi
familial congenital naevi. Congenital melanocytic naevi are classified
a Fair-skinned people tend to have more moles according to their actual or predicted adult size
than darker-skinned people. in maximum dimension.
a Moles that appear during childhood (aged a A small congenital melanocytic naevus is
2–10 years) tend to be the most prominent <1.5 cm.
and persistent moles throughout life. a A medium congenital melanocytic naevus is
a Moles that are acquired later in childhood or 1.5–19.9 cm.
adult life often follow sun exposure. a A large or giant congenital melanocytic
naevus is ≥20 cm.
Most white-skinned New Zealanders have
20–50 moles, but individuals in Northern Special types of congenital naevi include:
Europe and the USA tend to have fewer. a hairy melanocytic naevus (Fig. 5.72).
a bathing trunk naevus (Fig. 5.73).
What causes moles? a café au lait macule (Fig. 5.74).
Although the exact reason for local proliferation a speckled lentiginous naevus (Fig. 5.75).
of naevus cells is unknown, it is clear that the a dermal melanocytosis – Mongolian spot
number of moles a person has depends on (Fig. 5.76), naevus of Ota (Fig. 5.77) naevus
genetic factors, on sun exposure, and on immune of Ito, Hori naevus.
status.
a People with many moles tend to have family
members who also have many moles, and
their moles may have a similar appearance.
a Somatic mutations in RAS genes are
associated with congenital melanocytic
naevi.
a New melanocytic naevi may erupt following
the use of BRAF inhibitor drugs.
a People living in Australia and New Zealand
have many more naevi than their relatives
residing in Northern Europe.
a Immunosuppressive treatment leads to an
increase in numbers of naevi. Figure 5.72. Hairy melanocytic naevus.

5.10 Moles 345
The pathological classification of melanocytic a A compound naevus has nests of naevus

naevi relates to where naevus cells are found in cells at the epidermal–dermal junction
the skin. as well as within the dermis; a central
a A junctional naevus has groups or nests of raised area surrounded by a flat patch
naevus cells at the junction of the epidermis (Fig. 5.81).
and the dermis; a flat mole (Fig. 5.78). a A blue naevus has elongated, fusiform
a A dermal or intradermal naevus has naevus cells in the deep dermis. Flat or
naevus cell nests in the dermis. A papule, papular, the name describes its usual
plaque or nodule with a pedunculated, colour (Fig. 5.82).
papillomatous (Unna naevus; Fig. 5.79) a A combined naevus has two distinct types of
or smooth surface (Miescher naevus; mole within the same lesion – usually blue
Fig. 5.80). naevus and compound naevus (see Fig. 5.83).
Figure 5.73. Bathing trunk naevus. Figure 5.76. Mongolian spot.
Figure 5.74. Café au lait macule. Figure 5.77. Naevus of Ota.
Figure 5.75. Speckled lentiginous naevus. Figure 5.78. Junctional naevus.

Dermoscopy has given rise to a new Descriptive terms for signature naevi include
classification based on the pigment patterns of solid brown (Fig. 5.88), solid pink (Fig. 5.89),
melanocytic naevi. Examples include: eclipse/annular (Fig. 5.90), cockade/bull’s
a a junctional naevus described with reticular eye (Fig. 5.91), naevus with perifollicular
pattern of intersecting brown lines (Fig. 5.84). hypopigmentation (Fig. 5.92), more easily seen
a a dermal naevus described with aggregated by dermoscopy (Fig. 5.93), naevus with eccentric
cobblestones (Fig. 5.85) or globules (Fig. 5.86). pigmentation, fried-egg naevus, and lentiginous
a a blue naevus is hazy steel blue and uniform naevus (see Fig. 5.55).
structureless lesion (Fig. 5.87). Uncommon types of melanocytic naevi
include:
Signature naevi are the predominant type of
a Spitz naevus or epithelioid cell naevus –
naevus in an individual with multiple moles.
a pink (classic Spitz; Fig. 5.94) or brown
Figure 5.79. Unna or papillomatous naevus. Figure 5.82. Blue naevus.
Figure 5.80. Miescher naevus. Figure 5.83. Combined naevus.
Figure 5.81. Compound naevus. Figure 5.84. Dermoscopic appearance of junctional

naevus (reticular pattern).

5.10 Moles 347
(pigmented Spitz; Fig. 5.95) dome-shaped a A mole with specific characteristics: large
mole that arises in children and young adults. (>5 mm); ill-defined or irregular borders;
a Reed naevus – darkly pigmented type of Spitz varying shades of colour; with flat and bumpy
naevus with starburst dermoscopic pattern components (Fig. 5.98).
(Fig. 5.96). a Or, any funny-looking mole; large,
a Agminated naevi – a cluster of similar moles or different from the patient’s other
(Fig. 5.97). moles.
The term atypical naevus may be used in several Atypical naevi usually occur in fair-skinned
ways. individuals when they are due to sun exposure.
a A benign mole that has some clinical or They may be solitary or numerous. Pathology is
histopathological characteristics of melanoma. reported as dysplastic junctional or compound
Figure 5.85. Dermoscopic appearance of dermal naevus Figure 5.88. Solid brown compound naevus.
with aggregated cobblestones.
Figure 5.86. Dermoscopic appearance of dermal naevus Figure 5.89. Solid pink naevus.
with globules.
Figure 5.87. Dermoscopic appearance of blue naevus Figure 5.90. Annular naevus on scalp.
with structureless, steel-grey colour.

naevus and has specific histological features (the a People with a greater number of moles have
Clark naevus). a higher risk of developing melanoma than
those with few moles, especially if they have
What are the complications of moles? over 100 of them.
People worry about moles because they
Moles sometimes change for other reasons than
have heard about melanoma, a malignant
melanoma, for example, due to normal ageing,
proliferation of melanocytes that is the most
or following sun exposure or during pregnancy.
common reason for death from skin cancer.
They can enlarge, regress or involute (disappear).
a At first, melanoma may look similar to a
harmless mole, but in time it becomes more
a A Meyerson naevus is itchy and dry because
it is surrounded by eczema (Fig. 5.99).
disordered in structure and tends to enlarge.
Figure 5.91. Cockade naevus. Figure 5.94. Classic Spitz naevus.
Figure 5.92. Naevus with perifollicular hypopigmentation. Figure 5.95. Pigmented Spitz naevus.
Figure 5.93. Naevus with perifollicular Figure 5.96. Reed naevus.

hypopigmentation seen by dermoscopy.

5.10 Moles 349
a Sutton or halo naevus is surrounded by a consulted in person or with the help of clinical
white patch, and fades away over several and dermoscopic images. This is especially
years (Fig. 5.100). important if:
a A recurrent naevus is one that appears in a a a mole changes size, shape, structure or colour.
scar following surgical removal of a mole – a a new mole develops in adult life (>40 years).
this may have odd clinical and dermoscopic a it appears different from the person’s other
features (Fig. 5.101). moles (a so-called ugly duckling).
a it has ABCD characteristics (Asymmetry,
How is a mole diagnosed? Border irregularity, Colour variation,
Moles are usually diagnosed clinically by Diameter >6 mm).
their typical appearance. If there is any a it is bleeding, crusted or itchy.
doubt about the diagnosis, an expert may be
Most skin lesions with these characteristics
are actually harmless when evaluated by an
expert using dermoscopy. Short-term digital
dermoscopic imaging may be used in equivocal
flat lesions to check for change over time.
Naevi that remain suspicious for melanoma
are excised for histopathology (diagnostic
biopsy). Partial biopsy is not recommended, as it
may miss an area of cancerous change.
What is the treatment for moles?

Most moles are harmless and can be safely left
alone. Moles may be removed in the following
Figure 5.97. Agminated naevi.
circumstances:
Figure 5.98. Atypical naevus; large, irregular shape and Figure 5.100. Sutton or halo naevus.
colour.
Figure 5.99. Meyerson naevus. Figure 5.101. Recurrent naevus following shave excision
of benign dermal naevus.

a to exclude cancer. a Apply sunscreen to areas you can’t cover.

a the mole is a nuisance – perhaps irritated by Choose broad-spectrum high protection
clothing, comb or razor. (SPF 50+) sunscreens, applied frequently to
a cosmetic reasons – the mole is unsightly. exposed areas.
Surgical techniques include: What is the outlook for moles?
a excision biopsy of flat or suspicious mole. Most moles that appear in childhood remain
a shave biopsy of protruding mole. forever. Teenagers and young adults tend to
a electrosurgical destruction. have the greatest number of moles. There are
a laser to lessen pigment or remove coarse hair. fewer in later life because some of them slowly
Can moles be prevented? fade away.
To increase the chance of spotting melanoma
The number of moles can be minimised by strict
early, recommend:
protection from the sun, starting from birth.
a self-skin examination monthly.
Sunscreen alone is not sufficient to prevent new
a significant changes in moles or new lesions
moles from appearing.
are reported to doctor or dermatologist.
At any age, sun protection is important to
a regular skin examinations in patients with
reduce skin ageing and the risk of skin cancer.
many moles, atypical naevi or previous skin
a In New Zealand, the SunSmart’s Sun cancer.
Protection Alert advises when protection
a total body photography and digital
is required. Smartphone apps provide
dermoscopic imaging (mole mapping) for
UV protection advice specific for any
patients at high risk of melanoma, especially
geographical location.
if they have many moles.
a Cover up. Wear a hat, long sleeves and long
skirt or trousers. Choose fabrics designed for
the sun (UPF 40+) when outdoors.

5.11 Seborrhoeic keratoses 351
5.11 Seborrhoeic keratoses

What is a seborrhoeic keratosis? a Viral cause (e.g. human papillomavirus) has
been suspected but not proven.
A seborrhoeic keratosis is a harmless warty spot
that appears during adult life as a common sign
a Stable and clonal mutations or activation of
FRFR3, PIK3CA, RAS, AKT1 and EGFR genes
of ageing. Some people have hundreds of them.
are found in seborrhoeic keratoses.
Seborrhoeic keratosis (or seborrheic keratosis,
using US spelling) is also called SK, basal cell
a FRFR3 mutations are associated with
increased age and location on the head
papilloma, senile wart, brown wart or barnacle.
and neck, suggesting a role of ultraviolet
Who gets seborrhoeic keratoses? radiation.
Seborrhoeic keratoses are extremely common. It
a Seborrhoeic keratoses do not harbour tumour
suppressor gene mutations.
has been estimated that over 90% of adults over
the age of 60 years have one or more of them.
a Epidermal growth factor receptor inhibitors
(used to treat cancer) often result in an
They occur in males and females of all races,
increase in verrucal (warty) keratoses.
typically beginning to erupt in the 30s or 40s.
They are uncommon under the age of 20 years. What are the clinical features
What causes seborrhoeic keratoses? of seborrhoeic keratoses?
The precise cause of seborrhoeic keratoses is not Seborrhoeic keratoses can arise on any area of
known. skin, covered or uncovered, with the exception
The name is misleading, because they of palms and soles (Figs 5.102–5.107). They do not
are not limited to a seborrhoeic distribution arise from mucous membranes.
(scalp, mid-face, chest, upper back) as in Seborrhoeic keratoses have highly variable
seborrhoeic dermatitis, nor are they formed from appearance.
sebaceous glands, as is the case with sebaceous a Flat or raised papule or plaque.
hyperplasia. a 1 mm to several cm in diameter.
Seborrhoeic keratoses are considered a Skin-coloured (Fig. 5.103), yellow (Fig. 5.104),
degenerative in nature, appearing as part of the grey, light brown (Fig. 5.105), dark brown,
skin ageing process. As time goes by, seborrhoeic black or mixed colours.
keratoses become more numerous. Some a Smooth, waxy or warty surface
people inherit a tendency to develop a very large (see Figs 5.106 and 5.107).
number of them. Researchers have noted the a Solitary or grouped (see Fig. 5.102) in certain
following: areas, such as within the scalp, under the
a Eruptive seborrhoeic keratoses can follow breasts, over the spine or in the groin.
sunburn or dermatitis. They appear to stick on to the skin surface like
a Skin friction may be the reason they appear barnacles.
in body folds.
Figure 5.102. Multiple seborrhoeic keratosis. Figure 5.103. Skin-coloured seborrhoeic keratosis.

Variants of seborrhoeic keratoses include: a stucco keratosis – grey, white or yellow

a solar lentigo – flat circumscribed pigmented papules on the lower extremities (Fig. 5.109).
patches in sun exposed sites (see Fig. 5.17). a inverted follicular keratosis.
Thicker seborrhoeic keratoses may arise a large cell acanthoma.
within solar lentigo. a lichenoid keratosis: an inflammatory phase
a dermatosis papulosa nigra – small, preceding involution of some seborrhoeic
pedunculated and heavily pigmented keratoses and solar lentigo (Fig. 5.110),
seborrhoeic keratoses on head and neck of with characteristic grey dots on dermoscopy
darker-skinned individuals (Fig. 5.108). (Fig. 5.111).
Figure 5.104. Yellowish seborrhoeic keratosis. Figure 5.107. Melanoacanthoma: a brown seborrhoeic
keratosis with a waxy surface.
Figure 5.105. Flat brown seborrhoeic keratosis. Figure 5.108. Dermatosis papulosa nigra.
Figure 5.106. Seborrhoeic keratosis with warty surface. Figure 5.109. Stucco keratosis.

5.11 Seborrhoeic keratoses 353
Complications of seborrhoeic keratoses a A stuck-on, well-demarcated warty plaque.

Seborrhoeic keratoses are not premalignant a Other similar lesions.
tumours. However: Sometimes, seborrhoeic keratosis may resemble
a skin cancers are sometimes difficult to tell a skin cancer, such as basal cell carcinoma,
apart from seborrhoeic keratoses. squamous cell carcinoma or melanoma.
a a skin cancer may by chance arise within or Dermoscopy often shows a disordered
collide with a seborrhoeic keratosis. structure in a seborrhoeic keratosis, as is the
Very rarely, eruptive seborrhoeic keratoses have case in skin cancers. There are diagnostic
been reported to denote an underlying internal dermoscopic clues to seborrhoeic keratosis, such
malignancy, most often gastric adenocarcinoma. as multiple orange or brown clods (due to keratin
The controversial paraneoplastic syndrome in skin surface crevices), white “milia-like” clods
is known as the sign of Leser–Trélat. Eruptive (Fig. 5.113), curved thick ridges and furrows
seborrhoeic keratoses that are not associated forming a brain-like or cerebriform pattern
with cancer are sometimes called pseudo-sign of (Fig. 5.114).
Leser–Trélat. If doubt remains, a seborrhoeic keratosis
An irritated seborrhoeic keratosis is an may undergo partial shave or punch biopsy or
inflamed, red and crusted lesion (Fig. 5.112). diagnostic excision.
It may give rise to dermatitis around the The dominant histopathological features of
seborrhoeic keratosis. Dermatitis may also seborrhoeic keratosis may be described as:
trigger new seborrhoeic keratoses to appear. a melanoacanthoma (deeply pigmented,
see Fig. 5.107).
How is a seborrhoeic keratosis diagnosed? a acanthotic.
The diagnosis of seborrhoeic keratosis is a hyperkeratotic or papillomatous.
often easy. a adenoid or reticulated.
a clonal or nested.
Figure 5.110. Solar lentigo evolving into lichenoid Figure 5.112. Irritated seborrhoeic keratosis.
keratosis (Fig. 5.111).
Figure 5.111. Lichenoid keratosis (Fig. 5.110) confirmed Figure 5.113. Orange and white clods seen on
by grey dots on dermoscopy. dermoscopy of seborrhoeic keratosis.

a curettage and electrocautery.

a ablative laser surgery.
a shave biopsy (shaving off with a scalpel).
a focal chemical peel with trichloracetic acid.
All methods have disadvantages. Treatment-
induced loss of pigmentation is a particular issue
for dark-skinned patients. There is no easy way to
remove multiple lesions on a single occasion.
How can seborrhoeic keratoses

be prevented?
Unknown.
Figure 5.114. Cerebriform dermoscopic pattern in
seborrhoeic keratosis. What is the outlook for seborrhoeic
keratoses?
a adamantinoid or mucinous. Seborrhoeic keratoses tend to persist. From time
a desmoplastic. to time, individual or multiple lesions may remit
a irritated. spontaneously or via the lichenoid keratosis
mechanism.
What is the treatment for seborrhoeic
Those associated with dermatitis may regress
keratoses? after it has been controlled.
An individual seborrhoeic keratosis can easily be
removed if desired. Reasons for removal may be
that it is unsightly, itchy, or catches on clothing.
Methods used to remove seborrhoeic
keratoses include:
a cryotherapy (liquid nitrogen) for thinner
lesions (repeated if necessary).

5.12 Squamous cell carcinoma – cutaneous 355
5.12 Squamous cell carcinoma – cutaneous

What is cutaneous squamous cell in immunosuppressed populations. b-HPV
and HPV subtypes 5, 8, 17, 20, 24, and 38
carcinoma?
have also been associated with an increased
Cutaneous squamous cell carcinoma (SCC) is a risk of cutaneous SCC in immunocompetent
common type of keratinocytic or non-melanoma individuals.
skin cancer. It is derived from keratinising
cells within the epidermis. Keratin is the horny What are the clinical features of
protein that makes up skin, hair and nails. cutaneous squamous cell carcinoma?
Cutaneous SCC is an invasive disease,
Cutaneous SCCs present as enlarging scaly or
referring to cancer cells that have grown beyond
crusted lumps (Figs 5.115–5.116). They usually
the epidermis. SCC can sometimes metastasise
arise within pre-existing actinic keratosis or
and may prove fatal.
intraepidermal carcinoma.
Intraepidermal carcinoma (SCC in situ) and
mucosal SCC are considered elsewhere.
a Grow over weeks to months.
a May ulcerate (Fig. 5.115).
Who gets cutaneous squamous cell a Often tender or painful.
carcinoma? a Often located on sun-exposed sites,
particularly the face, lips, ears, hands,
Risk factors for cutaneous SCC include the forearms and lower legs.
following. a Size varies from a few millimetres to several
a Age and gender: SCCs are particularly centimetres in diameter.
prevalent in elderly males. However, they
also affect females and younger adults.
a Previous SCC or other form of skin cancer
(basal cell carcinoma, melanoma).
a Actinic keratosis.
a Smoking.
a Fair skin, blue eyes and blond or red hair.
a Previous cutaneous injury, thermal burn,
disease (e.g. cutaneous lupus, epidermolysis
bullosa, leg ulcer).
a Inherited syndromes: SCC is a particular
problem for families with xeroderma
pigmentosum and albinism.
a Other risk factors include ionising
radiation, exposure to arsenic, and immune
suppression due to disease (e.g. chronic
Figure 5.115. Ulcerated cutaneous SCC.
lymphocytic leukaemia) or treatment. Organ
transplant recipients have a massively
increased risk of developing SCC.
What causes cutaneous squamous cell

carcinoma?
More than 90% of cases of SCC are associated
with DNA mutations in the p53 tumour
suppressor gene, caused by exposure to
ultraviolet radiation (UV), especially UVB.
Mutations in signalling pathways including
epidermal growth factor receptor, RAS, Fyn, or
p16INK4a signalling are also implicated.
Beta-genus human papillomaviruses (wart
virus) are thought to play a role in SCC arising Figure 5.116. Crusted cutaneous SCC.

Types of cutaneous squamous a location on the ear, vermilion of lip

cell carcinoma (see Fig. 5.1), central face, hands, feet,
genitalia.
Distinct clinical types of invasive SCC include: a arising in elderly or immune suppressed
a cutaneous horn – the horn is due to excessive patient.
production of keratin (see Fig. 5.117). a histological thickness >2 mm, poorly
a keratoacanthoma – a rapidly growing differentiated histology, or with invasion of
keratinising nodule that may resolve without the subcutaneous tissue, nerves and blood
treatment (see Figs 5.118 and 5.119). vessels.
a carcinoma cuniculatum (‘verrucous
carcinoma’), a slow-growing, warty tumour Metastatic SCC is found in regional lymph nodes
on the sole of the foot (Fig. 5.120). (80%), lungs, liver, brain, bones and skin.
The pathologist may classify the SCC as well Staging SCC
differentiated, moderately well differentiated, In 2018, the American Joint Committee on
poorly differentiated or anaplastic. There are Cancer (AJCC) published a new staging system
other variants. for cutaneous SCC for the 8th edition of the AJCC
Manual. This evaluates the dimensions of the
High-risk cutaneous squamous original primary tumour (T) and its metastases
cell carcinoma to lymph nodes (N).
Cutaneous SCC is classified as low-risk or
high-risk, depending on the chance of tumour Tumour staging for cutaneous SCC
recurrence and metastasis. Characteristics of TX Primary tumour cannot be assessed
high-risk SCC include: T0 No evidence of primary tumour
a diameter ≥2 cm.
Figure 5.117. Cutaneous horn. Figure 5.119. Keratoacanthoma.
Figure 5.118. Keratoacanthoma. Figure 5.120. Carcinoma cuniculatum.

5.12 Squamous cell carcinoma – cutaneous 357
Tis Carcinoma in situ a Surgery.

T1 Tumour ≤2 cm a Radiotherapy.
T2 Tumour ≥2 cm a Experimental targeted therapy using
Tumour ≤4 cm epidermal growth factor receptor inhibitors.
T3 Tumour >4 cm or with perineural invasion
Many thousands of New Zealanders are treated
T4 Tumour with invasion of bone
for SCC each year, and more than 100 die from
their disease. In the UK, more than 750 non-
Nodal staging for cutaneous SCC melanoma skin cancer deaths were recorded in
NX Regional lymph nodes cannot be assessed 2014, mostly due to cutaneous SCC.
N0 No regional lymph node metastasis
N1 Metastasis in one local lymph node ≤3 cm How can cutaneous squamous cell
N2 Metastasis in one local lymph node ≥3 cm carcinoma be prevented?
Metastasis in >1 local lymph node ≤6 cm
There is a great deal of evidence to show that
N3 Metastasis in lymph node ≥6 cm
very careful sun protection at any time of life
reduces the number of SCCs. This is particularly
How is squamous cell carcinoma important in ageing, sun-damaged, fair skin;
diagnosed? in patients who are immunosuppressed; and
Diagnosis of cutaneous SCC is based on clinical in those who already have actinic keratoses or
features. The diagnosis and histological subtype previous SCC.
is confirmed pathologically by diagnostic biopsy a Stay indoors or in the shade in the middle of
or following excision. the day.
Patients with high-risk SCC may also undergo a Wear covering clothing.
staging investigations to determine whether it a Apply broad-spectrum sunscreens
has spread to lymph nodes or elsewhere. These generously to exposed skin if outdoors.
may include: a Avoid indoor tanning (sun beds and solaria).
a ultrasound scan, X-rays, CT scans, MRI scans. Oral nicotinamide (vitamin B3) in a dose of
a lymph node or other tissue biopsy. 500 mg twice daily may reduce the number and
severity of SCCs in people at high risk.
What is the treatment for cutaneous Patients with multiple squamous cell
squamous cell carcinoma? carcinomas may be prescribed an oral retinoid
Cutaneous SCC is nearly always treated (acitretin or isotretinoin). These reduce the number
surgically. Most cases are excised with a of tumours but have some nuisance side effects.
3–10 mm margin of normal tissue around the
visible tumour. A flap or skin graft may be What is the outlook for cutaneous
needed to repair the defect. squamous cell carcinoma?
Other methods of removal include: Most SCCs are cured by treatment. Cure is most
a shave, curettage and electrocautery for likely if treatment is undertaken when the lesion
low-risk tumours on trunk and limbs. is small.
a aggressive cryotherapy for very small, thin, About 50% of people at high risk of SCC
low-risk tumours. develop a second one within 5 years of the first.
a Mohs micrographic surgery for large facial They are also at increased risk of other skin
lesions with indistinct margins or recurrent cancers, especially melanoma. Regular self-skin
tumours. examinations and long-term annual skin checks
a radiation therapy for inoperable tumour, by an experienced health professional are
patients unsuitable for surgery, or as recommended.
adjuvant.
What is the treatment for advanced or

metastatic squamous cell carcinoma?
Locally advanced primary, recurrent or metastatic
SCC requires multidisciplinary consultation.
Often a combination of treatments is used.

5.13 Vascular lesions

Introduction according to the size and type of vessel. They
may remain stable or become more prominent
Terminology of vascular conditions can be
with maturity. There are various associated
confusing, with several lesions being incorrectly
syndromes (see DermNet NZ).
named or classified. Vascular skin lesions
include:
a Capillary malformation – salmon patch
(Fig. 5.121) and port wine stain (Fig. 5.122).
1. Vascular naevi.
2. Angiomas.
a Venous malformations – glomovenous
malformation, arteriovenous malformations,
3. Telangiectasias.
blue rubber bleb syndrome (Fig. 5.123)
4. Vascular sarcomas.
(associated gastrointestinal lesions).
A paediatric dermatologist, paediatrician, a Arteriovenous malformations: of mixed
vascular specialist or surgeon should assess blood vessel origin.
significant infantile capillary malformations a Lymphatic malformation: Lymphangioma
or proliferative haemangiomas, especially circumscriptum, cavernous lymphangioma
when large, symptomatic (e.g. ulcerated), (Fig. 5.124).
located on the head and neck or close to eye, a Angioma serpiginosa: a crop of swirling
nose or mouth. vascular papules (Fig. 5.125).
a Naevus anaemicus – in this naevus, blood
Vascular naevi flow is interrupted resulting in pale areas
Vascular naevi or anomalies are present at birth (Fig. 5.126).
or appear in early childhood. They are classified
Figure 5.121. Capillary malformation. Figure 5.123. Blue rubber bleb syndrome.
Figure 5.122. Port wine stain. Figure 5.124. Cavernous lymphangioma.

5.13 Vascular lesions 359
Angiomas a Angiokeratoma: acquired scaly angiomas,

Angiomas are benign tumours formed by usually on vulva or scrotum, or in association
dilation of blood vessels or formation of new with Fabry disease (see Fig. 5.129).
ones by proliferation of endothelial cells. a Glomus tumour: tender papule on nail bed or
a Infantile proliferative haemangioma palm arising in young to middle-aged adult
(capillary, cavernous or mixed): (Fig. 5.130).
proliferates in the first few weeks of life, Pyogenic granuloma (see Fig. 5.132) occurs
followed by involution later in childhood in children and young adults on skin and
(Fig. 5.127). mucosa, most often lower lips, fingers and toes
a Congenital haemangioma is at full size at in response to a minor, often unnoticed, injury.
birth and may rapidly involute (RICH) or It grows rapidly and may become pedunculated
persist (NICH). or polypoid and surrounded by a collarette of
a Kaposiform haemangioendothelioma is a normal skin. It bleeds and crusts.
rare aggressive haemangioma that results Bacillary angiomatosis is a rare opportunistic
in platelet trapping – the Kasabach–Merritt bacterial infection due to Rochalimaea henselae.
phenomenon.
a Tufted angioma: rare childhood tumour with Telangiectasias
characteristic histology. Prominent cutaneous blood vessels can be
a Cherry angioma (Fig. 5.128) adult onset, physiological or pathological (e.g. feeding a
common degenerative lesions, usually tumour such as basal cell carcinoma, and they
multiple. Dermoscopy shows red, purple or are a common sign of rosacea). There are some
blue clods (Fig. 5.131). named conditions in which telangiectasia is
characteristic.
Figure 5.125. Angioma serpiginosa. Figure 5.127. Infantile proliferative haemangioma.
Figure 5.126. Naevus anaemicus. Figure 5.128. Cherry angioma.

Figure 5.129. Angiokeratoma seen on dermoscopy. Figure 5.132. Pyogenic granuloma.
Figure 5.130. Glomus tumour. Figure 5.133. Spider angioma.
Figure 5.131. Purple clods of angioma seen on Figure 5.134. Venous lake.
dermoscopy.
a Spider angioma (Fig. 5.133) or spider a Venous lake (Fig. 5.134): blue or purple
telangiectasis consists of central arteriole and compressible papule due to venous dilation,
radiating capillaries. Very common in healthy often on lower lip or ear.
individuals, but more arise in response to a Unilateral acquired telangiectasia:
oestrogen, e.g. pregnancy, liver disease. telangiectasia with naevoid distribution.

5.13 Vascular lesions 361
Figure 5.135. Essential telangiectasia. Figure 5.137. Hereditary haemorrhagic telangiectasia.
Figure 5.136. Benign hereditary telangiectasia. Figure 5.138. Acquired lymphangiectasia.
Malignant vascular tumours

a Essential telangiectasia: idiopathic
telangiectasia and venulectasia (see
a Kaposi sarcoma: due to human herpesvirus
8 (HHV8) and immunosuppression, e.g.
Fig. 5.135).
infection with human immunodeficiency
a Benign hereditary telangiectasia: familial
virus (HIV). There are four types. Kaposi
condition in which matt telangiectases
sarcoma presents with multiple purple
appear (Fig. 5.136).
macules, papules and plaques on skin and
a Hereditary haemorrhagic telangiectasia:
mucous membranes (see Fig. 5.139).
telangiectasia on skin and mucous
membranes associated with bleeding
a Angiosarcoma: idiopathic or secondary to
chronic lymphoedema or radiation. Often
from nose and gut causing anaemia (see
an aggressive cancer, it mostly presents in
Fig. 5.137).
elderly people with spreading purple patches
a Acquired lymphangiectasia: “frog-spawn”
and plaques that may bleed and ulcerate
appearance that follows lymphatic
(Fig. 5.140).
obstruction, e.g. tumour or surgery
(see Fig. 5.138).

Figure 5.139. Kaposi sarcoma. Figure 5.140. Angiosarcoma.

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DERMATOLOGY MADE EASY

The book concludes with a comprehensive section on further investigations and

Reviews of the first edition

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Scion Publishing Limited

Important Note from the Publisher

Typeset by Medlar Publishing Solutions Pvt Ltd, India

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3.7 Erythema multiforme.................................203 5.4 Basal cell carcinoma.....................................320

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If you notice errors or omissions, don’t forget to tell us by emailing info@scionpublishing.com

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5.1 Actinic cheilitis

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Physical treatments for actinic cheilitis include:

What is the outlook for actinic cheilitis?

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5.2 Actinic keratosis

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What is the treatment for actinic

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Figure 5.13. The day of treatment with photodynamic

Prevention of actinic keratoses

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5.3 Ageing skin

What causes the skin to age? Smoking

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How are signs of ageing skin diagnosed?

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5.4 Basal cell carcinoma

What causes basal cell carcinoma?

What are the clinical features of basal cell

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Superficial BCC a Potentially more aggressive than other forms

Figure 5.24. Nodular BCC. Figure 5.26. Morphoeic BCC.

Figure 5.25. Superficial BCC. Figure 5.27. Pigmented BCC.

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Advanced BCC Mohs micrographically controlled excision

What is the treatment for primary

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Targeted therapy refers to the hedgehog

How can basal cell carcinoma

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Figure 5.34. Trichilemmal cyst. Figure 5.36. Milia.

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A The origin of secondary milium is a Trichilemmal cyst

Figure 5.37. Epidermoid cyst. Figure 5.39. Steatocystoma multiplex.

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