DERMATOLOGICAL DISORDERS

ACNE VULGARIS
• Acne is an inflammatory eruption almost ubiquitous in the
teenage years, characterised clinically by open comedones
(blackheads), closed comedones (white heads) and seborrhoea.
• More severe manifestations include inflammatory papules,
pustules, nodules and cysts. The latter may cause significant
scarring. The distribution is predominantly on the face,
shoulders, upper chest and back. There are three pathogenetic
factors:
• • Elevated sebum excretion.
• • Occlusion or blockage of the pilosebaceous unit.
• • Colonisation with Propionibacterium acnes.
 Management
• • Mild disease may be treated with topical antibiotics such as
erythromycin, dessicants such as benzoyl peroxide, or topical
retinoids.
• • Oral antibiotics, particularly of the tetracycline group, are
used as prolonged courses for more stubborn disease.
• • The anti-androgenic oral contraceptive Dianette (cyproterone
acetate with ethinylestradiol) is also an option in female
patients.
• • For the most severe cases, oral retinoid therapy with isotretinoin
has revolutionised the management of acne. The side-effect profile
includes drying of the skin and mucous membranes but this is
generally manageable. Isotretinoin may elevate serum
triglycerides and derange liver function; both should be checked
prior to commencing the drug. Isotretinoin is highly teratogenic,
and female patients must be counselled about this prior to
commencing treatment.
 PSORIASIS
• Psoriasis is a non-infectious, chronic inflammatory disease of the
skin, characterised by well defined erythematous plaques with
silvery scale, which have a predilection for the extensor surfaces
and scalp, and by its chronic fluctuating course. The prevalence is 2%
in European populations, but less in African and Asian populations.
• Pathology reveals keratinocyte proliferation and an inflammatory
infiltrate.
• The cause is unknown, but there is a large familial component.
Precipitating factors include:
• • Trauma.
• • Intercurrent infection.
• • Certain drugs (β-blockers, antimalarials, lithium).
• • Stress/anxiety.
• There are five main clinical presentations:
 Stable plaque psoriasis: This the most common type, consisting of
the well-recognised salmon-pink plaques with silvery scale
arising on the elbows, knees and back (Fig. 17.6). The scalp is
involved in ∼60% of patients. Nail disease is common, with
pitting of the nail plate, onycholysis or subungual hyperkeratosis
(Fig. 17.7). Psoriasis of the flexures (e.g. natal cleft, axillae,
submammary folds) looks red, shiny and symmetrical, but not scaly.
 Guttate psoriasis: This occurs more frequently in children and
adolescents, and often follows a streptococcal sore throat. The
onset is rapid, and the lesions consist of small raindrop-sized scaly
plaques. Guttate psoriasis responds well to phototherapy. The
majority of these patients later develop plaque psoriasis.
 Erythrodermic psoriasis: This is one of the dermatological
emergencies. Over 90% of the body surface becomes erythematous
and scaly. It is often accompanied by systemic upset due to the high
losses of heat and fluid from the inflamed skin.
 Pustular psoriasis: This may be generalised or localised. The rare
generalised form is a dermatological emergency, presenting with large
numbers of sterile pustules on an erythematous base. The patient is
unwell with swinging pyrexia, and requires hospital admission. The
localised form is less serious, though extremely uncomfortable, and
generally affects the palms and the soles (palmoplantar pustulosis).
This condition particularly affects middle aged female smokers.
 Psoriatic arthropathy: This involves joints.

Diagnosis and management

• The diagnosis is clinical.
• Management depends on the patient, his or her expectations, the subtype
of psoriasis and the extent of the disease. Limited chronic plaque psoriasis
should be manageable with topical agents only, whereas more
extensive disease may require phototherapy or systemic agents.
Inpatient treatment with a combination of dithranol and UVB (Ingram’s
regimen) is an excel-lent and safe option, which can clear psoriasis.
 Topical agents: Dithranol, tar, and vitamin D analogues
(calcitriol, calcipotriol) all reduce plaques. Corticosteroids
should be used sparingly, mainly for flexures.

 Phototherapy: UVB or psoralen (photosensitiser) plus UVA

(PUVA) are effective in moderate to severe psoriasis, but
carry a long-term risk of skin cancer.

 Systemic agents: Acitretin (a retinoid), methotrexate and

ciclosporin are effective but may cause significant side
effects.

 Newer biological agents: Infliximab, etanercept and

efalizumab may be considered when other treatments have
failed.
 BOILS & CARBUNCLES
FOLLICULITIS, FURUNCLES AND CARBUNCLES
• Folliculitis can be superficial, involving just the ostium of the hair follicle (folliculitis), or
deep (furuncles and carbuncles).

 Superficial folliculitis: This is an extremely common condition that can be subacute or

chronic. It is often infective, caused by Staph. aureus, but can also be due to
physical (e.g. traumatic epilation) or chemical (e.g. mineral oils) injury. In these cases
the folliculitis is usually sterile. Staphylococcal folliculitis is most common in children
and often occurs on the scalp or limbs. The pustules usually heal in 7–10 days but can
become more chronic, and in older children and adults can progress to a deeper form of
folliculitis.

 Deep folliculitis (furuncles and carbuncles): A furuncle (or boil) is an inflammatory

nodule, follicularly based, which becomes pustular and fluctuant and is often exquisitely
tender. The lesions eventually rupture to discharge pus and, because they are deep,
leave a scar. They can progress to form a carbuncle, which is an exquisitely tender
nodule, often on the neck, shoulders or hips and associated with severe
constitutional symptoms. It implies the involvement of several contiguous hair follicles.
Treatment, as for furuncles, is with an appropriate anti-staphylococcal antibiotic.
 ALOPECIA
• The term means nothing more than loss of hair and is a sign rather
than a diagnosis. There are many causes and patterns, but an important
distinction is whether the alopecia is scarring or non-scarring.
• The causes of alopecia are summarised in Box 17.7; the most common
are discussed here.
 Tinea capitis: Fungal scalp infection is increasingly common in the UK. Any
patient developing an area of hair loss and scaling in the scalp should have
the area scraped and affected hairs plucked for mycological
examination.
 • Endothrix (within the hair shaft) infections, e.g. Trichophyton tonsurans,
cause relatively uninflamed patchy baldness with breakage of the hairs
at the skin surface (‘black dot’). There is no fluorescence under Wood’s light.
 • Ectothrix (outside the hair shaft) species of fungi, such as Microsporum
audouinii, show minimal inflammation, although M. canis infections (from
dogs and cats) are more inflamed and can be identified by green
fluorescence with Wood’s light.
 Kerions are boggy, highly inflamed areas of tinea capitis and are usually
caused by zoophilic fungi (from animals, e.g. cattle ringworm, T.
verrucosum). Treatment is systemic, with oral terbinafine, griseofulvin or
itraconazole. Topical therapy with an antifungal shampoo is
recommended as an adjunct and arachis oil (Peanut oil) is used to
remove crusting.

 Alopecia areata: This non-scarring condition appears as sharply defined,

non-inflamed bald patches, usually on the scalp. During the active stage
of hair loss pathognomonic ‘exclamation mark’ hairs are seen
(broken-off hairs 3–4 mm long, which taper off towards the scalp). The
condition may affect the eyebrows, eyelashes and beard. The hair
usually regrows spontaneously in small bald patches, but the
outlook is less good with larger patches and when the alopecia
appears early in life or is associated with atopy. Alopecia totalis
describes complete loss of scalp hair and alopecia universalis
complete loss of all hair. There is an association of alopecia areata
with autoimmune disorders, atopy and Down’s syndrome.
 Androgenetic alopecia: Male-pattern baldness is physiological in men >20 yrs
old, although rarely it may be extensive and develop at an alarming pace in the late
teens. It also occurs in females, most obviously after the menopause. The
distribution is of bitemporal recession and then crown involvement.

Investigations
• • Laboratory tests, including an FBC, ESR, U&Es, LFTs and TFTs, an
autoantibody profile and, in cases where lupus or lichen planus is suspected, a biopsy
should allow a diagnosis to be reached in most cases.
• • Mycological assessment is advisable in cases of localised hair loss with scaling.

Management
• • Specific causes such as fungal infection should be treated.
• • Alopecia areata sometimes responds to topical or intralesional corticosteroids,
such as 0.3 ml triamcinolone (10 mg/ml).
• • Some males with androgenetic alopecia may be helped by systemic finasteride or
topical 2% minoxidil solution.
• • In females, anti-androgen therapy such as cyproterone acetate is sometimes
useful.
• • A wig may be the most appropriate treatment for extensive alopecia.
 MYCOSIS FUNGOIDES
(CUTANEOUS T-CELL LYMPHOMA )
• In contrast to B-cell lymphomas, which usually present as sudden
focal skin tumours, cutaneous T-cell lymphoma often has an indolent
course, developing slowly over many years from polymorphic patches
and plaques through to nodules and then a systemic stage. Given
that it can appear clinically similar to a number of other more
common inflammatory skin conditions such as eczema and
psoriasis, a high index of suspicion is required for diagnosis.
• Staging with CT may be required.
• Treatment options include corticosteroids and phototherapy in early-
stage disease. Chemotherapy and physical therapies such as
radiotherapy and electron beam radiotherapy are reserved for more
advanced disease.
 POLYMORPHIC LIGHT ERUPTIONS
• Polymorphous light eruption, also known as polymorphic light eruption, is a rash
caused by sun exposure in people who have developed sensitivity to sunlight.

 Sign & Symptoms

• The term "eruption" refers to the rash, which usually appears 30 minutes to
several hours after exposure to sunlight. The rash typically appears on areas of the
body that tend to be covered during winter but exposed in summer: the upper
chest, front of the neck and arms.
• Characteristics of the rash may include:
 Dense clusters of small bumps and blisters
 Red, raised rough patches
 Itching or burning

• Rarely people may have other signs or symptoms, such as fever, chills, headache
or nausea. These conditions may be the result of an associated sunburn rather
than polymorphous light eruption.
 Causes
• The exact cause of polymorphous light eruption isn't well-understood. The
rash appears in people who have developed sensitivity to components of
sunlight, and in particular ultraviolet (UV) radiation from the sun or other
sources, such as tanning beds or tanning lamps. This sensitivity is called
photosensitivity. It results in immune system activity that causes a rash.

 Risk factors
• Anyone can develop polymorphous light eruption, but several factors are
associated with an increased risk of the condition:

 Being female
 Experiencing the first episode during the teenage years or 20s
 Having light skin and living in northern regions
 Having a family history of the condition

 Diagnosis is by history & Examination or may need; Skin Biopsy, Blood Tests
or Photo Testing.
 Treatment
• Treatment of polymorphous light eruption usually isn't necessary
because the rash typically goes away on its own within 10 days.
• In case of severity Corticosteroids (Local or Systemic) can be
used.
• Treatment is also available to help prevent a rash like
Phototherapy.
 VITILIGO
• Vitiligo is an acquired condition in which circumscribed
depigmented patches develop; it affects 1% of the population world-
wide.
Clinical assessment: Segmental vitiligo is restricted to one part of
the body but not necessarily a dermatome. Generalised vitiligo is
often symmetrical and frequently involves the hands, wrists, knees and
neck, as well as the area around the body orifices. The hair of the scalp
and beard may also depigment (Fig. 17.3). The patches of
depigmentation are sharply defined. Some spotty perifollicular
pigment may be seen within the depigmented patches and is
sometimes the first sign of repigmentation. Sensation in the
depigmented p atches is normal (in contrast to tuberculoid leprosy). The
course is unpredictable but most patches remain static or enlarge;
a few repigment spontaneously.
Management: This is unsatisfactory. Patients should be
warned that their patches of vitiligo will be more
susceptible to sunburn, and should take appropriate
precautions. Camouflage cosmetics are found useful by
some patients. Phototherapy can produce some
successful results, but must be used cautiously due to
the susceptibility of the vitiliginous patches to burning.
The patient should also be warned of the possibility of the
vitiligo becoming more prominent as surrounding skin
darkens during the course of phototherapy.
Repigmentation tends to occur perifollicularly.
 PITYRIASIS
 PITYRIASIS ROSEA
• Pityriasis rosea is a viral rash which lasts about
6–12 weeks. It is characterised by a herald
patch followed by similar, smaller oval red
patches that are located mainly on the chest
and back.
• Pityriasis rosea most often affects teenagers
and young adults. However, it can affect males
and females of any age.
 Sign & Symptoms
• Many people with pityriasis rosea have no other symptoms, but
the rash sometimes follows a few days after an upper respiratory
viral infection (cough, cold, sore throat or similar).
 The herald patch
• The herald patch is a single plaque that appears 1–20 days before
the generalised rash of pityriasis rosea. It is an oval pink or red
plaque 2–5 cm in diameter, with a scale trailing just inside the
edge of the lesion like a collaret.
 Secondary rash
• A few days after the appearance of the herald patch, more scaly patches (flat
lesions) or plaques (thickened lesions) appear on the chest and back. A few plaques
may also appear on the thighs, upper arms and neck but are uncommon on the face
or scalp. These secondary lesions of pityriasis rosea tend to be smaller than the
herald patch. They are also oval in shape with a dry surface. Like the herald patch,
they may have an inner collaret of scaling. Some plaques may be annular (ring-
shaped).
• Pityriasis rosea plaques usually follow the relaxed skin tension lines or cleavage
lines (Langer lines) on both sides of the upper trunk. The rash has been described as
looking like a fir tree. It does not involve the face, scalp, palms or soles.
• Pityriasis rosea may be very itchy, but in most cases, it doesn't itch at all.
 Causes
• Pityriasis rosea is associated with reactivation of herpesviruses 6 and 7, which
cause the primary rash roseola in infants. Influenza viruses and vaccines have
triggered pityriasis rosea in some cases.
 Clinical Course
• Pityriasis rosea clears up in about six to twelve weeks. Pale marks or brown
discolouration may persist for a few months in darker-skinned people but
eventually, the skin returns to its normal appearance.
• Second attacks of pityriasis rosea are uncommon (1–3%), but another viral
infection may trigger recurrence years later.
• Pityriasis rosea during early pregnancy has been reported to cause miscarriage in
8 of 61 women studied. Premature delivery and other perinatal problems also
occurred in some women.
 Diagnosis
• The diagnosis of pityriasis rosea is usually made clinically but may be supported by
the finding of subacute dermatitis on histopathology of a skin biopsy. Eosinophils
are typical of drug-induced pityriasis rosea. Blood testing for HHV6 (IgG or PCR) is
not indicated because nearly 100% of individuals have been infected with the virus
in childhood and existing commercial tests do not measure HHV6 activity.
• Fungal scrapings are sometimes sent for mycology to exclude fungal infection
 Treatment
 General advice
• Bathe or shower with plain water and bath oil, aqueous cream, or another soap
substitute.
• Apply moisturising creams to dry skin.
• Expose skin to sunlight cautiously (without burning).

 Medical Treatment
• The following medicines have been reported to speed up clearance of pityriasis
rosea, based on small case series.
• A 7-day course of high-dose aciclovir
• A 2-week course of oral erythromycin has also been reported to help, probably
because of a nonspecific anti-inflammatory effect. Other studies have found that
erythromycin and azithromycin are not effective in pityriasis rosea.
• Topical steroid cream or ointment; this may reduce the itch while waiting for the rash
to resolve.

 Phototherapy
• Extensive or persistent cases can be treated by phototherapy (ultraviolet light, UVB).
 Pityriasis Versicolor
• Pityriasis versicolor is a common yeast infection of the skin, in
which flaky discoloured patches appear on the chest and back.
• Pityriasis versicolor most frequently affects young adults and is
slightly more common in men than in women. It can also affect
children, adolescents, and older adults.
• Pityriasis versicolor is more common in hot, humid climates than
in cool, dry climates. It often affects people that perspire heavily.
It may clear in the winter months and recur each summer.
• Although it is not considered infectious in the conventional
sense, pityriasis versicolor sometimes affects more than one
member of a family.
 Sign & Symptoms
• Pityriasis versicolor affects the trunk, neck, and/or arms, and is
uncommon on other parts of the body. The patches may be coppery
brown, paler than surrounding skin, or pink. Pale patches may be more
common in darker skin; this appearance is known as pityriasis versicolor
alba. Sometimes the patches start scaly and brown, and then resolve
through a non-scaly and white stage.
• Pityriasis versicolor is usually asymptomatic, but in some people it is mildly
itchy.
• n general, pale or dark patches due to pityriasis versicolor do not tend to
be more or less prone to sunburn than surrounding skin.
 Causes
• Pityriasis versicolor is caused by mycelial growth of fungi of the genus
Malassezia.
• Malassezia are part of the microbiota (microorganisms found on normal skin).
They are dependent on lipid for survival. Fourteen different species of
malassezia have been identified. The most common species cultured from
pityriasis versicolor are M. globosa, M. restricta and M. sympodialis.
• Usually malassezia grow sparsely in the seborrhoeic areas (scalp, face and
chest) without causing a rash. It is not known why they grow more actively on
the skin surface of patients prone to pityriasis versicolor. One theory
implicates a tryptophan-dependent metabolic pathway.

 Diagnosis
• Pityriasis versicolor is usually diagnosed clinically. However, the following
tests may be useful.
• Wood lamp (black light) examination— yellow-green fluorescence may be
observed in affected areas
• Dermoscopy of pityriasis versicolor - pallor, background faint pigment
network, and scale is seen
• Microscopy using potassium hydroxide (KOH) to remove skin cells—
hyphae and yeast cells that resemble spaghetti and meatballs are
observed
• Fungal culture—this is usually reported to be negative, as it is quite
difficult to persuade the yeasts to grow in a laboratory
• Skin biopsy—fungal elements may be seen within the outer cells of the
skin (stratum corneum) on histopathology. Special stains may be
required.

 Treatment
• Mild pityriasis versicolor is treated with topical antifungal agents.
• Topical azole cream/shampoo (econazole, ketoconazole)
• Selenium sulfide
• Terbinafine gel
• Ciclopirox cream/solution
• Propylene glycol solution
• Sodium thiosulphate solution
• Oral antifungal agents, itraconazole and fluconazole, are used
to treat pityriasis versicolor when extensive or if topical agents
have failed. Oral terbinafine, an antifungal agent used to treat
dermatophyte infections, is not effective for malassezia
infections such as pityriasis versicolor.
• Vigorous exercise an hour after taking the medication may
help sweat it onto the skin surface, where it can effectively
eradicate the fungus. Bathing should be avoided for a few
hours. A few days' treatment will clear many cases of pityriasis
long term, or at least for several months.
 HYPERHIDROSIS
• Hyperhidrosis is the name given to excessive and uncontrollable
sweating.
• Sweat is a weak salt solution produced by the eccrine sweat
glands. These are distributed over the entire body but are most
numerous on the palms and soles (with about 700 glands per
square centimetre).
• Primary hyperhidrosis is reported to affect 1–3% of the US
population and nearly always starts during childhood or
adolescence. The tendency may be inherited, and it is reported to
be particularly prevalent in Japanese people.
• Secondary hyperhidrosis is less common and can present at any
age
 Causes
 Primary hyperhidrosis appears to be due to overactivity of the hypothalamic
thermoregulatory centre in the brain and is transmitted via the sympathetic nervous
system to the eccrine sweat gland.
• Triggers to attacks of sweating may include:
• Hot weather
• Exercise
• Fever
• Anxiety
• Spicy food
 Causes of secondary localised hyperhidrosis include:
• The auriculotemporal syndrome (gustatory hyperhidrosis)
• Stroke
• Spinal nerve damage
• Peripheral nerve damage, when it may be associated with cutaneous dysaesthesia
• Surgical sympathectomy
• Neuropathy
• A brain tumour
• Chronic anxiety disorder
 Causes of secondary generalised hyperhidrosis include:
• Obesity
• Diabetes
• Menopause
• Overactive thyroid
• Cardiovascular disorders
• Respiratory failure
• Other endocrine tumours, such as phaeochromocytoma
• Parkinson disease
• Hodgkin lymphoma
• Drugs: alcohol, caffeine, corticosteroids, cholinesterase inhibitors, tricyclic
antidepressants, selective serotonin reuptake inhibitors, nicotinamide and
opioids.

 Diagnosis
• Hyperhidrosis is usually diagnosed clinically. Tests relate to the potential
underlying cause of hyperhidrosis and are rarely necessary for primary
hyperhidrosis.
• The precise site of localised hyperhidrosis can be revealed using the Minor test.
• Iodine (orange) is painted onto the skin and air-dried.
• Starch (white) is dusted on the iodine.
• Sweating is revealed by a change to dark blue/black colour.
• Screening tests in secondary generalised hyperhidrosis depend on other clinical
features but should include as a minimum:
• Blood sugar / glycosylated haemoglobin
• Thyroid function.

 Treatment
• General measures
• Wear loose-fitting, stain-resistant, sweat-proof garments.
• Change clothing and footwear when damp.
• Socks containing silver or copper reduce infection and odour.
• Use absorbent insoles in shoes and replace them frequently.
• Use a non-soap cleanser.
• Apply corn starch powder after bathing.
• Avoid caffeinated food and drink.
• Discontinue any drug that may be causing hyperhidrosis.
• Topical Antiperspirant
• Oral Anticholionergics
• Beta Blockers
• Botulinum Toxin Injections
• Surgical removal of Axillary glands
• Sypathectomy