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Chapter: Clinical Dermatology: Sebaceous and sweat gland disorders

Eccrine sweat glands

There are 2 –3 million sweat glands distributed all over the body surface but they are most numerous on the palms, soles and axillae.

Sweat glands

Eccrine sweat glands

There are 2 –3 million sweat glands distributed all over the body surface but they are most numerous on the palms, soles and axillae. The tightly coiled glands lie deep in the dermis, and the emerging duct passes to the surface by penetrating the epidermis in a corkscrew fashion. Sweat is formed in the coiled gland by active secretion, involving the sodium pump. Some damage occurs to the membrane of the secret-ory cells during sweating. Initially sweat is isotonic with plasma but, under normal conditions, it becomes hypotonic by the time it is discharged at the surface, after the tubular resorption of electrolytes and water under the influence of aldosterone and antidiuretic hormone.

In some ways the eccrine sweat duct is like a renal tubule. The pH of sweat is between 4.0 and 6.8; it contains sodium, potassium chloride, lactate, urea and ammonia. The concentration of sodium chloride in sweat is increased in cystic fibrosis, and sweat can be analysed when this is suspected.

Sweat glands have an important role in temperature control, the skin surface being cooled by evaporation. Up to 10 L/day of sweat can be excreted. Three stim-uli induce sweating.

1  Thermal sweating is a reflex response to a raisedenvironmental temperature and occurs all over the body, especially the chest, back, forehead, scalp and axillae.

2 Emotional sweatingis provoked by fear or anxietyand is seen mainly on the palms, soles and axillae.

3 Gustatory sweatingis provoked by hot spicy foodsand affects the face.

The eccrine sweat glands are innervated by cholinergic fibres of the sympathetic nervous system. Sweating can therefore be induced by cholinergic, and blocked by anticholinergic drugs. Central control of sweating resides in the preoptic hypothalamic sweat centre.

Clinical disorders can follow increased or decreased sweating, or blockage of sweat gland ducts. 

Generalized hyperhidrosis

Thermal hyperhidrosis

The ‘thermostat’ for sweating lies in the preoptic area of the hypothalamus. Sweating follows any rise in body temperature, whether this is caused by exercise, environmental heat or an illness. The sweating in acute infections, and in some chronic illnesses (e.g. Hodgkin’s disease), may be a result of a lowering of the ‘set’ of this thermostat.

Other causes of general hyperhidrosis

   Emotional stimuli, hypoglycaemia, opiate with-drawal, and shock cause sweating by a direct or reflex stimulation of the sympathetic system at hypothalamic or higher centres. Sweating accompanied by a general sympathetic discharge occurs on a cold pale skin.

   Lesions of the central nervous system (e.g. a cerebral tumour or cerebrovascular accident) can cause gener-alized sweating, presumably by interfering directly with the hypothalamic centre.

   Phaeochromocytoma, the carcinoid syndrome, dia-betes mellitus, thyrotoxicosis, Cushing’s syndrome and the hot flushes of menopausal women have all been associated with general sweating. The mechan-isms are not clear. 

Local hyperhidrosis (Fig. 12.16)

Local hyperhidrosis plagues many young adults. The most common areas to be affected are the palms, soles and axillae. Too much sweating there is embarrassing, if not socially crippling. 

A sodden shirt in contact with a dripping armpit, a wet handshake and stinking feet are hard crosses to bear. Seldom is any cause found, but organic disease, especially thyrotoxicosis, acromegaly, tuberculosis and Hodgkin’s disease should be considered. A blatant anxiety state is occasionally present, but more often an otherwise normal person is understandably concerned about his or her antisocial condition. A vicious circle emerges, in which increased anxiety drives further sweating.

These problems may be no more than one end of the normal physiological range. How many students sitting examinations have to dry their hands before putting pen to paper? It is only when the sweating is gross, or continuous, that medical advice is sought. Such sweating is often precipitated by emotional stimuli and stops during sleep.


Topical applications. The most useful preparation foraxillary hyperhidrosis is 20% aluminium chloride hexahydrate in an alcohol base. At first it is applied to the dry axillae every night. Soon the interval can be increased, and many need the preparation only once or twice a week. The frequency may have to be cut down if the preparation irritates the skin, which is most likely if it is applied after shav-ing or when the skin is wet. Aluminium chloride also helps hyperhidrosis of the palms and soles, but it is less effective there.

Potassium permanganate soaks (1 : 10 000 aqueous solution) combat the bacterial superinfection of sweaty feet that is responsible for their foul smell. Patients should soak their feet for 15 min twice a day until the smell has improved and be warned that potassium permanganate stains the skin and everything else brown. Occasionally glutaraldehyde solutions are used instead, but allergy and yellow-stained skin are potential com-plications. Topical clindamycin is also effective.

Iontophoresis. This is the passage of a low-voltagedirect current across the skin. Iontophoresis with tap water or with the anticholinergic drug glycopyrro-nium bromide (glycopyrolate, USA) may help palmar or plantar hyperhidrosis. Patients attend two or three times a week for treatment until the condition improves. Repeated courses or maintenance therapy may be required.

Botulinum toxin. This binds to presynaptic nervemembranes and then inhibits the release of acetyl-choline. It is now the treatment of choice for severe axillary or plantar hyperhidrosis, unresponsive to medical measures. Subdermal aliquots of the toxin are injected into the hyperhidrotic area of the axilla or sole, one region at a single session. Sweating is abolished after a delay of 2–3 days. Repeat injections (about every eighth month) are necessary as the sweating returns when the toxin has gone. Antibodies may form against the toxin and diminish its long-term effectiveness. Botulinum toxin is used less often for palmar hyperhidrosis because of the risk of paralys-ing the intrinsic muscles of the hand.

Systemic treatment. Oral anticholinergic agents suchas Pro-Banthine and glycopyronium bromide (USA) are sometimes tried but their side-effects limit their value.

Surgery. This is used less nowadays as the abovemeasures are usually effective. However, recalcitrant axillary hyperhidrosis can be treated by removing the vault of the axilla, which bears most of the sweat glands. These can be identified preoperatively by apply-ing starch and iodine, which interact with sweat to colour the sweat gland openings blue. Thoracoscopic sympathetic trunkotomy (between the first and sec-ond thoracic ganglia) is effective for severe palmar hyperhidrosis alone but is a last resort.

Hypohidrosis and anhidrosis

Anhidrosis caused by abnormality of the sweat glands

Heat stroke. Caused by sweat gland exhaustion, thisis a medical emergency seen most often in elderly

people moving to a hot climate. It can also occur in the young, during or after prolonged exercise, especially in hot climates. Patients present with hyperthermia, dry skin, weakness, headache, cramps and confusion, leading to vomiting, hypotension, oliguria, metabolic acidosis, hyperkalaemia, delirium and death. They should be cooled down immediately with cold water, and fluids and electrolytes must be replaced.

Hypohidrotic ectodermal dysplasia. This rare disor-der is inherited as an X-linked recessive trait, in which the sweat glands are either absent or decreased. Affected boys have a characteristic facial appearance, with poor hair and teeth (Figs 13.13 and 13.14), and are intolerant of heat.

Prematurity. The sweat glands function poorly inpremature babies nursed in incubators and hot nurseries.

Anhidrosis caused by abnormalities of the nervous system

Anhidrosis may follow abnormalities anywhere in the sympathetic system, from the hypothalamus to the peripheral nerves. It can therefore be a feature of multiple sclerosis, a cerebral tumour, trauma, Horner’s syndrome or peripheral neuropathy (e.g. leprosy, alcoholic neuropathy and diabetes). Patients with widespread anhidrosis are heat-intolerant, develop-ing nausea, dizziness, tachycardia and hyperthermia in hot surroundings.

Anhidrosis or hypohidrosis caused by skin disease

Local hypohidrosis has been reported in many skin diseases, especially those that scar (e.g. lupus erythe-matosus and morphoea). It may be a feature of Sjogren’s syndrome, ichthyosis, psoriasis and miliaria profunda .

Interference with sweat delivery

Miliaria. This is the result of plugging or rupture ofsweat ducts. It occurs in hot humid climates, at any age, and is common in over-clothed infants in hot nurseries. The physical signs depend on where the ducts are blocked.

Miliaria crystallina. This presents as tiny clear non-inflamed vesicles that look like dew. This is the most superficial type.

Miliaria rubra (prickly heat). Tiny erythematous andvery itchy papules.

Miliaria profunda. These consist of larger erythema-tous papules or pustules. This is the deepest type.

Treatment. The best treatment is to move to a coolerclimate or into air conditioning. Clothing that pre-vents the evaporation of sweat (e.g. nylon shirts) should be avoided; cotton is best. Claims have been made for ascorbic acid by mouth, but in our hands it rarely if ever helps. Topical steroids reduce irritation but should only be used briefly. Calamine lotion cools and soothes.


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