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SECTION THREE
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Endocrine and metabolic disorders
421
Box 19.11
History
Patient concerns
Events: life and medical
Glucose diary (urine or blood)
Current treatment
Hypoglycaemia
Driving
Pregnancy/contraception in women
Impotence
Symptoms of coronary artery disease or peripheral
vascular disease
Smoking habit
Examination
Weight/body mass index
Blood pressure: erect and supine
Injection sites
Urinalysis
Eye examination
Foot examination
Tests
Renal function, liver function
Glycated haemoglobin (HbA1c)
Lipids
Urine for albumin excretion
The diabetic annual review
Figure 19.20 Necrobiosis lipoidica diabeticorum.
presenting with coma or reduced conscious level to
have their blood glucose checked immediately.
Characteristically, the cardinal symptoms of severe
polyuria, polydipsia and weight loss will have been
present for some time prior to coma; such symptoms
should never be ignored in a diabetic person. Patients
with acute hyperglycaemic crises are frequently
severely dehydrated, with hypotension (including
postural hypotension), tachycardia, dry mucous
membranes and reduced skin turgor. Other signs
of DKA include rapid deep sighing respiration
(Kussmaul breathing—a respiratory compensation
for metabolic acidosis) and ketones on the breath
(a sweet odour reminiscent of nail polish remover).
Diabetic ketoacidosis can occasionally present with
symptoms of an acute abdomen.
In the non- acute setting, it is desirable for all
patients with diabetes to undergo a full medical
assessment once a year—the so- called diabetic
annual review (Box 19.11).
Skin, nails and hands
Dermatological manifestations of diabetes are
common. Fungal nail infections, particularly of the
feet, are common, as are dermatophyte infections of
the skin of the feet (tinea pedis). Staphylococcal skin
infections leading to pustules, abscesses or carbuncles
can also be seen. Other skin lesions seen in diabetes
include necrobiosis lipoidica diabeticorum (Fig.
19.20). This is a rare complication of diabetes,
Figure 19.21 Granuloma annulare. (Courtesy of Dr David
Peterson.)
predominantly seen in young women aged 15 to 40
years. This presents as a painless red macule, usually
over the anterior shin, which then heals with scarring
to form a yellowish/brown lesion. The condition can
be unsightly, and little effective treatment is available.
Vitiligo is seen in a small number of patients with
type 1 diabetes, reflecting its autoimmune nature.
Diabetic dermopathy is characterized by brown
macules on the lower legs that heal to form
atrophic, shiny white scars. A further skin lesion
seen in patients with diabetes is granuloma annulare,
pale, shiny rings and nodules usually seen on the
arms or hands (Fig. 19.21). Bullosis diabeticorum
is a rare manifestation, characterized by tense
blistering, mainly on the feet. Acanthosis nigricans
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Endocrine and metabolic disorders
Figure 19.22 Acanthosis nigricans.
Figure 19.25 The prayer sign in diabetic cheiroarthropathy.
Figure 19.23 Lipohypertrophy. (Courtesy of Dr David Peterson.)
Figure 19.24 Lipoatrophy. (Courtesy of Dr David Peterson.)
is characterized by a dark velvety appearance in the
axillae or neck of people with insulin resistance (Fig.
19.22) and frequently accompanies type 2 diabetes,
but may occur in people with insulin resistance in
the absence of diabetes.
Diabetic patients treated with insulin should
have their injection sites examined for signs of
lipohypertrophy (a physiological response to insulin
Figure 19.26 Tinel’s sign in carpal tunnel syndrome: tapping on
the median nerve at the wrist induces pain in the median nerve
distribution.
injected near fat cells; Fig. 19.23) or lipoatrophy (an
allergic response to non- human insulins—now rarely
seen) (Fig. 19.24). Continuous glucose monitoring
and continuous subcutaneous insulin infusion
(insulin pump) devices are increasingly common
in people with type 1 diabetes and has transformed
the quality of life and susceptibility to dangerous
hypoglycaemia in many. The sampling and delivery
needles remain in the subcutaneous space for several
days at a time and careful inspection of these sites is
particularly important.
Diabetic cheiroarthropathy (‘stiff hand syndrome’
or ‘limited joint mobility’) is seen in some patients
with long- standing diabetes. It is characterized
by skin thickening and sclerosis of the tendon
sheaths, leading to reduced joint mobility and the
characteristic prayer sign (Fig. 19.25). Examination
of the hands for signs of carpal tunnel syndrome (see
Chapter 16) is important if the patient has suggestive
symptoms. Thus, the presence of Tinel’s sign
Figure 19.27 Phalen’s sign in carpal tunnel syndrome:
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hyperflexion of the wrist leads to pain in the median nerve
distribution.
Endocrine and metabolic disorders
Figure 19.29 Diabetic cataract.
SECTION THREE
423
Figure 19.28 Corneal arcus and xanthelasmata in a patient with
diabetic dyslipidaemia.
(Fig. 19.26) and Phalen’s sign (Fig. 19.27) should be
sought. Thenar eminence wasting may also be seen.
Eyes
Examination of the eyes is mandatory in patients with
diabetes. External examination may indicate signs
of dyslipidaemia (corneal arcus and xanthelasmata;
Fig. 19.28). A reduced pupillary response to
light may indicate autonomic neuropathy. Visual
acuity should be assessed yearly with a Snellen
chart, and unexplained loss of acuity should be
investigated. Fundoscopy should be undertaken with
pharmacological dilatation of the pupils in order to
obtain an adequate view. Loss of the red reflex on
fundoscopy may indicate cataract formation, and the
lens should be assessed for opacities (Fig. 19.29). The
vitreous and retina should be examined carefully,
starting from the optic disc and radiating into each
quadrant of the eye. The macula is examined last,
because this can be quite uncomfortable for the
patient. The use of green light may aid the detection
of microaneurysms. Ideally, all patients with
diabetes should have annual fundal photography. A
Box 19.12
Non- proliferative retinopathy
Microaneurysms
Dot haemorrhages
Hard exudates (lipid deposits) not involving the macula
Mild
<5 microaneurysms
Haemorrhages and/or exudates
Moderate
Extensive (>5) blot haemorrhages and/or
microaneurysms and/or cotton wool spots (retinal
ischaemia)
Venous beading
Looping or reduplication
Intraretinal microvascular anomaly (IRMA)
Severe
Intraretinal deep blocked haemorrhages in four
quadrants
Venous beading in two quadrants
Severe IRMA in one quadrant
Proliferative retinopathy
New vessels on disc (NVD) or elsewhere (NVE)
Maculopathy
Any retinopathy 1 disc diameter around the macula
Focal or exudative maculopathy
Diffuse
Ischaemic
classification of diabetic retinopathy is shown in Box
19.12 (Figs 19.30–19.34).
Characteristic features of diabetic retinopathy
Cardiovascular system
Examination of the heart and vasculature is important
in patients with diabetes. Palpation of peripheral
pulses, especially of the feet, is extremely important,
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Endocrine and metabolic disorders
Figure 19.30 Background retinopathy (dot haemorrhages and
microaneurysms) in the inferior nasal region. (Courtesy of Dr Paul
Dodson.)
Figure 19.33 New vessel formation and laser photocoagulation
burns in severe proliferative retinopathy. (Courtesy of Dr Paul
Dodson.)
Figure 19.31 Preproliferative changes with multiple dot and blot
haemorrhages and cotton wool spots. (Courtesy of Dr Paul Dodson.)
Figure 19.32 Retinal haemorrhage owing to new vessel formation
in severe proliferative retinopathy. (Courtesy of Dr Paul Dodson.)
as is auscultation of the carotid and femoral
arteries to detect bruits. Blood pressure should be
measured frequently in patients with diabetes to
detect hypertension (classed at >140/80 mmHg
Figure 19.34 Exudative diabetic maculopathy. (Courtesy of Dr
Paul Dodson.)
in patients with diabetes) or postural hypotension
(drop in systolic BP >20 mmHg on standing).
A resting tachycardia, loss of sinus arrhythmia
(reflex bradycardia on expiration) and loss of
reflex bradycardia during a Valsalva manoeuvre can
indicate autonomic neuropathy, although these are
best assessed by electrocardiography (ECG).
Feet
The feet of patients with diabetes should be
examined at least once a year. Signs of deformity;
callus (a sign of excessive pressure at this site); fungal
infection, especially between the toes; nail care and
ulceration should be carefully assessed. Peripheral
pulses and nail- fold refill should be assessed for signs
of peripheral vascular disease. Nerve function should
be assessed by testing vibration sense at the great toe,
medial malleolus and knee, and testing fine touch on
the toes, metatarsal heads, heels and dorsum of the
feet with a 10- g monofilament (Semmes Weinstein
monofilament) (Fig. 19.35). Loss of ankle jerks
Figure 19.35 Testing for neuropathy using a Semmes Weinstein
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monofilament giving standard 10 g of fine touch.
is also a sign of early diabetic peripheral sensory
neuropathy.
A complication of diabetic peripheral neuropathy
is the neuropathic joint—Charcot neuroarthropathy
(see Fig. 19.18). This usually affects the ankle and
presents with a painless, swollen, hot red joint,
sometimes with a history of minor local trauma. The
natural history is of progressive deformity until the
process settles, usually over a few months. Untreated,
the joint develops severe deformity, which then puts
the foot at high risk of ulceration, infection and
amputation. Treatment is with immobilization in a
plaster- cast boot and intravenous bisphosphonates.
Diabetic patients with signs of peripheral
vascular disease or peripheral neuropathy, even if
asymptomatic, should be classified as at high risk for
ulceration and be given careful education on foot
care by a podiatrist.
SECTION THREE
Endocrine and metabolic disorders
combination of its longer half- life and the fact that
the liver metabolizes large amounts of portal vein
insulin, but not C- peptide, dictates that it is a good
measure of endogenous insulin secretory capacity.
Close to the diagnosis of type 1 diabetes when there
may be some, but reduced, insulin secretion, levels
of C- peptide can overlap with those seen in type 2
diabetes. However, 3 to 5 years after the diagnosis,
if there is still diagnostic uncertainty between type
1, type 2 or monogenic diabetes, measurement of
C- peptide may be extremely helpful because lowundetectable levels confirm the absolute need for
insulin replacement therapy.
In acute hyperglycaemic decompensation of
diabetes, urgent investigations are required, including
a laboratory glucose estimation, assessment of renal
function (urea and electrolytes), urinalysis testing for
ketones and glucose and arterial blood gas assessment
to determine pH and bicarbonate level. A search for
precipitating causes should be undertaken, including
a chest radiograph, ECG, white cell count and, in
younger women, a pregnancy test.
To reduce the risk of chronic complications, it is
important to ensure a full biochemical assessment
is undertaken yearly as part of an annual diabetic
review. Renal and liver function should be checked,
along with assessment of urine albumin excretion.
Glycaemic control can be assessed using the HbA1c,
which is well correlated to prevailing glycaemic
control over the preceding 10 to 12 weeks. Glycaemic
targets are individualized according to the patient’s
age, comorbid conditions, risk of hypoglycaemia
and the patient’s own preferences. An HbA1c less
than 53 mmol/mol (7.0%) is generally deemed to
show acceptable glycaemic control. Lipid profile
(cholesterol, triglycerides, low- density lipoprotein
(LDL) cholesterol and high- density lipoprotein
(HDL) cholesterol) should be checked yearly.
425
Investigation
Diagnosis of diabetes is based on a fasting plasma
glucose, oral glucose tolerance test (OGTT) or
glycated haemoglobin (HbA1c) using the WHO
criteria (see Box 19.9). Although clinically it is
relatively simple to distinguish between type 1 and
type 2 diabetes, occasionally the diagnosis is not clear,
especially in younger- onset type 2 diabetes without
a family history. In these circumstances, the use of
immunological tests, such as anti- islet cell (ICA),
anti- glutamic acid decarboxylase (GAD), anti- zinc
transporter 8 (ZnT8) or anti- islet antigen- 2 (IA2)
antibody, may be helpful. Positivity of either is a good
indicator of autoimmune islet cell destruction (and
hence probable type 1 diabetes), insulin deficiency
and a subsequent requirement for insulin therapy.
Measurement of C- peptide may also be helpful; this
is the connecting peptide that joins the A and B chains
of insulin in the proinsulin molecule. Insulin and
C- peptide are secreted in equimolar amounts, but a
Communication, phraseology and mental
health
Diabetes is a lifelong condition, with relentless
self- care requirements, from which there are no
holidays. Maintaining euglycaemia whilst avoiding
hypoglycaemia is extremely difficult, particularly
in type 1 diabetes, and oscillations in blood
glucose can be very dispiriting. Although the longterm outcome studies in diabetes relate almost
exclusively to prevailing levels of HbA1c, this can
sometimes translate into this value forming the sole
focus of the clinical interaction, with the unintended
consequence that the person with diabetes feels
‘adversely judged’ if the result is unfavourable. Be
careful when presenting cases to colleagues and
avoid phrases such as ‘poorly controlled diabetic’ or
‘frequent flyer’ if someone has repeated admissions
to hospital. People live with diabetes; they are not
‘diabetics’. Always remember that most people with
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Endocrine and metabolic disorders
diabetes are likely to have more experience and
understanding of the condition than you.
Depression, eating disorders and anxiety are
more common in people with diabetes than in the
background population. The interaction between
insulin replacement therapy and body weight has
potential consequences for mental health and selfesteem. Insulin is an anabolic hormone and its
deliberate omission or restriction by people with
type 1 diabetes can sometimes be used as a strategy
for weight control. Many experienced diabetes
physicians make use of the diabetes distress scale: a
clinical instrument for opening a conversation with
a person with diabetes that uses a 17- item scale to
capture four critical dimensions of distress: emotional
burden, regimen distress, interpersonal distress and
physician distress. Others take a less structured
approach and simply start the consultation with an
open- ended question such as: ‘Before we get on to
the glucose measurements, how is life in general?’
Even if the person with diabetes is coping well and
has no mental health issues, he will appreciate that
you understand living with diabetes is hard work.
Lipid disorders
The two circulating lipids, cholesterol and
triglyceride, are transported within lipoproteins in
the circulation. The apolipoproteins over the surface
of these molecules enable their recognition by cells
in organs such as the liver. Lipid disorders, which are
common, contribute significantly to the burden of
cardiovascular disease. Primary lipid disorders are
usually inherited, whereas secondary disorders are
acquired as a result of other medical disorders, such
as thyroid disease, diabetes, liver disease, nephrotic
syndrome or alcohol excess.
History
Lipid disorders rarely cause significant symptoms,
unless the patient presents with an acute feature,
such as acute pancreatitis or myocardial infarction.
Thus, any previous history of vascular disease or acute
abdominal pain should be sought. Acute pancreatitis,
a rare complication of severe hypertriglyceridaemia,
presents with acute, severe, generalized abdominal
pain. Although alcohol and cholelithiasis are the
two most common causes of acute pancreatitis,
hypertriglyceridaemia is a well- recognized and
easily overlooked cause of the condition; any patient
presenting with acute pancreatitis should have his
serum lipids checked.
In the assessment of patients with lipid disorders, it
is important to enquire about symptoms of ischaemic
heart disease (chest pain history, admissions for
ischaemic heart disease and any cardiological/
cardiothoracic interventions), peripheral
vascular disease (intermittent claudication) and
Figure 19.36 Tendon xanthoma of the hands. (Courtesy of Dr
David Peterson.)
cerebrovascular disease (transient ischaemic attacks,
amaurosis fugax and strokes). Other cardiovascular
risk factors should also be assessed. The smoking
history is very important and a family history
of premature vascular disease (under the age of
55 years) should be carefully sought. In familial
hypercholesterolaemia, half of men and a fifth of
women die before the age of 60 from coronary
artery disease. Possible symptoms of secondary
causes should also be assessed. Thus, symptoms of
hypothyroidism (above), diabetes (above), renal
failure or nephrotic syndrome (see Chapter 17) and
liver disease (see Chapter 14) should be sought.
Alcohol intake and dietary history should also be
assessed.
Examination
The diagnostic hallmark of familial hypercholesterolaemia is tendon xanthomata. These are
localized infiltrates of lipid- containing macrophages
that resemble atherosclerotic plaques; they
develop from the third decade onwards. The most
common sites are the Achilles tendon and the
extensor tendons of the hands, particularly over the
knuckles (Fig. 19.36). Other sites include the tibial
tuberosities, at the site of insertion of the patellar
tendon (subperiosteal xanthomata) or at the triceps
tendon at the elbow.
As the cholesterol deposition is deep within
the tendon and the swelling is fibrous, tendon
xanthomata are felt as hard nodules along the length
of the tendon. They occasionally become inflamed,
and a tenosynovitis develops. On the extensor
surface of the hands, they may overlie the knuckle
and be very hard and quite easy to miss.
Xanthelasmata are deposits of lipid in the skin of
the eyelids, more commonly the upper rather than
the lower (see Fig. 19.28). Although a dramatic sign,
they are not present in the majority of patients with
familial hypercholesterolaemia. More common is a
corneal arcus, seen as a rim of lipid deposit around
the iris (see Fig. 19.28). This can be seen at any
age, although it is more common in older people;
Figure 19.37 Eruptive xanthomata in severe
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hypertriglyceridaemia. (Courtesy of Dr David Peterson.)
Figure 19.38 Lipaemia retinalis. (Courtesy of Dr Paul Dodson.)
only in the minority is this sign associated with
hypercholesterolaemia.
The characteristic sign of hypertriglyceridaemia
is eruptive xanthomata (Fig. 19.37). These are
yellow nodules or papules that usually appear on
the extensor surface of the elbows, knees, buttocks
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Endocrine and metabolic disorders
and back. Striate palmar xanthomas are yellowish
discolouration of the skin creases, usually seen best in
the hands; they are caused by hypertriglyceridaemia.
In severe forms of hypertriglyceridaemia,
hepatosplenomegaly may be seen. Fundoscopy in
severe hypertriglyceridaemia may show lipaemia
retinalis, characterized by optic pallor and the retinal
vessels appearing white (Fig. 19.38).
A careful cardiovascular examination should
be performed in all patients with significant
hyperlipidaemia, including a search for carotid
or femoral bruits and signs of peripheral vascular
disease. Patients with homozygous familial
hypercholesterolaemia may have signs of aortic
stenosis.
427
Investigation
All patients with lipid disorders should undergo a
fasting lipid profile, composed of total cholesterol,
LDL cholesterol, HDL cholesterol and triglycerides.
In severe hypertriglyceridaemia, the serum may
become turbid and take on the appearance of
milk. Investigations to exclude secondary causes
should include thyroid, liver and renal function and
fasting glucose. Resting or exercise ECG may be
checked to look for signs of ischaemic heart disease.
Genotyping to determine the type of familial lipid
abnormality may be required, especially for familial
hypercholesterolaemia, although usually this is
available only in specialist centres.
Acute pancreatitis can be diagnosed using
serum amylase or lipase, which is frequently
very elevated in the condition. In severe hypertriglyceridaemia, however, falsely low serum
amylase can lead to diagnostic confusion, because
triglycerides interfere with the amylase/lipase
assay. Severe hypertriglyceridaemia can lead to a
pseudohyponatraemia, and care should be exercised
when interpreting serum sodium levels in the
condition.
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BASIC SYSTEMS
Skin, nails and hair
Rino Cerio
20
Introduction
The skin is the largest organ in the human body.
Forming a major interface between man and his
environment, it covers an area of approximately 2 m
and weighs about 4 kg. The structure of human skin
is complex (Figs 20.1 and 20.2), consisting of four
distinct layers and tissue components with many
important functions (Box 20.1). Reactions may occur
in any of the components of human skin and their
clinical manifestations reflect, among other factors,
the skin level in which they occur, and sometimes
they act as a ‘window’ of systemic changes elsewhere
in the body, e.g. medical conditions discussed
later in the chapter, such as those associated with
pruritus (see Box 20.9), systemic causes of erythema
nodosum (see Box 20.10) or paraneoplastic skin
conditions (Box 20.2).
The accurate diagnosis of most skin lesions requires
an adequate history, careful examination of the
patient and, occasionally, laboratory investigation,
but dermatology is predominantly a visual specialty.
History
Detailed information should be sought concerning
the present skin condition. This should include the
site of onset, mode of spread and duration of the
disorder. Any personal history or family history of
skin disease, including skin cancer and atopy (an
allergic skin reaction becoming apparent more or
less immediately on contact), is important. Previous
medical conditions should be noted and a full
drug history obtained, including the use of overthe- counter and other preparations. The social and
occupational history and, in some circumstances,
details of recent travel, environmental exposure,
especially sunshine and artificial ultraviolet light,
and sexual activity are often important (Box 20.3).
Examination
The whole skin, including hair, nails and assessable
mucosae, should be fully inspected (preferably in
natural light), but the patient’s modesty should
be protected. Sometimes a magnifying lens or
dermatoscope is useful.
Colour and pigmentation
Before inspecting any rash or lesion, note the colour
of the skin. Normal skin colour varies, depending on
lifestyle and light exposure as well as constitutional
and ethnic factors.
Pallor can have many causes. It may be:
Temporary, owing to shock, haemorrhage or
intense emotion
Persistent, owing to anaemia or peripheral
vasoconstriction
Vasoconstriction is seen in patients with severe
atopy—an inherited susceptibility to asthma,
eczema and hay fever. Pallor is a feature of anaemia,
but not all pale persons are anaemic; conjunctival
and mucosal colour is a better indication of
anaemia than skin colour. A pale skin resulting from
diminished pigment occurs with hypopituitarism
and hypogonadism.
Normal skin contains varying amounts of brown
melanin pigment. Brown pigmentation owing to
deposited haemosiderin is always pathological.
Albinism is an inherited generalized absence of
pigment in the skin; a localized form is known as
piebaldism. Patches of white and darkly pigmented
skin (vitiligo) (Fig. 20.3) are owing to a local
and complete absence of melanocytes. Several
autoimmune endocrine disorders are associated with
vitiligo.
Abnormal redness of the skin (erythema) is seen
after overheating, extreme exertion and sunburn
and in febrile, exanthematous and inflammatory
skin diseases. Flushing is a striking redness, usually
of the face and neck, which may be transient
or persistent. Local redness may be caused by
telangiectasia, especially on the face. Cyanosis is a
blue or purple- blue tint caused by the presence of
excessive reduced haemoglobin, either locally, as in
impaired peripheral circulation, or generally, when
oxygenation of the blood is defective. The skin
colour in methaemoglobinaemia is more leaden than
in ordinary cyanosis; it is caused by drugs, such as
dapsone, and certain poisons.
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Skin surface
Keratinocytes
Subcutaneous
Erector pilorum
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Skin, nails and hair
Epidermis
Capillary loop
Sebaceous
gland
Dermis
tissue
Figure 20.1 The anatomy of the full thickness of the skin in section.
Stratum
corneum
Langerhans’
cell
Basal cell
layer
Melanocyte
Figure 20.2 The anatomy of the epidermis.
Basement
membrane
Jaundice varies from the subicteric lemon- yellow
tints seen in pernicious anaemia and haemolytic
jaundice to various shades of yellow, orange or dark
olive- green in obstructive jaundice. Jaundice, which
stains the conjunctivae, must be distinguished from
the rare orange- yellow of carotenaemia, which does
Hair follicle
muscle
Eccrine sweat
gland
Hair matrix
Box 20.1
Functions of the human skin
Protection: physical, chemical, infection—immune and
innate
Physiological: homoeostasis of electrolytes, water and
protein
Thermoregulation
Sensation: specialized nerve endings—pain, touch and
temperature
Lubrication and waterproofing: sebum
Immunological reactions: Langerhans’ cells,
lymphocytes, macrophages
Wound healing
Ultraviolet- induced vitamin D synthesis
Body odour: apocrine glands
Psychosocial: cosmetic
not. Slight degrees of jaundice cannot be seen in
artificial light.
Increased pigmentation may be racial, owing
to sunburn or connected with various diseases.
In Addison’s disease, a brown or dark- brown
pigmentation affects exposed parts and parts not
normally pigmented, such as the axillae and the
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Skin, nails and hair
431
Box 20.2
Paraneoplastic skin disorders
Dermatosis Associated tumour
Dermatomyositis Lung, gastrointestinal (GI)
tract, genitourinary tract
Acanthosis nigricans GI tract, lung, liver
Paget’s disease of the
Adenocarcinoma
nipple/extra- mammary
Paget’s disease of the
perineum
Erythroderma Haematological
Tylosis- thickening of palms
Oesophageal carcinoma
and soles
Ichthyosis Lymphoma
Erythema gyratum repens Lung, breast
Necrolytic migratory
Glucagonoma
erythema
Box 20.3
Approach to dermatological patient history
Time course of skin eruption
Distribution of lesions including initially
Symptoms: pruritus
Family history: atopy and psoriasis
Drug/allergy history
Past medical history
Contacts: family and partners
Provocating factors: sunlight and foods
Previous and current treatments
Figure 20.3 Vitiligo, a disorder of cutaneous pigmentation that is
often autoimmune in origin and associated with other autoimmune
disorders.
palmar creases; the lips and mouth may exhibit
dark bluish- black areas. Note, however, that mucosal
pigmentation is a normal finding in a substantial
proportion of black patients.
More or less generalized pigmentation may also be
seen in the following:
Haemochromatosis, in which the skin has a
peculiar greyish- bronze colour with a metallic
sheen, owing to excessive melanin and iron
pigment
Chronic arsenic poisoning, in which the skin
is finely dappled affecting covered more than
exposed parts
Argyria, in which the deposition of silver in the
skin produces a diffuse slate- grey hue
The cachexia of advanced malignant disease
In pregnancy, there may be pigmentation of
the nipples and areolae, of the linea alba and
sometimes a mask- like pigmentation of the face
(chloasma). Chloasma may also be induced by
oral contraceptives containing oestrogen. A similar
condition, melasma, may be seen in Asian and AfroCaribbean males.
Localized pigmentation may be seen in pellagra
and in scars of various kinds, particularly those owing
to X- irradiation therapy. Venous hypertension in
Figure 20.4 Flat- topped papules of lichen planus.
the legs is often associated with chronic purpura,
leading to haemosiderin pigmentation. The mixture
of punctate and fresh purpura and haemosiderin
may produce a golden hue on the lower calves and
shins. Pigmentation may also occur with chronic
infestation by body lice. Erythema ab igne, a
reticular pattern of pigmentation, can be seen in
patients who use local heat to relieve chronic pain
or on the shins of people who habitually sit too
near a fire. Livedo reticularis, a web- like pattern of
reddish- blue discolouration mostly involving the
legs, occurs in autoimmune vasculitis, especially
in systemic lupus erythematosus (SLE) and
antiphospholipid syndrome, when it is associated
with cerebral infarction. The violet- coloured lesions
of lichen planus are slightly raised, flat- topped
papules (Fig. 20.4). Psoriasis usually presents as a
symmetrical plaque on extensor surfaces (Fig. 20.5).
Keloid consists of raised and inflamed, overgrown
tender scar tissue (Fig. 20.6). Dermatomyositis
often produces swelling and heliotrope- coloured
erythema of the eyelids without scaling of the skin.
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