Disorders of sweat glands

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					Section 10: Disorders of the skin appendages

Chapter 50: Disorders of sweat glands
Physiology of eccrine sweat glands                  through the dermis to the intraepidermal sweat
      Sweat glands are described as merocrine;      duct unit which opens onto the epidermis.
unlike the holocrine sebaceous glands, their              The secretory coil contains 3 types of
cells are not destroyed in the process of           cells: large clear cells which are the main
secretion. Merocrine glands are further             secretory cells, small dark cells, which
subdivided into 2 types: apocrine and eccrine.      resemble mucus-secreting cells of other organs
Apocrine secretion occurs by small portions of      but whose function is not known, and
apical cytoplasm becoming pinched off.              myoepithelial cells which support the gland
Apocrine gland sweat duct opens into the hair       and help propel the sweat towards the surface.
follicle while that of eccrine glands open onto     The function of the coil is to produce from
the epidermis.                                      plasma a watery isotonic secretion which can
      Eccrine sweat glands have 2 distinct          subsequently be modified by the duct. The
functions: they allow body cooling by               ducts consist of 2 or more cuboidal cells and
evaporation and thus contribute to adaptation       the intra-epidermal sweat unit is lined by one-
to a hot environment (major illness or death        layer of specialized cells.
may ensue with sweat gland failure); they also
                                                    Control of eccrine sweating
moisten the skin on the palms and soles at
                                                          Eccrine glands alter their activity in
times of activity, and thus improve their grip.
                                                    response to thermal, osmotic, mental and
Apocrine glands are responsible for body
                                                    gustatory factors. When the core temperature
                                                    of the body rises above a certain level, termed
      Eccrine sweat glands are distributed over
                                                    the temperature set point, eccrine sweating is
the whole skin surface, including the glans
                                                    initiated. Thermosensitive receptors are
penis and foreskin, but not on the lips, external
                                                    present both in the preoptic area and the
auditory canal, clitoris or labia minora. The
                                                    anterior hypothalamus. Different receptors
number varies greatly with site, from 620/cm2
                                                    respond to heat and cold. Thermoregulatory
on the soles and about 120/cm2 on the thighs
                                                    sweating occurs especially on the upper trunk
to 60/cm2 on the back. The total number on
                                                    and the face, but also occurs over the whole
the body surface is between 2 and 5 million.
                                                    body surface, including the palms and soles.
The weight of the eccrine glands totals 100 g.
                                                    The hypothalamic thermal set point is also
The glands vary in size from person to person
                                                    influenced by alterations in blood osmotic
and this probably accounts for individual as
                                                    pressure. Hyperosmolarity results in elevation
well as regional differences in sweat rate
                                                    of the thermal set point and reduced sweating
(maximal individual gland secretion rates
                                                    (as sweat is hypotonic, this is a response to
ranging from 2 to 20 nL/min/gland).
                                                    conserve further water loss).
Anatomy of eccrine sweat glands                           The centres and pathways controlling
     Embryologically, sweat glands are              mental sweating are not fully known. Mental
derived from a specialized down-growth of the       stimuli produce sweating, especially on the
epidermis at about the third month of               palms and soles, perhaps to improve the grip
intrauterine life on the palms and soles and at     at times of activity. Mental activity also
about 5 months elsewhere, and they resemble         produces some general increase in sweating
adult glands by 8 months. Sweat glands are          over the body surface. The activity may be
morphologically normal at birth, but may not        emotional or intellectual.
function fully until about 2 years of age. No             The efferent sudomotor pathway
new eccrine glands develop after birth. Unlike      consists of the cerebral cortex to the
the apocrine glands, they have no                   hypothalamus, hypothalamus to medulla,
developmental       relationship   with     the     medulla (mostly crossed) to the lateral horn of
pilosebaceous follicle. The gland consists of a     the spinal cord, then to the sympathetic
secretory coil in the lower dermis and              ganglia, and finally from to ganglia to the
subcutaneous tissue, and a duct leading             sweat gland as post-ganglionic non-

myelinated fibres. The sympathetic nerve           (peripheral    neuropathies    as     familial
supply of sweat glands is unusual in being         dysautonomia     and    brain    disease    as
cholinergic. The quantity and quality of the       diencephalic lesions), drugs (e.g. fluoxetine,
sweat may be varied greatly. Under basal           aspirin, NSAIDs, amphetamine, caffeine,
conditions, some insensible perspiration           insulin, sulphonylureas, SSRIs, MAOIs,
always occurs, partly due to transepidermal        chlorpromazine) and phaeochromocytoma
water loss and partly to sweat gland activity.     (attacks of hyperhidrosis, hypertension,
Only the latter is suppressed by atropine.         tachycardia and headache).
Under maximal stimulation, the body can
                                                   Emotional         (cortical)      hyperhidrosis
produce up to 12 L in 24 h, or for short
                                                   (palmoplanter, axillary, craniofacial)
periods 3 L in 1h; this rate exceeds the ability
                                                         Emotional or mental activity increases
of human to drink.
                                                   sweating, especially on the palms, soles,
      The composition of sweat varies greatly
                                                   axillae and to a lesser extent face and groin.
from person to person, time to time and site to
                                                   Mental activity devoid of any emotional
site. The sweat duct is largely responsible for
                                                   content may provide sweating. Most cases of
the modification in sweat constituent
                                                   hyperhidrosis presenting to the dermatologist
concentration which occurs, and this will
therefore vary according to how rapidly the        are of this type, affecting especially the palms,
sweat is passing through the duct. The most        soles and axillae in any combination. The
important constituents are sodium, chloride,       head, neck and scalp may be affected in
potassium, urea and lactate. Urea and lactate      craniofacial hyperhidrosis. The sweating of
probably act to moisturize the stratum             the palms and soles may be either continuous
corneum. Sweat is hypotonic and this is            or phasic. The hands may be cold and show
largely due to reabsorption of sodium in the       tendency to acrocyanosis. Hyperhidrosis may
duct. At increased sweat rates, the sodium         be a significant disability, in that sweat drips
concentration rises, presumably because there      from the hands onto the floor.
is reduced time for ductal absorption.                   The disorder occurs in either sex, and
      The normal sodium concentration is 10-       commonly begins in childhood or around
20 mmol/L at low sweat rates, and up to 100        puberty, and it is one of the components of
mmol/L at high rates. In Addison's disease         various syndromes in which palmoplanter
there is high sweat sodium. An increase in         keratoderma occurs. Hyperhidrosis may
sweat electrolytes occurs in cystic fibrosis and   persist for some years, but there is a tendency
this is a useful diagnostic test. Glucose is       to spontaneous improvement after the age of
present in a concentration of 0-3 mg/100 ml.       25 years. Complications include pompholyx
High sweat glucose may be found in                 and contact dermatitis. The condition of pitted
uncontrolled diabetes and this may create a        keratolysis of the feet, due to infection with
favorable environment for skin infections. The     Micrococcus sendentarius, is associated with
pH of sweat is 4-6.8. Active excretion or          hyperhidrosis. Axillary hyperhidrosis is due to
secretion of drugs such as griseofulvin and        overacting eccrine glands unlike axillary odor
ketoconazole may contribute to their efficacy.     which is apocrine in origin. Craniofacial
                                                   hyperhidrosis is often phasic and occurs in
Hyperhidrosis                                      middle age.
Generalized (hypothalamic) hyperhidrosis           Localized hyperhidrosis
      There is marked physiological variation
                                                         This may be caused by spinal cord injury,
in thermo-regulatory sweating from person to       intrathoracic       neoplasia,       gustatory
person in the absence of disease. An increase      hyperhidrosis, granulosis rubra nasi, sweat
in the temperature of blood bathing the
                                                   gland naevi, idiopathic, compensatory (around
hypothalamus increases heat loss by sweating       an area of partial anhidrosis or after
and vasodilatation. The causes of generalized      sympathectomy) or around local skin disorders
hyperhidrosis include fevers (e.g. tuberculosis,
                                                   (e.g. glomus tumor, pretibial myxoedema,
malaria, brucellosis, endocarditis), metabolic     burning feet syndrome).
diseases        (diabetes,       hypoglycemia,
hyperthyroidism),        menopause,        solid   Gustatory (autonomic) hyperhidrosis
malignancy and lymphoma, congestive heart                Sweating on the lips, forehead and nose
failure, cold-induced, neurological disorders      after    eating    certain     foods    occur

physiologically in many people. Hot spicy          and aluminium chloride (axillae, hands and
foods are the most likely cause. The central       feet). Applying 20% solution of aluminium
connections of this reflex are not fully known.    chloride in absolute ethyl alcohol at night
Gustatory hyperhidrosis also occurs in             when the axilla is dry, at first nightly and later
pathological      conditions     involving   the   every 1-4 week, is effective.
autonomic nervous system. The commonest                  Iontophoresis: This is a satisfactory
cause is damage to the sympathetic nerves          method of treatment for the hands and feet by
around the head and neck. Regeneration after       using tap water iontophoresis. The axilla is
damage to sympathetic nerves occurs with           satisfactorily controlled        by    aluminium
abnormal parasympathetic connections. Thus,        chloride topically. The mode of action of tap
the reflex arcs which normally allow chewing       water iontophoresis is not known and duct
or taste stimulation to cause parotid or gastric   occlusion does not occur. Direct current is
secretion may cause sweating in a localized        used with each palm or sole being treated for
zone corresponding to the area of the skin in      30 min with 20 mA initially 3 times a week,
which the sympathetic innervation has been         but     once    anhidrosis      is    established,
damaged. The commonest site is within the          maintenance treatment once a month only may
distribution of the auriculotemporal nerve         be required.
following injury, abscess or operation in the            Botulinum toxin A injection: This
parotid region (Von Frey's syndrome).              compound produces prolonged block of
      Submental gustatory sweating follow          neuronal acetylcholine release at the
injuries of the chorda tympani, and sweating       neuromuscular      junction.      0.1   mL      of
in the distribution of the greater auricular       appropriately     diluted     botulinum      toxin
nerve commonly follows radial neck surgery.        administered by high intradermal injections
Gustatory sweating may occur in diabetes due       can be given to 1 cm2 areas of skin
to autonomic neuropathy. It may also follow        appropriately anaesthetized, topical EMLA
herpes zoster. Gustatory sweating occurs in        cream for axillary skin and regional nerve
50% of patients subjected to operation on the      block for the palms and soles. Each axilla
parotid gland and usually appears 4 months         usually requires 12 injections, one hand 20
after operation and either persist indefinitely    and each foot 24-36 injections. It will produce
or wane after 3-5 years. As well as sweating       reduction in sweating for up to 8 months in
there is usually vasodilatation.                   axillary and 6 months in palmer hyperhidrosis.
      Treatment of severe cases may require        This treatment can be used also for
surgical interruption of the parasympathetic       circumscribed and gustatory hyperhidrosis.
pathway e.g. section of the glossopharyngeal       Systemic therapy
nerve within the skull, or tympanic                      Atropine-like drugs (e.g. propantheline)
neurectomy. Excision of the auriculotemporal       have been used to block the effect of
nerve is usually followed by recurrence.           acetylcholine on the sweat glands, but their
Topical therapy with aluminium chloride,           side effects (dryness of mouth, constipation,
topical glycopyrronium bromide or botulinum        glaucoma, hyperthermia and convulsions) are
toxin may be helpful.                              often more troublesome than the hyperhidrosis
Treatment of hyperhidrosis                         itself. Ganglion blocking drugs inhibit
     In many patients all that is necessary is     sweating but hypotension is too troublesome.
simple reassurance and explanation that the        Surgical treatment
disorder is likely to improve spontaneously,             Only those patients in whom a severe
perhaps in several years. Topical and systemic     disability is arising from the hands or axillae
treatments are only temporarily suppressive.       warrant       surgery.      Pedal     sympathetic
Topical therapy                                    denervation requires removal of the second
     Topical anticholinergics: Topical 0.5%        lumbar sympathetic ganglion; bilateral
glycopyrronium bromide cream is successfully       operations will usually result in ejaculatory
used for gustatory hyperhidrosis in diabetics.     failure, so it is best avoided. Sympathectomy,
     Eccrine duct blocking agents: These           when complete causes anhidrosis, whether
drugs act by impeding the delivery of sweat to     performed       cervically,    transaxillary   or
the skin surface and include formalin soaks        endoscopically. Endoscopic approach, done
1% (feet only), glutaraldehyde 10% (feet only)     for both sides at one session, via a

pneumothorax done through a small axillary           dermatitis, eczema, lichen planus and
incision,    is   the preferred        approach.     psoriasis.
Interruption of the sympathetic fibres between             Ross's syndrome consists of widespread
the second and fourth thoracic ganglia is done       anhidrosis      combined       with      patchy
by surgical transection or clipping. Reduction       compensatory hyperhidrosis, together with
of palmar hyperhidrosis is achieved in 95%           tonic pupils (appearing asymmetrical and
and of axillary hyperhidrosis is a little bit less   irregular in their outline, constricting and
successful.                                          dilating slowly to light and dark, respectively),
      Complications of sympathectomy include         and loss of deep tendon reflexes. The changes
pneumothorax,         haemothorax,         nipple    are due to selective degeneration of the
sensitivity,    Horner's     syndrome         and    sympathetic pathways.
bradycardia. Compensatory hyperhidrosis,
which is mild, occurs in 80% of treated
patients, affecting the trunk, legs and face.
                                                           The 3 forms of miliaria, miliaria
Axillary hyperhidrosis may also be greatly
                                                     crystallina (sudamina), miliaria rubra (prickly
helped by local excision of the axillary vault
                                                     heat), and miliaria profunda, occur as a result
by subcutaneous curettage of the axillary skin       of either obliteration or disruption of the
or tumescent liposuction of the axilla.              eccrine duct. They differ in clinical form due
                                                     to the different levels at which obliteration
Anhidrosis                                           occurs. In miliaria crystallina, the obstruction
      Anhidrosis is the absence of sweat from
                                                     is very superficial within the stratum corneum
the surface of the skin in the presence of an        and the vesicle is subcorneal. In miliaria rubra,
appropriate stimulus. This may be caused by          the changes include keratinization of the
an abnormality of the sweat gland itself, or at      intraepidermal part of the sweat duct, with
any level in the nervous pathway. Extensive          leakage and then formation of a vesicle around
anhidrosis may impair heat regulation to such        the duct. In miliaria profunda there is rupture
a degree that hyperpyrexia occurs on exposure        of the duct at the level or below the dermo-
to heat. Cessation of sweating is the cause of       epidermal junction.
heat hyperpyrexia. It occurs in anhidrotic                 Miliaria crystallina is often seen in
ectodermal dysplasia and in neonates.                febrile illnesses associated with profuse
Localized areas of anhidrosis may help in            sweating. It occurs in neonates due to delay in
diagnosis of leprosy or neurologic lesions.          patency development in the sweat duct. The
Sweat gland function can be a useful way to          incidence of miliaria rubra is highest in hot,
assess damage to the sympathetic nervous             humid conditions and there is striking
system e.g. in patients with postural                variation in individual susceptibility. Infants
hypotension. Sweat retention is the cause of         are especially prone. It is due to prolonged
miliaria and plays an important role in              exposure of the skin to sweat. The first event
producing crises of irritation in patients with      is an increase in the flora staphylococcus
atopic dermatitis, eczema or psoriasis.              epidermidis which produces a substance that
         The causes of anhidrosis include            blocks the lumen of the sweat duct. The
lesions of the nervous system, lesions of sweat      parakeratotic plugs which occur in the later
glands, plugging of the eccrine duct and             stages of the disease are not the primary cause
idiopathic acquired anhidrosis. Lesions of the       of the obstruction, but arise in the repair
nervous system include hyperthermia, organic         process, and may further aggravate the
brain lesions, syringomyelia of spinal cord,         obstruction. Leakage of sweat into the
lesions of peripheral nerves (e.g. leprosy,          epidermis is responsible for the final
diabetes,      alcoholism,      sympathectomy),      production of the lesions, and for their further
ganglion blocking and anticholinergic drugs,         aggravation. Miliaria profunda is due to more
Ross's syndrome and botulism. Sweat gland            severe damage to the sweat duct, and usually
lesions     include     anhidrotic   ectodermal      follows repeated attacks of miliaria rubra.
dysplasia, icthyosis, scleroderma, Sjögren's         Clinical features
syndrome and any cause of atrophy e.g.                    Miliaria crystallina: Clear, thin-walled
acrodermatitis chronica atrophicans. Plugging        vesicles, 1-2 mm in diameter, without an
of the eccrine duct occurs in miliaria, atopic       inflammatory areola are usually symptomless

and develop in crops, mainly on the trunk. In       chemotherapy exposure. Cases arise after
persistent febrile illness recurrent crops may      administration      of     a     cocktail     of
occur. The vesicles soon rupture and are            chemotherapeutic drugs.
followed by superficial branny desquamation.              Drugs secreted by eccrine sweat glands:
     Miliaria rubra: The lesions develop in         Some drugs are concentrated and secreted by
areas of friction with clothing, and in flexures.   eccrine glands, and in part this may account
They are minute erythematous papules, most          for their therapeutic effect. These drugs
common on the trunk and may be numerous.            include sulfadiazine, amphetamines, iodides,
They produce intense discomfort. Relief is          phenytoin, phenobarbital, carbamazepine,
often instantaneous when the stimulus to            griseofulvin,     ketoconazole,     fluconazole,
sweating is abolished by a cool shower.             ciprofloxacin and cocaine.
     Miliaria profunda: This follows repeated             Coma induced necrosis: Necrosis of the
attacks of miliaria rubra, and is uncommon          eccrine glands is a consistent feature of drug-
except in the tropics. The lesions are easily       induced coma caused by barbiturates,
missed because there is no itching or               benzodiazepines, narcotics or antidepressants.
discomfort. They are pale, firm papules 1-3         Similar changes are seen in blisters resulting
mm across, on the body and sometimes also           from coma induced by hypoglycemia or
on the limbs.                                       neurological events.
                                                          Radiation induced eccrine damage: High
                                                    dose radiation (>50 Gy) resulting in radiation
     The course depends mainly on
                                                    dermatitis will abolish eccrine function. Lower
environmental factors. If continued sweating
                                                    doses will reduce eccrine function temporarily
occurs, recurrent episodes lasting a few days
                                                    for several months.
are usual, but discomfort may be continuous.
                                                          Disorders with sweat gland cellular
Secondary bacterial infection is common such
                                                    inclusions: Accumulation of substances within
as impetigo and pustular miliaria. Periporitis
                                                    the secretory cells occurs in a number of
staphylogenes is the name given to multiple
                                                    metabolic diseases and their identification in
staphylococcal abscesses superimposed on
                                                    skin biopsies can be used diagnostically e.g.
miliaria rubra in young infants. In most cases
                                                    membrane-based vacuoles in secretory cells in
of miliaria rubra, the changes are reversible if
                                                    Hurler        type      mucopolysaccharidosis,
further sweating is avoided.
                                                    intracytoplasmic lipid in Niemann-pick lipid
Treatment                                           storage disease, secretory cell inclusions seen
     The only really effective prevention or        in Fabry's disease and fucosidosis.
treatment for miliaria is avoidance of further            Granulosis rubra nasi: The cause is
sweating. Air-conditioned office or bedroom         unknown. The disease starts in childhood and
is preferable, also avoidance of excessive          usually subsides spontaneously at puberty, but
clothing and friction with clothing is              may persist indefinitely. Diffuse erythema first
important. Oral ascorbic acid 500 mg twice          appears on the tip of the nose, gradually
daily may diminish the severity of miliaria.        extends to involve the cheeks, the upper lip
Calamine lotion is probably as effective as         and the chin. The erythema is covered by
anything for the relief of discomfort.              small beads of sweat. Small red macules and
                                                    papules and sometimes vesicles later form at
Other disorders of the eccrine                      the sweat duct orifices. The cases that persist
sweat glands                                        after puberty may show telangiectasia and
       Neutrophilic eccrine hidradenitis: This is   small     cysts.    Treatment      is    usually
necrosis of eccrine epithelium and secretory        disappointing.
coil with a dense surrounding neutrophilic
infiltrate. It occurs with cancer chemotherapy      Apocrine sweat glands
and with Behcet's disease and HIV infection.             Anatomy and physiology: Apocrine sweat
Painful erythematous papules and plaques            glands derive their name from the way their
arise on the limbs, neck, face and ears 10 days     secretion appears, on light microscopy, to be
after the start of chemotherapy, often              delivered by pinching off parts of the
associated with fever and a neutropenia. The        cytoplasm. However, electron microscopy
eruption lasts about 10 days resolving without      shows that this may be partly an artefact. They
therapy and only rarely recurs at subsequent        develop as part of the pilosebaceous follicle in

the fourth to fifth month of intrauterine life. In   apocrine sweat prevents its decomposition. A
the embryo they are present over the entire          strong axillary odour is associated with richer
skin surface, but most glands subsequently           bacterial flora especially corynebacteria.
disappear, so that in the adult they are present     Increased axillary pH may facilitate the
only in the axillae, perianal region and areolae     overgrowth of these bacteria, and some
of breasts. So called ectopic glands may be          deodorants may help by acidifying the axillary
present elsewhere. The mammary glands and            skin. There is marked individual and racial
glands in the external auditory meatus are           variation in body odour.
modified apocrine glands.                                   Treatment of axillary bromidrosis
      Apocrine glands are poorly developed in        includes omission of foodstuffs like garlic
childhood, and begin to enlarge with the             from the diet, frequent washing of the axillae
approach of puberty. The activity of the glands      and local antibacterial substances. There is
is androgen-dependent and they show marked           little evidence that topical treatment of eccrine
5α-reductase activity. The glands are larger         hyperhidrosis e.g. by aluminium chloride,
than eccrine glands. They are situated in the        have much effect on the apocrine glands.
subcutaneous tissue. Each consists of a tubule       Surgical excision of axillary subcutaneous
and a duct. The latter is quite short, and opens     tissue by a variety of surgical techniques,
into the neck of the hair follicle above the         which removes both eccrine and apocrine
sebaceous gland. The secretory coil is a simple      glands, gives good effects in those dissatisfied
convoluted tubule lined by a single layer of         with conservative measures.
columnar or cuboidal cell. The apocrine duct                Fish odour syndrome: This syndrome is
closely resembles the eccrine duct and consists      present in 7% of patients complaining of sweat
of a double layer of cuboidal cells. Outside the     malodour. It results from excessive amounts of
basement membrane of the gland and duct is a         trimethylamine appearing in both eccrine and
longitudinal layer of myoepithelial cells. Their     apocrine sweat, breath and urine and imparts
function is to support the duct and to propel        an unpleasant fishy smell to sufferers.
the secretion to the surface.                        Affected individuals are unable to oxidize this
      Apocrine glands secrete very small             substance, which is produced by the intestinal
quantities of an oily fluid. The secretion is        bacterial degradation of choline and carnitine
odourless on reaching the surface, and               in food to the odourless trimethylamine N-
bacterial decomposition is responsible for the       oxide. This can occur as a primary genetic
characteristic odour. Expulsion of apocrine          condition or secondary to increased production
sweat may occur continuously or be provoked          from its precursors (fish, eggs) by gut bacteria,
by emotional stimuli. The ducts have an              in diseases such as blind loop syndrome,
adrenergic sympathetic supply. Only the              chronic uraemia and liver disease. A diet low
axillary glands are important in producing           in choline and carnitine may help. Short
body odour.                                          courses of metronidazole or neomycin may
      Bromidrosis (abnormal sweat odour):            temporarily reduce the bacteria that degrade
Odour of the skin is to a large extent               choline and carnitine in the gut. Activated
determined by apocrine gland secretion.              charcoal and copper chlorophylline have been
Eccrine secretion is odourless but some              shown to reduce urinary trimethylamine
substances may be secreted in it e.g. garlic.        concentrations to normal levels in sufferers.
Characteristic mousy odor may be associated                 Chromidrosis: This, most commonly
with     phenylketonuria.      Other     patients    blue black, yellow or green, results from the
complaining of malodour may be suffering             secretion of lipofuscins in apocrine sweat, and
from phobias of malodour or from organic             may be associated with coloured breast milk.
lesions of the CNS. Apocrine glands are larger       The condition starts at puberty and persists
in size and have more 5α-reductase activity          until there is regression of apocrine gland
than in persons without bromidrosis.                 function in old age. Coloured sweat may be
      Apocrine secretion is odourless as it          discharged from the glands in response to
reaches the surface apart from excreted              exercise and emotional stimuli, and after
substances such as garlic. Bacterial                 manipulation of the skin. Pseudochromidrosis
decomposition liberates fatty acids etc., with       refers to coloration of otherwise colorless
characteristic smells. The process occurs only       eccrine sweat when it reaches the surface of
after some hours and frequent removal of             the skin due to dyes (eccrine chromidrosis)

and is usually weak in hue. In alkaptonuria the    shaped, follicular papules develop. Hair loss in
sweat may be dark.                                 the axillae usually ensues. The itching is often
     Fox-Fordyce disease: It is a disorder of      provoked by those emotional stimuli which
the apocrine glands comparable to prickly heat     normally cause apocrine secretion. The
of the eccrine glands. The aetiology is            disease runs a prolonged course and may
unknown. Obliteration of the apocrine duct at      persist until menopause. Some remission may
the infundibulum is the cause and this is          occur during pregnancy.
followed by rupture and apocrine sweat                   Treatment is unsatisfactory. Various
retention therefore follows.                       regimens have produced some improvement in
     The disease occurs mainly in women            some patients e.g. topical and intralesional
soon     after    puberty,    but     can     be   steroids, topical clindamycin, topical retinoic
postmenopausal. It can occur in males or in        acid, oral contraceptives, UVR sufficient to
children. Itching, which may be intense,           cause exfoliation (6 settings), oral retinoids,
occurs in the axillae, and to a lesser extent in   electrocautery, surgical excision of affected
the anogenital region and around the breasts.      skin or subcutaneous removal of the apocrine
Skin colored, or slightly pigmented, dome-         glands.


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