The bulbous digital deformity known as clubbing (Figure 2.1a,b) was described as early

as the fifth century BC when Hippocrates noted such changes in patients suffering from

empyema. The diagnostic signs comprise:

1 Overcurvature of the nails in the proximal to distal and transverse planes (Figure

2.2).

2 Enlargement of periungual soft tissue structures confined to the tip of each digit.

A simple method to detect clubbing is measurement of the phalangeal depth ratio (Figure

2.3). In a normal finger the distal phalangeal depth is smaller than the interphalangeal

depth. In clubbing this relationship is reversed (>1). The measurement can easily be taken

using a caliper in less than a minute.

 
 

 

Figure 2.1

 
 

(a, b) Clubbing.

 
 

 
 

 
 

Figure 2.2

Clubbing, demonstrating typical nail curvature and obliteration of the

‘window’.

 
 

 
 

 
 

 
 

Figure 2.3 In clubbing the phalangeal depth ratio is greater than

1. (a/b>1)

 
 

The increased nail curvature usually affects all 20 digits, but may be particularly

obvious on the thumbs, index and middle fingers. The ‘watch-glass’ shape of the nail

may occur as an isolated deformity without any associated enlargement of the tip of the

digit. The shape of the curved nails is variable and may appear fusiform, like a bird’s

beak, or clubbed like a watch-glass. The matrix quite often appears abnormally large.

There are three main types of clubbing:

1 Simple clubbing.

2 Hypertrophic pulmonary osteoarthropathy.

3 Pachydermoperiostosis.

 
 

Simple clubbing

Simple clubbing is the most common category and has several distinctive characteristics:

1 Increased nail curvature occurs with a transverse furrow separating it from the rest

of the nail both in the early stage and after resolution. The onset is usually gradual

and painless, except in some cases of carcinoma of the lung in which clubbing may

develop abruptly and be associated with severe pain.

2 Hypertrophy of the soft parts of the terminal segment caused by firm, elastic,

oedematous infiltration of the pulp, which may spread to the dorsal surface with

marked periungual swelling.

3 Hyperplasia of the dermal fibrovascular tissue may extend to involve the adjacent

matrix. This accounts for one of the earliest signs of clubbing—abnormal mobility

of the nail base, which can be rocked back and forth giving the impression that it is

floating on a soft oedematous pad. The increased vascularity is responsible for the

slow return of colour when the nail is pressed and released.

4 Acral cyanosis is often observed.

In the early stages clubbing may involve one hand only, though eventually both hands

become affected symmetrically. Several stages of clubbing or acropachy may be

distinguished: suspected, slight, average and severe. In practice the degree of the

deformity may be gauged by Lovibond’s ‘profile sign’ which measures the angle between

the curved nail plate and the proximal nail fold when the finger is viewed from the radial

aspect. This is normally 160°, but exceeds 180° in clubbing. A modified profile sign is

assessed by measuring the angle between the middle and the terminal phalanx at the

interphalangeal joint: in normal fingers the distal phalanx forms an almost straight (180°)

extension of the middle phalanx, whereas in severe clubbing this angle may be reduced to

160° or even 140°. However, the best indicator may be the simple clinical method

adopted by Schamroth: in normal individuals a distinct aperture or ‘window’, usually

diamond-shaped, is formed at the base of the nail bed; early clubbing obliterates this

window. (Fig 2.2).

Radiological changes occur in less than one-fifth of cases. These include phalangeal

demineralization and irregular thickening of the cortical diaphysis. Ungual tufts generally

show considerable variations and may be prominent in advanced stages of the disease.

Bony atrophy may be present.

Congenital finger clubbing may be accompanied by changes such as hyperkeratosis of

the palms and soles, and cortical hypertrophy of the long bones. Familial clubbing may

be associated with hypertrophic osteoarthropathy; some authors regard simple clubbing

as a mild form of the latter. Isolated watch-glass nails without other deformities are also

constitutionally determined. Rare cases of unilateral Hippocratic nails have been reported

due to obstructed circulation, oedema of the soft tissues and dystrophy of the affected

parts. The pathological process apparently responsible for clubbing and its associated

changes is the increased blood flow due to the opening of many anastomotic shunts.

 
 

 
 

 
 

Hypertrophic pulmonary osteoarthropathy

This disorder is characterized by the following five signs:

1 Clubbing of the nails.

2 Hypertrophy of the upper and lower extremities similar to the deformity found in

acromegaly.

3 Joint changes with pseudo-inflammatory, symmetrical, painful arthropathy of the

large limb joints, especially those of the legs. This syndrome is almost

pathognomonic of malignant chest tumours, especially lung carcinoma and

mesothelioma of the pleura; less commonly bronchiectasis is seen. Gynaecomastia

may also be present.

4 There may be bone changes such as bilateral, proliferative periostitis and moderate,

diffuse decalcification.

5 Peripheral neurovascular disorders such as local cyanosis and paraesthesia are not

uncommon.

Hypertrophic osteoarthropathy confined to the lower extremities appears as a

manifestation of arterial graft sepsis.

 
 

Pachydermoperiostosis

Pachydermoperiostosis (idiopathic hypertrophic osteoarthropathy) is rare. In most of the

reported cases the digital changes typically begin at or about the time of puberty. The

ends of the fingers and toes are bulbous and often grotesquely shaped, with hyperhidrosis

of the hands and the feet (Figure 2.4). The clubbing stops abruptly at the distal

interphalangeal joint. In this type the lesions of the finger tips are clinically identical to

those of hypertrophic pulmonary osteoarthropathy. However, in pachydermoperiostosis

the thickened cortex appears homogeneous on X-ray examination and does not impinge

on the medullary space. Acro-osteolysis of the distal phalanges has been reported.

 
 

 
 

Figure 2.4

Clubbing in pachydermoperiostosis.

 
 

 
 

The pachydermal change of the extremities and face, with furrowing and oiliness of the

skin, is the most characteristic feature of the disorder; it is termed the Touraine-Solente-

Golé syndrome. Nevertheless, in hypertrophic pulmonary osteoarthropathy there may be

facial    skin    and    scalp    changes    indistinguishable    from those    seen in

pachydermoperiostosis; this may be due to a common genetic factor. In the differential

diagnosis acromegaly must be considered; this enhances tufting of the terminal phalanges

and presents an anchor-like appearance, but without acro-osteolysis. Thyroid acropachy

is usually associated with exophthalmos, pretibial myxoedema and abnormal thyroid

function.

It should be noted that only rarely will any type of clubbing present to a dermatologist,

since in most cases it is simply one sign among many relating to the primary cause.

 
 

 
 

Classification of clubbing

The principal general causes of clubbing are listed in Table 2.1; a more comprehensive

list of causes is given below.

 
 

Idiopathic forms

Hereditary and congenital forms, sometimes associated with other anomalies:

• familial and genotypic pachydermoperiostosis

• racial forms (Africans)

• syndrome of pernio, periostosis and lipodystrophy

• Muckle-Wells syndrome.

 
 

Acquired forms

1 Thoracic disorders are involved in about 80% of cases of clubbing, often with the

common denominator of hypoxia:

• bronchopulmonary diseases, especially chronic and infective bronchiectasis,

abscess and cyst of the lung, pulmonary tuberculosis

• sarcoidosis, pulmonary fibrosis, emphysema, Ayerza’s syndrome, chronic

pulmonary venous engorgement, asthma in infancy, mucoviscidosis

• blastomycosis, pneumonia, Pneumocystis carinii infection, AIDS.

2 Thoracic tumours:

• primary or metastatic bronchopulmonary cancers, pleural tumours, mediastinal

tumours

• Hodgkin’s disease, lymphoma, pseudotumour due to oesophageal dilatation.

 
 

 
 

Figure 2.5

Pseudoclubbing due to trauma—hooked nail deformity.

 
 

3 Cardiovascular disease:

• congenital heart disease associated with cyanosis (rarely non-cyanotic)

• thoracic vascular malformations; stenoses and arteriovenous aneurysms

• Osler’s disease (subacute bacterial endocarditis)

• congestive cardiac failure

• myxoma

• Raynaud’s disease, erythromelalgia, Maffucci’s syndrome.

4 Disorders of the alimentary tract (5% of cases):

• oesophageal, gastric and colonic cance

 
 

• disease of the small intestine

 
 

 
 

Figure 2.6

Clubbed appearance in acromegaly. (Courtesy of D.Wendling.)

 
 

 
 

 
 

Figure 2.7

Pseudoclubbing in yellow nail syndrome.

 
 

 
 

• colonic disease

• amoebiasis and inflammatory states of the colon

• ulcerative colitis

• familial polyposis, Gardner’s syndrome

• ascariasis

• active chronic hepatitis

• primary or secondary cirrhoses

• purgative abuse.

5 Endocrine origin:

 
 

 
 

• Diamond’s syndrome (pretibial myxoedema, exophthalmos and finger

clubbing)

• acromegaly.

6 Haematological causes:

• methaemoglobinaemia

• sulphaemoglobinaemia

• haemoglobinopathies

• primary or secondary polycythaemia associated with hypoxia

• poisoning by phosphorus, arsenic, alcohol, mercury or beryllium.

7 Hypervitaminosis A.

8 Malnutrition, kwashiorkor.

9 Addiction (hashish, heroin).

10 Syringomyelia, POEMs syndrome (peripheral neuropathy, organomegaly,

endocrinopathy, monoclonal plasmaproliferative disease, skin changes).

11 Lupus erythematosus.

12 Unilateral or limited to a few digits:

• subluxation of the shoulder (with paralysis of the brachial plexus), medial nerve

neuritis

• Pancoast-Tobias syndrome

• aneurysm of the aorta or the subclavian artery

• sarcoidosis

• tophaceous gout.

13 Lower extremities:

• arterial graft sepsis.

14 Isolated forms:

• local injury, whitlow, lymphangitis

• subungual epidermoid inclusions.

15 Transitory form: physiological in the newborn child (due to reversal of the

circulation at birth).

16 Occupational acro-osteolysis (exposure to vinyl chloride).

Childhood
In early childhood, the nail plate is thin and may show temporary koilonychia. Because of
the shape of the matrix, some children show ridges that start laterally by the proximal nail
fold and join at a central point just short of the free margin, to give a ‘herringbone’
arrangement of the ridges (chevron nails). In one study 92% of normal infants aged 8–9
weeks showed a single transverse line (Beau’s line) on the finger nails. One child
demonstrated a transverse depression through the whole nail thickness on all 20 digits.

Old age
Many of the changes seen in old age may occur in younger age groups with impaired
arterial blood supply. Elastic tissue changes diffusely affecting the nail bed epidermis are
often seen historically; these changes may
be due to the effects of ultraviolet (UV) radiation, although it has been stated that the nail
plate is an efficient filter of UVB radiation. The whole subungual area in old age may
show thickening of blood vessel walls with vascular elastic tissue fragmentation. Pertinax
bodies are often seen in the nail plate; they are probably remnants of nuclei of
keratinocytes. Nail growth is inversely proportional to age; related to this slower growth,
corneocytes are larger in old age. Since nails tend to thicken with age and some diseases,
it may well be that the volume of nail production per unit of time does not change.
The nail plate becomes paler, dull and opaque with advancing years and white nails
similar to those seen in cirrhosis, uraemia and hypoalbuminaemia may be seen in normal
individuals. Longitudinal ridging is present to some degree in most people after 50 years
of age and this may give a ‘sausage links’ appearance. 

Clinicians used to observing the slow rate of clearance of diseased or damaged nails are
apt to view the nail apparatus as a rather inert structure, although it is in fact the centre of
marked kinetic and biochemical activity.

Cell kinetics
Unlike the hair matrix, which undergoes a resting or quiescent (telogen) phase every few
years, the nail matrix germinative layers
continue to undertake DNA synthesis, to divide and to differentiate throughout life, akin
to the epidermis in this respect. Exactly which parts of the nail apparatus contribute to the
nail plate has been debated; it is now usually accepted that the three-layer nail plate is
produced from the proximal matrix, the distal matrix and the nail bed (sterile ventral
matrix).

Why the nail grows flat, rather than as a heaped-up keratinous mass, has generated
much thought and discussion. Several factors probably combine to produce a relatively
flat nail plate; the orientation of the matrix rete pegs and papillae, the direction of cell
differentiation, and the fact that since keratinization takes place within the confines of the
nail base, limited by the proximal nail fold dorsally and the terminal phalanx ventrally,
the differentiating cells can only move distally and form a flat structure—by the time they
leave the confines of the proximal nail fold all the cells are dead, keratinized and
hardened.

Linear nail growth
Many studies have investigated the linear growth rates of the nail plate in health and
disease; their findings are summarized in Tables 1.1 and 1.2. Finger nails grow
approximately 1 cm every 3 months and toe nails at half this rate.

Table 1.1 Physiological and environmental factors affecting the rate of linear
nail growth

Faster growth
Day-time
Pregnancy
Minor trauma/nail biting
Right-hand nails
Youth, increasing age
Fingers
Summer
Middle, ring and index fingers
Male (?)

Slower growth
Night-time
First day of life

Left-hand nails
Old age
Toes
Winter or cold environment
Thumb and little finger
Female (?)

There is a rich arterial blood supply to the nail bed and matrix derived from paired digital
arteries (Figure 1.2). The main supply passes into the pulp space of the distal phalanx
before reaching the dorsum of the digit. The volar digital nerves (Figure 1.2c) are
similarly important in providing nerves to the deep nail apparatus structures. An
accessory blood supply arises further back on the digit and does not enter the pulp space.
There are two main arterial arches (proximal and distal) supplying the nail bed and
matrix, formed from anastomoses of the branches of the digital arteries. In the event of
damage to the main supply in the pulp space, such as might occur with trauma, infection
or scleroderma, there may be sufficient blood from the accessory vessels to permit
normal growth of the nail.
There is a capillary loop system to the whole of the nail fold, but the loops to the roof
and matrix are flatter than those below the exposed nail. There are many arteriovenous
anastomoses below the nail—glomus bodies, which are concerned with heat regulation.
Glomus bodies are important in maintaining acral circulation under cold conditions—
arterioles constrict with cold, but glomus bodies dilate. The nail beds of fingers and toes
contain such bodies (93–501 per cm2). Each glomus is an encapsulated oval organ 300
µm long, made up of a tortuous vessel uniting an artery and venule, a nerve supply and a
capsule; also within the capsules are many cholinergic muscle cells.

Figure 1.2

Digital blood and nerve supply: (a) showing arterial anastomoses; (b)
arterial supply from hand to digits (radio-opaque dye seen in arterises);
(c) major digital arteries and nerve supply.

Periungual and subungual warts are usually difficult to treat and frequently recur. The
life span of periungual warts may be such that they—and the various treatments—may
exceed the patience of both patient and physician! Under such circumstances intelligent
placebo therapy may well be appropriate. A great variety of treatments are listed in all
pharmacopoeias, reflecting their individually limited success rates. The choice of
treatment depends on:
• number of warts
• location (periungual and subungual)
• duration
• age of the patient
• immunological status
• skills of the doctor.
Surgical procedures should be restricted to selected cases.

Topical treatment
Topical agents include: keratolytic agents, virucidal agents and immunomodulators.

Keratolytic agents
Keratolytic agents are the most popular first-line treatment of warts and are particularly
suitable for young children, who can apply at home creams, ointments, tapes or quick-
drying acrylate lacquers containing salicylic acid in concentrations ranging from 10% to
40%.

Virucidal agents
Both glutaraldehyde and formaldehyde combine with keratin and produce skin
desiccation with viral destruction. Effectiveness is comparable to that of keratolytic
agents.

Immunotherapy
Topical immunotherapy with strong topical sensitizers—squaric acid dibutylester
(SADBE) or diphenylcyclopropenone (DPCP)—is an effective and painless treatment for
multiple warts. A preparation of SADBE or DPCP 2% in acetone is used for
sensitization. After 21 days weekly applications are carried out with dilutions ranging
from 0.001% to 1% according to the patient’s response. The objective of treatment is to
induce a mild contact dermatitis.
Imiquimod acts as an immunomodulator owing to its capacity to induce cytokine
(especially interferon alpha) production. Although imiquimod has only been used for
treatment of genital and facial warts, its effectiveness in these regions suggests its
possible use for periungual warts.

Systemic treatment

Oral immunomodulators 
The efficacy of cimetidine 750–1200 mg per day has never been definitively proved. The
drug is expensive and not always well tolerated.

Interferon
The efficacy of interferons is still debated and the necessity of intravenous administration
together with cost of treatment do not recommend its routine use. However, complete
cure of recalcitrant and extensive periungual and subungual warts has been reported after
interferon beta treatment.

Antimitotics 
Intralesional injections of bleomycin are effective in the treatment of periungual warts.
After local anaesthesia, the bleomycin solution (1 U bleomycin per 1 ml sterile saline) is
dropped on the wart surface. The wart is then punctured using a disposable needle
approximately 40 times per 5 mm2area. The wart slowly undergoes necrosis with
formation of an eschar that can be scraped away 3–4 weeks after treatment. Residual
warts can be retreated.

Surgical treatment

Cryotherapy 
Freezing warts with liquid nitrogen is a rapid method of treatment. It is contraindicated
in small children, since it is frequently associated with intense pain secondary to oedema
under the nail bed. Application of a surface anaesthetic cream 1–2 hours prior to therapy
does not help to reduce pain in the periungual region. Hyperkeratotic warts should be
pared off before treatment to permit freezing of the deeper portions of the wart. Freezing
takes 10–15 seconds using cryogen spray. A 1 mm halo ring should form in the normal
skin surrounding the wart. Cryosurgery should be used with caution for warts on the
proximal nail fold, since nail matrix damage is a common complication, with
leukonychia, Beau’s lines and onychomadesis. Irreversible matrix destruction with nail
atrophy has been reported after overzealous cryosurgery.

Surgical excision 
Excision of periungual warts is not recommended since it produces scarring and is
associated with a high frequency of recurrence.
•   Electrosurgery should be avoided, since it produces considerable scarring.
•   Infrared coagulation is another destructive method that is not recommended.
•   Localized heating using a radiofrequency heat generator has been successfully used
to treat hand warts (86% cure). This treatment is not particularly painful, but may
cause scarring and does not seem suitable for periungual warts.

Laser techniques 
•   Carbon dioxide laser: this causes thermic destruction of the wart, producing a loss
of skin which heals by secondary intention. When warts extend into the nail folds or
the nail bed, laser treatment should be preceded by partial or total nail avulsion. Re-
epithelialization takes a long time (approximately 9 weeks) and is associated with
risk of infections and pain. Some authors reported complete cures in 71% of
patients with periungual warts exclusively treated with one or two sessions of CO2
laser. Temporary or permanent nail dystrophy were observed in 29% of treated
patients. Pain sometimes persists after wound healing. Scarring is not rare, as well
as disturbance of function. This technique is suggested only as a secondary
approach for recalcitrant warts.
•   Pulsed dye laser: this laser acts through a selective microvascular destruction of the
dilated capillaries of the warts, since the oxyhaemoglobin contained in the vessels
preferentially absorbs yellow light. Healing of the wart is due both to thermic
damage and to removal of the blood supply. Stimulation of a cell-mediated immune
response may be another contributing factor. A few days after the procedure the
wart becomes dry and black, as a result of necrosis. Since no wound is produced,
patients may return to work immediately and postoperative pain is minimal. Healing
occurs after 2–4 weeks. Periungual warts are less responsive to treatment than
palmar or common warts. Although this technique is associated with a very low
incidence of scarring, cure is achieved in only a third of cases, and usually after two
to four treatments.
•   Erbium:YAG laser: the erbium:ytrium-aluminium-garnet (YAG) laser produces a
controlled tissue ablation with minimal thermal damage compared with the CO2
laser. This laser has been used for periungual warts with an excellent safety profile
and minimal morbidity and pain.

Frequent application of distasteful topical preparations on the nail and periungual skin
can discourage patients from biting and chewing their finger nails. Possible alternatives
include:
•   1% clindamycin
•   quaternary ammonium derivatives
•   4% quinine sulphate in petrolatum.
Patients with severe onychophagia or median nail dystrophy can be helped by daily
bandaging the injured fingers with permeable adhesive tape. Fluoxetine at high dosages
(60 mg/day) can be helpful in interrupting this compulsive disorder in adults.

Yellow nail syndrome is an uncommon disorder of unknown aetiology, characterized by
the triad of yellow nails, lymphoedema and respiratory tract involvement. Vitamin E at
dosages ranging from 600 to 1200 IU daily can induce a complete clearing of the nail
changes. Although the mechanism of action of vitamin E in yellow nail syndrome is still
unknown, antioxidant properties of alpha-tocopherol may account for its efficacy. A 5%
solution of vitamin E in dimethyl sulphoxide produced marked clinical improvement in a
double-blind controlled study. The efficacy of topical vitamin E, however, still needs
confirmation. Oral itraconazole, 400 mg daily one week a month for several months, or
oral flucouazole, may be beneficial in some cases.

Twenty-nail dystrophy, characterized by nail roughness, can be idiopathic or associated
with alopecia areata and less often with lichen planus. It is a benign condition that never
causes nail scarring. The nail changes usually regress spontaneously in a few years.
Reassuring the patient is probably the best approach to this nail disorder. Although
topical PUVA can be effective, continuous treatment is required to maintain the results.

Specific nail involvement occurs in about 10% of patients with lichen planus and
permanent damage of at least one nail occurs in approximately 4% of patients. However,
if lichen planus is correctly diagnosed and treated, permanent damage to the nail unit is
rare, even where there is diffuse involvement of the nail matrix.
Systemic steroids are effective in treating nail lichen planus: intramuscular
triamcinolone acetonide 0.5 mg/kg every month for 2–3 months usually produces
recovery of the nail abnormalities. Intralesional injections of triamcinolone acetonide
10mg/ml represent a possible, but painful, alternative when the disease is limited to a few
finger nails. Mild relapses are frequently observed, but recurrences are usually
responsive to therapy. Steroid treatment is not useful in pterygium, since the nail matrix
cannot be regenerated. Systemic retinoids at dosages suitable for psoriasis are a good
alternative.

Since treatment of nail psoriasis is always disappointing, before treatment is started the
individual problems of every patient should be carefully considered, and in particular the
degree of discomfort that results from the nail lesions. Reassuring the patient is probably
the best approach for isolated nail pitting, oily patches, mild onycholysis and splinter
haemorrhages. However, diffuse onycholysis, subungual hyperkeratosis and severe nail
plate surface abnormalities may require a positive therapeutic approach.

Local therapies of nail psoriasis only rarely induce complete
remission of the disease

When the nail folds are affected, regular application of topical emollients is useful to
reduce scaling and prevent self-induced trauma.
Topical steroids, or combinations of topical steroids with salicylic acid and/or retinoic
acid, are widely prescribed. Their efficacy is poor, even when applied with occlusive
dressing after chemical or mechanical avulsion of the onycholytic nail plate. Long-term
application of topical steroids may result in marked atrophy of the soft tissues of the
digits or even in focal resorption of the distal phalanges.
A nail lacquer containing 8% clobetasol propionate, formulated to optimize
penetration of the drug through the nail plate, has been developed for use in this
condition. This topical treatment, which is effective and well tolerated, produces
improvement in most cases of nail psoriasis, with effects directly related to the duration
of treatment.
Topical calcipotriol is effective when onycholysis and subungual hyperkeratosis are
prominent symptoms. Topical tazarotene 0.1 % gel has also been used with good results
and tolerability in psoriasis. The latter drug is especially effective in reducing
onycholysis (in occluded and non-occluded nails) and pitting (in occluded nails).
Topical psoralens followed by exposure to ultraviolet-A (PUVA) are not very effective
owing to poor penetration of the UVA through the nail plate, especially when the plate is
thickened. However, this treatment may be useful in pustular psoriasis when recurrent
pustular lesions have destroyed the nail plate. Intralesional injections of triamcinolone
acetonide 10 mg/ml, at a dose of 0.2–0.5 ml per nail, have proved effective in some cases
of nail matrix psoriasis. In patients with nail-plate surface abnormalities the steroids
should be injected in the nail matrix, whereas in patients with subungual hyperkeratosis
the site of injection should be the nail bed. Injections should be repeated monthly for 6
months, then every 6 weeks for the next 6 months and finally every 2 months for 6–12
months. A digital block is sometimes useful to make the treatment less painful, but when
several digits are involved, a wrist block may be the appropriate anaesthesia. However,
routine use of this treatment is not recommended because of the pain caused by the
injections, the local side-effects and recurrence of the nail abnormalities after
discontinuation of the therapy. In addition, the efficacy of intralesional steroids in nail
matrix psoriasis is limited, with only 50% success in treating nail pits.
Systemic treatment with methotrexate or cyclosporin can clear the nail changes, but
this can be recommended only when nail psoriasis is associated with widespread disease
or psoriatic arthritis.
Retinoids are of little value in the treatment of nail psoriasis except for hyperkeratotic
nails and pustular psoriasis. Oral administration of etretinate or acitretin can even worsen
the nail changes owing to the development of nail brittleness, pyogenic granuloma-like
lesions and chronic paronychia. Oral photochemotherapy can improve crumbling of the
nail plate and psoriatic involvement of the proximal nail fold, but is less effective in nail
pitting or subungual hyperkeratosis. Superficial radiotherapy can have a beneficial effect
on psoriatic nails but is not recommended because the benefits are short-lived.
Pustular psoriasis of the nail unit usually fails to respond to conventional topical
treatments. Local treatment with topical anti-metabolites (mechlorethamine, 1 %
fluorouracil) is an option, even though results are variable. Systemic steroids, PUVA and
cyclosporin can arrest the development of pustular lesions and avoid permanent scarring
of the nail apparatus. A study of 46 patients with pustular psoriasis of the nails indicates
that systemic retinoids at low dosage (less than 0.5 mg of acitretin per day) are the
treatment of choice in patients with multiple nail involvement, whereas topical
calcipotriol is the best option for pustular psoriasis limited to one or two nails. Topical
calcipotriol is also useful as maintenance therapy in patients who responded to retinoids,
in order to prevent recurrence.