Psoriasis of the palms and hyperkeratotic eczema are often confused.

Differentiation is sometimes
somewhat arbitrary. Often, hyperkeratotic plaques are localized at points of contact, `for example
with tools, but not all frictional hyperkeratosis is necessarily an expression of psoriasis. The
possibility of psoriasis koebnerizing into areas of contact dermatitis should not be forgotten
Allergic and irritant contact dermatitis and constitutional eczema of the hands may only be
distinguishable by a careful history and patch testing. They commonly coexist. Superimposed
irritant contact dermatitis from home and work exposures is common.
This is an unusual form of cutaneous candidiasis that manifests as a diffuse eruption beginning as
individual vesicles and spreading into confluent areas involving the trunk, thorax, and extremities.
The associated generalized pruritus is increased in severity in the genitocrural folds, anal region,
axillae, and hands and feet.

Topical therapy includes witfield oinment, azole (miconazole and clotrimazole), imidazole
( ketoconazole), or allylamines ( terbinafine or naltifine cream), these are applied twice daily for 4
weeks.
Pathogenesis Dermatophytes are not endogenous pathogens. Transmission of dermatophytes to
humans occurs via three sources, each resulting in typical features (Table 76.6). While

dermatophytes are not especially virulent and typically invade only the outer, cornified layers of
the skin, they can be responsible for considerable morbidity. Their adaptation to different hosts
has evolved, allowing greater chronicity and further spread of infection. The first stage of
infection involves both contact with and adherence of the infectious elements of the fungus
(arthroconidia) to the skin. The ability of certain fungi to adhere to a particular host arises from
numerous mechanisms and host factors, including the ability of certain fungi to adapt to the
human body2. Dermatophytes, unlike most other fungi, produce keratinases (enzymes that break
down keratin), which allow for invasion of the fungi into keratinized tissue. Mannans in the cell
walls of dermatophytes have immuno-inhibitory effects. In T. rubrum, the mannans may also
decrease proliferation, thereby decreasing the likelihood of the fungus being sloughed off prior to
invasion. This mechanism is thought to contribute significantly to the chronicity of infections
caused by T. rubrum12. The invasion of dermatophytes is subject to host factors including
protease inhibitors and possibly hormones, which may limit the extent of invasion. If invasion is
successful, disease occurs. The severity of clinical disease is affected by several host factors:
sebum has an inhibitory effect on dermatophytes, and the degree of disease activity may be
related to the number and activity of sebaceous glands in a particular body region; breaks in the
skin barrier or macerated skin can encourage dermatophyte invasion; and increased susceptibility
may be inherited or related to the competency of the immune system. Once dermatophytes have
invaded and begun to proliferate in the skin, there are additional factors that aid in limiting the
infection to keratinized tissue. These include the preference of dermatophytes for the cooler
temperature of the skin compared to the normal body temperature, the presence of factors in the
serum that inhibit dermatophyte growth (e.g. b-globulins, ferritin and other metal chelators)2, and
the host immune system. Further invasion or dissemination is actually quite unusual (see below).
Other conditions influencing dermatophyte infections include thymomas and underlying skin
disorders such as Darier disease and HaileyHailey disease.
Defi nition. Any species of dermatophyte may affect the skin of
the hand. Infections of the dorsal surface present no specifi c features
and are considered as ringworm of the glabrous skin under
tinea corporis. This section is therefore concerned with ringworm
of palmar skin and with infections beginning under rings.
Species concerned. For the most part, the organisms concerned
are the three anthropophilic species involved in tinea pedis. T.
rubrum is, among cases coming to the skin clinics, the most common
cause by far. E. fl occosum and T. mentagrophytes var. interdigitale are
involved in a small minority of cases and mainly in the presence
of pre-existing palmar plantar keratoderma such as tylosis.
The anthropophilic species T. violaceum may also produce this
clinical picture and animal species may occasionally infect the
palmar skin. T. mentagrophytes var. erinacei from contact with
hedgehogs has been notable in this regard.
Pathogenesis. In most cases, apart from animal infections, there
is pre-existing foot infection with or without toenail involvement.

A special mention should be made of ringworm beginning under

rings, wrist watches, and where anatomical deformities or occupational
usage predispose to maceration between the fi ngers.
Here, there may be a particular susceptibility to T. mentagrophytes
var. interdigitale infections, and in such cases infection may occur
without obvious foot involvement [1]. Poor peripheral circulation
and palmar keratoderma are other possible predisposing factors
[2].
Clinical features. T. rubrum infection may take several different
clinical forms. Hyperkeratosis of the palms and fi ngers affecting
the skin diffusely is the most common variety, and is unilateral in
about half of cases. The accentuation of the fl exural creases is a
characteristic feature. Other clinical variants include crescentic
exfoliating scales, circumscribed vesicular patches, discrete red
papular and follicular scaly patches, and erythematous scaly
sheets on the dorsal surface of the hand. The latter forms are more
likely to be zoophilic infections.
Differential diagnosis. Dermatophyte infections of the palm
are often quiet and chronic, commonly passing unnoticed or
misdiagnosed. Contact dermatitis, especially the primary irritant
variety, psoriasis, pityriasis rubra pilaris, constitutional eczemas,
keratoderma, syphilis and post-streptococcal peeling must all be
considered. In ring infections and web space cases with anatoSuperfi
cial mycoses 36.33
mical deformity, candidosis and bacterial intertrigo should be
excluded.
Unilateral scaling should always alert the clinician to the necessity
of taking scrapings. Nail changes may help: pitting suggests
psoriasis, but subungual hyperkeratosis if present should always
be scraped. If the palmar infection spreads to the dorsal surface,
more classical annular lesions may be seen, although this happens
relatively infrequently. Tinea manuum, like tinea cruris and tinea
faciei, is sometimes modifi ed by inappropriate treatment with
topical steroids leading to further diagnostic diffi culties.
Control. The prevalence of tinea manuum is directly related to
the level of tinea pedis in the population. Prompt treatment of
tinea pedis and the use of separate towels are sensible measures
that can be recommended, but it is likely that tinea manuum will
continue to occur sporadically and a greater awareness of this
condition, so that it may be recognized promptly, is of prime
importance.
Mild interdigital tinea pedis without bacterial involvement
is treated topically with allylamine, imidazole,
ciclopirox, benzylamine, tolnaftate, or undecenoic
acid based creams.74 Terbinafine cream applied twice
daily for 1 week is effective in 66% of cases.75 The dosing
schedule of oral terbinafine is 250 mg daily for
2 weeks. Itraconazole in adults is given 400 mg daily
for 1 week, 200 mg daily for 24 weeks, or 100 mg daily
for 4 weeks with similar efficacies of all regimens,76
whereas itraconazole in children is administered at
5 mg/kg/day for 2 weeks. Fluconazole 150 mg weekly
for 34 weeks is also effective.71 Topical or systemic
corticosteroids may be helpful for symptomatic relief

during the initial period of antifungal treatment of

vesiculobullous tinea pedis. Maceration, denudation,
pruritus, and malodor obligate a search for bacterial
coinfection by Gram stain and culture, the results of
which most often demonstrate the presence of Gramnegative
organisms including Pseudomonas and Proteus.
Patients suspected of having Gram-negative coinfections
should be treated with a topical or systemic
antibacterial agent based on the culture and sensitivity
report. Associated onychomycosis is common; if present,
more durable treatment of the onychomycosis is
necessary to prevent recurrence of tinea pedis. Newer
oral antifungal agents have replaced griseofulvin as
the treatments of choice for severe or refractory tinea
pedis when this infection is also accompanied by onychomycosis.
Itraconazole (Fig. 232-1) is a highly lipophilic compound
that has a wide spectrum of activity.44 In vitro,
it is fungistatic and effective against dermatophytes,
yeast, molds, and dimorphic fungi.4547
MECHAN ISM OF ACTION . Itraconazole inhibits
14--demethylase, a microsomal cytochrome
P450 enzyme, in the fungal membrane (Fig. 232-2).48
14--Demethylase is necessary for the conversion of
lanosterol to ergosterol, which is the principal structural
component of the fungal cell membrane.46 Consequently,
the accumulation of 14--methylsterols leads
to the impairment of membrane permeability and
membrane-bound enzyme activity and to the arrest of
fungal cell growth.
ND ICAT ION S. Itraconazole has the broadest efficacy
compared to other commonly prescribed antifungals.
47 Thus, it is a first-line therapy for infections
due to Candida and other nondermatophyte species
(Box 232-3).
Pediatric. Itraconazole can be used to treat tinea
capitis in children. It is more often prescribed in the
capsule formulation with food or acidic beverages
such as colas because the cyclodextrin in the liquid
form of itraconazole causes more gastrointestinal side
effects such as diarrhea and also due to reports of neoplasms
associated with high doses in murine and rat
models.54 Nevertheless, for children who cannot swallow
capsules or take capsules with food, the solution
has a pleasant taste and is considered to be safe.55 Itraconazole
is dosed at 5 mg/kg per day for 46 weeks.56
Children who weigh between 15 and 30 kg require
one 100 mg capsule daily; children weighing 3040 kg
require 100 mg 1 day alternating with 200 mg the next
day, to average 150 mg daily.57 Children weighing over
50 kg can be dosed as adults.55 Tinea capitis caused
by T. tonsurans requires a course lasting 24 weeks58;
however, a longer treatment course is recommended
for M. canis.59 Because onychomycosis is less common
in children than in adults, there is much less data available

for treatment of pediatric onychomycosis. For better

compliance due to decreased adverse effects, lower
cost, and overall reduced exposure to drug, one can
prescribe a pulsed regimen of 5 mg/kg/day for 1 week
alternating with 3 weeks off; two pulses are recommended
for fingernail involvement and three pulses
for toenail involvement.9
The oral solution is a good option for oropharyngeal or
esophageal candidiasis in children, even in fluconazoleresistant
infections.53
Adult. Itraconazole has been approved for the treatment
of onychomycosis caused by dermatophytes54
and is effective as continuous or pulse therapy. A
2-month course of itraconazole pulse therapy is necessary
for fingernail onychomycosis, while toenail onychomycosis
requires a 3-month course. A single course
consists of 200 mg twice daily for 1 week per month.
Itraconazole pulse therapy is at least equal in efficacy, if
not superior, in the treatment of toenail onychomycosis
Fluconazole, like
itraconazole, inhibits 14--demethylase, a microsomal
cytochrome P450 enzyme, in the fungal membrane
riseofulvin (Fig. 232-1; Box 232-7) has been used since
1958 for the treatment of dermatophyte infections.59
Griseofulvin is not effective for candidiasis, deep fungal
infections, or pityriasis versicolor.
MECHANISM OF ACTION
Griseofulvin is fungistatic in vitro,59 and has a narrow
spectrum of antimycotic activity. It disrupts microtubule
mitotic spindle formation, thereby causing mitotic
arrest at the metaphase stage.102
Terbinafine inhibits the enzyme squalene epoxidase in
the fungal cell membrane, thereby blocking the biosynthesis
of ergosterol (Fig. 232-2).3 Squalene epoxidase, a
complex, microsomal noncytochrome P450 enzyme,
catalyzes the first enzymatic step of ergosterol synthesis:
the conversion of squalene into squalene epoxide.
Consequently, terbinafine causes an abnormal intracellular
accumulation of squalene and a deficiency in
ergosterol.4 In-vitro accumulation of squalene accounts
for the drugs fungicidal activity by weakening the cell
membrane, while deficiency of ergosterol is associated
with the drugs fungistatic activity, as ergosterol is a
component of fungal membranes required for normal
growth.4
Because of its high selectivity, terbinafine is generally
well tolerated with a low incidence of adverse side
effects. The most common side effects after oral administration
are of a gastrointestinal nature (3.5%5.0%).29
Other rare side effects include headache, exanthematous
eruption, acute generalized exanthematous pustulosis,
pustular psoriasis, subacute cutaneous lupus
erythematosus, chest pain, elevated laboratory parameters,

loss of taste, fatigue, and malaise.2833 A few cases

of hepatocellular injury (including fulminant hepatic
failure),34,35 reversible agranulocytosis,36 and severe
skin reactions, including toxic epidermal necrolysis
and erythema multiforme, were also reported.37
Risks and Precautions
Terbinafine should be prescribed with caution in
patients with hepatic disease or history of hepatic
toxicity with other medications (Box 232-2). Furthermore,
there is insufficient data to recommend its use
in patients with renal impairment. Because terbinafine
rarely causes a lupus-like rash and neutropenia,
patients with known systemic lupus erythematosus or
immunodeficiency also may not be good candidates
for this medication.10