SKIN SYMPTOMS DUE TO DIABETIC
VASCULAR ABNORMALITIES Diabetic microangiopathy Both small and large blood vessels are affected in diabetes
In diabetic microangiopathy, there is proliferation of
endothelial cells and deposits of PAS-positive material in
the basement membrane of arterioles, capillaries and
venules with resulting decreased luminal area .
Basement membrane thickening is a characteristic finding
in diabetic and prediabetic patients
Microangiopathy is responsible for the retinopathy,
nephropathy and possibly also neuropathy and
dermopathy associated with diabetes.
Erysipelas-like erythema –
This condition is seen mostly in elderly diabetic
patients with an average duration of diabetes mellitus
of 5 years.
Well-demarcated, red areas occur on the legs or feet,
and there may be underlying destructive bone disease
caused by a small vessel insufficiency.
Wet gangrene of the
foot This is a late
manifestation of diabetic
tend to develop a dry
form as a result of large
Diabetic rubeosis –
A peculiar rosy reddening
of the face, and sometimes
of the hands and feet, may
be seen in long-standing
The changes have been
attributed to decreased
vascular tone or diabetic
Diabetic dermopathy (diabetic shin spots) This is the most common dermatosis associated with
Microangiopathy and neuropathy are involved .
Lesions are predominantly situated on the shins, forearms,
thighs and over bony prominences.
The initial lesion is an oval, dull-red papule 0.5–1 cm in
diameter. It evolves slowly, producing a superficial scale,
leaving an atrophic brownish scar.
The colour is due to haemosiderin in histiocytes near the
Large vessel disease –
Atherosclerosis is the second form of vascular disease
frequently associated with diabetes mellitus.
The patient shows intermittent claudication with
pallid and cool skin distally on the extremities.
Common clinical sequelae are myocardial infarction,
cerebral thrombosis, nephrosclerosis and ischaemic
gangrenous lesions of the legs and feet.
There is a distal symmetrical polyneuropathy with mixed
motor and sensory nerve involvement.
The motor neuropathy of the foot is characterized by
dorsally subluxed digits, distally displaced plantar fat pads,
depressed metatarsal heads, hammer toes and pes cavus .
A painless and slowly penetrating ulcer of the sole and of
other pressure sites is suggestive of diabetic neuropathy.
The ulcer is circular and punched out in shape, occurring
in the middle of a callosity .
An initial subepidermal haemorrhagic bulla may
give rise to discoloration of the surrounding skin.
Loss of temperature and pain sensation and absence of
the ankle reflex (an early sign of diabetic neuropathy)
indicate a neuropathic origin.
Sensory abnormalities of the lower extremities include
numbness, tingling, aching and burning.
Burning feet and restless legs are common complaints.
Damage to autonomic nerves of the skin in chronic
advanced cases is manifested by oedema, erythema
Complex nature of diabetic foot requires special
There is a multifactorial aetiology.
Predisposing factors include abnormal plantar
pressure points, foot deformities and minor trauma
Cutaneous infections in diabetes
Skin infections due to Staphylococcus aureus and group A
Streptococcus haemolyticus are common in diabetic
infections causing severe furuncles, carbuncles and styes
were frequent among diabetic individuals.
Invasive Pseudomonas infection of the ear can progress
through cellulitis and osteitis to cranial nerve damage and
meningitis with a high mortality rate, so-called malignant
Non-clostridial gas gangrene This complication develops in the soft tissues near a
gangrenous focus. It was diagnosed in 17% of diabetics
who were admitted to hospital because of gangrene or
The commonest pathogens are Escherichia coli,
Klebsiella, Pseudomonas and Bacteroides spp. in
Candida albicans Candida albicans infections of mouth, nail folds, genitals
and intertriginous skin areas are frequent in diabetics.
Candidiasis may be the presenting feature of diabetes, and
is frequently seen in diabetic patients whose disease is not
A high glucose level of the saliva seems to account for
the oral infection .
Phimosis is a common complaint of diabetic men, and
recurring candidal infection is usually the cause.
Insulin resistance and acanthosis
Acanthosis nigricans is characterized by symmetric, velvety
to verrucous, hyperkeratotic and hyperpigmented plaques
that have a predilection for the axillae, the nape, and other
High plasma levels of insulin are thought to contribute to
the development of acanthosis nigricans.
Various skin disorders associated
with diabetes mellitus
Necrobiosis lipoidica Frequencies of diabetes between 42% and 62% have been
reported in patients with necrobiosis lipoidica.
whereas necrobiosis lipoidica is uncommon (0.3%) among
Nonscaling plaques with a yellow atrophic center, surface
telangiectases, and an erythematous or violaceous border
that may be raised.
yellow aspect in central area
of the lesions is most likely
due to thinning of the dermis,
making subcutaneous fat
Ulceration occurs in up to
35% of cases.
Disseminated granuloma annulare –
This is rarely seen in diabetic patients
Pruritus. Pruritus was once considered a typical symptom of
The frequency of generalized pruritus in diabetic
patients is unknown.
Anogenital pruritus may be due to secondary infection
with candidiasis or haemolytic streptococci.
Stiff joints and waxy skin Waxy tight skin on the backs of the hands and limited
joint mobility may be seen in patients with insulindependent diabetes
diabeticorum The most common sites of
are the neck and upper
The condition is mainly
seen in overweight adults
with non-insulindependent diabetes, is
painless and causes no
Finger pebbles Thickening of the skin on
the dorsum of the hand
due to many causes,
diabetes among them, is
often manifest by a
pebbling of the skin on the
Skin tags Skin tags are small, soft,
occurring on eyelids, neck
and axillae, often
associated with obesity.
of the skin Eruptive xanthomas may
develop in diabetic
lesions slowly resolve when
the diabetes is properly
Vitiligo occurs more frequently in diabetic individuals. In
late-onset diabetes, a 4.5% frequency has been reported .
Lichen planus –
An increased incidence of abnormal glucose tolerance
tests in patients with lichen planus, especially oral lichen
planus, has been reported .
The overall support for a true association seems limited .
Haemochromatosis - The main symptoms are liver
disease, hyperpigmentation, joint disease, hypogonadism
and eventually, diabetes.
Diabetic bullae Diabetic bullae are uncommon,
but believed to be a distinct
marker for diabetes .
The location is the lower legs
and feet, occasionally hands and
They range in size from less
than one centimetre to several
A typical blister arises on a noninflamed base, and heals
without scarring in 2–5 weeks.
There have been reports of
perforating collagenosis in
patients with diabetes with
and without renal insuffi
The cause is attributed to
and lesions are due to
minor injury such as
pressure or scratching
Insulin lipodystrophy Insulin lipodystrophy is
Patients present with
atrophic plaques at the
sites of insulin injection.
There is atrophy of the
Local insulin reactions –
Insulin may cause immediate local reactions, starting as
erythema, which turn urticarial within 30 min and subside
within an hour; these are probably IgE mediated.
Serious generalized immediate reactions are rare.
The most common reactions are delayed, starting about 2
weeks after onset of insulin therapy.
An itchy nodule develops at the site of injection.
It lasts for days and heals with hyperpigmentation
and perhaps a scar.
Delayed hypersensitivity is involved.
This condition is due to insufficient secretion or supply of
adrenocortical hormones or hormonal compounds—
mainly cortisol and mineralocorticoids.
General symptoms include wasting, fatigue, orthostatic
hypotension, dizziness, anorexia, abdominal pain and
Self-mutilation, presenting as gouges in the skin, has been
reported as a result of psychiatric symptoms
hyperpigmentation of the skin, due to increased secretion
of pituitary MSH and ACTH as a response to low adrenal
corticosteroid levels, is the cardinal dermatological feature.
In women, in whom the adrenal gland is the main
source of androgens, there may be loss of axillary
and pubic hair and improvement in acne.
Features of associated autoimmune disease may be
present, notably vitiligo in 15% of patients with
Cushing’s disease and syndrome
Chronic glucocorticoid excess may occur due to
Increased secretion of adrenocorticotrophic
hormone (ACTH, corticotrophin), usually from the
2. Glucocorticoid hypersecretion of adrenal origin .
3. Exogenous administration of glucocorticoids.
Skin manifestations of thyroid dysfunction may be
divided into three categories:
(1) Direct action of thyroid hormone on skin tissues
(2) Skin manifestations of direct thyroid hormone
action on non-skin tissues
(3) Autoimmune skin disease associated with thyroid
dysfunction of autoimmune etiology
Direct thyroid hormone action on skin tissues
-Coarsened, thin, scaly skin
-Non-pitting edema (myxedema)
-Edema (hands, face, eyelids)
Hair and Nail Changes
-Dry, brittle, coarse hair
-Loss of lateral third of eyebrows
-Coarse, dull, thin, brittle nails
Clubbing of the fingers and toes in Graves’ disease,
associated with soft-tissue swelling of hands and feet and
with periosteal new bone formation, is termed thyroid
It occurs in less than 1% of thyrotoxic patients, and is
usually associated with exophthalmos and pretibial
myxoedema (Diamond’s triad).
The proximal phalanges and first or second metacarpals
are most commonly affected.
Most patients have minimal or no symptoms, but in those
with symptoms, stiffness is the most frequent.
Localized oedematous and thickened pretibial plaque
formation occurs in 1–10% of patients with
It is usually a late feature, occurring after
ophthalmopathy and diagnosis of hyperthyroidism.
Also occurs on the dorsum of the hallux, and may
affect other sites, including the lower abdomen, arms,
shoulders, neck and pinnae.
Clinical features The lesions first appear on the anterolateral aspect of
the lower limbs and only later extend to the back of
the legs, and feet .
The nodules are pink or skin-coloured, sometimes
yellow-brown and waxy, with prominent hair follicles
giving a ‘peau d’orange’ appearance.
They may occur in old or recent scars
localized pruritus or hypertrichosis over the lesions may be
localized hyperhidrosis has also been reported .
Three clinical types are recognized:
(1) Sharply circumscribed, in which both nodular and
tuberous lesions appear on the shins and toes
(2) Diffuse, producing solid non-pitting oedema of the shins
(3) Elephantiasic, in which there is both oedema and nodule
Excessive secretion of growth hormone (GH, somatotrophin)
causes an increase in plasma insulin-like growth factor-1 (IGF-1).
These hormones stimulate synthesis of collagen and
glycosaminoglycan in the skin and skeleton, leading to insidious
hypertrophy of skin, subcutaneous tissues and viscera, and to
periosteal bone growth.
This causes acromegaly in the adult
Gigantism in children whose bony epiphyses have not yet closed.
Acromegaly and gigantism
Periosteal new bone formation of the facial bones and skin
causes the characteristic facies.
Features are prognathism, frontal bossing, widely spaced
teeth and acral hypertrophy,
which causes elongated, blunt and thickened fingers.
Dermatological features include a protruding, thickened
lower lip, oedematous thick eyelids, a large and furrowed
tongue, triangular large ears, numerous skin tags (‘fibroma
widened skin pores, wet and oily skin due to hyperhidrosis
and increased sebum production, acne and cutis gyrata of
the scalp in more extreme cases.
Eruptive seborrhoeic keratoses mimicking the sign of
Leser–Trélat have been reported in acromegaly .
Hyperpigmentation develops in about half of the affected
individuals due to increased levels of melanocytestimulating hormone (MSH), and acanthosis nigricans may
The scalp hair is initially coarse and there may be
hirsutism, but later in the disease there is a decrease in
gonadotrophin production, which causes the hair to
become finer, with loss of secondary sexual hair.
The nails are flat and wide and grow fast.
Non-cutaneous features include macroglossia, visual
field defect and headache due to the neoplasm,
arthropathy, carpal tunnel syndrome and proximal
Cardiovascular morbidity and mortality is markedly
Insufficiency of the adenohypophysis (anterior pituitary) may
involve individual or multiple hormones.
In classical hypopituitarism, all endocrine cell functions of the
pituitary gland are involved to a varying degree.
Pallor of the skin due to decreased MSH secretion results in
generalized hypopigmentation, most apparent in the skin of the
nipple areola and genitalia; in contrast with anaemia, the
mucous membranes retain their normal colour.
There is an increased sunburn tendency and lack of tanning, and
there may be a degree of carotenaemia due to hypothyroidism.
Loss of terminal hair due to decreased gonadotrophin
secretion is observed in all patients, fi rst in the axillae
and later, but not invariably, in the pubic area.
Fine wrinkling and dryness of the skin simulates
The face appears expressionless due to diminution of
the facial skinfolds.
The activity of sebaceous and sweat glands is reduced.
Pituitary dwarfism is characterized by proportionate
retardation of somatic growth in conjunction with
normal mental development.