This document summarizes disorders of sweat glands. It discusses the normal structure and function of eccrine sweat glands. It then describes various disorders that can cause either hyperhidrosis (excessive sweating) or anhidrosis (lack of sweating). Hyperhidrosis can be generalized, focal (affecting hands, feet, or axillae), or localized. Specific conditions that can cause hyperhidrosis like gustatory sweating are also outlined. The document concludes with descriptions of management options for different sweat disorders.

1. DISORDERS OF SWEAT
GLANDS
DR ASMA AYAZ
RESIDENT DERMATOLOGY KTH

3. INTRODUCTION
 Allow body cooling by evaporation
 Moisten the skin on the palms and soles at times of
activity, and thus improve their grip.
 Distributed over the whole skin surface including
the glans penis and foreskin
 Not present on the lips, external ear canal, clitoris
or labia minora.

4.  The number varies greatly with site, from 620/cm2
on the soles, about 120/cm2 on the thighs to
60/cm2 on the back.
 The total number on the body surface is between 2
and 5 million, and is the similar in different ethnic
groups.
 Total weight is 100g.
 Maximal individual gland secretion rates ranging
from 2 to 20 nL/min/gland).

5.  Embryologically, sweat glands are derived from a
specialized down‐growth of the epidermis at about
the third month of intrauterine life on the palms and
soles and at about 5 months elsewhere;
 They resemble adult glands by 8 months.
 Sweat glands are morphologically normal at birth
but may not function fully until about 2 years of age.
 No new eccrine glands develop after birth.

6.  The secretory coil contains 3 types of cells
 LARGE CLEAR CELLS
 SMALL DARK CELLS
 MYOEPITHEILIAL CELLS

8. TECHNIQUES FOR STUDYING THE FUNCTION OF THE
ECCRINE SWEAT
GLANDS
 Collection of sweat in bags or pads at rest, after
exposure to heat, or after injection or iontophoresis
of pilocarpine or other cholinergic agonists.
 Direct measurement of water loss.
 Microcannulation of the duct or coil
 Measurement of electrical potentials and electrical
resistance of the skin
 Visualization of the individual sweat droplets.
 Isolated glands.

9. VISUALIZATION OF THE INDIVIDUAL SWEAT
DROPLETS
 Direct microscopy, by in vivo staining, by forming
plastic impressions or by indicators that become
coloured on contact with water, such as the
starch/iodine technique bromophenol blue
quinizarin and the food dye Edicol ponceau.
 A simple modification of the starch/iodine test is to
dry the skin, paint it with 2% iodine in alcohol, allow
it to dry, and then press the skin against a
good‐quality paper.
 The starch in the paper reacts with iodine in the
presence of water, so that each sweat droplet
shows up as a minute dark spot.

12. CONTROL OF ECCRINE SWEATING
 Central control
 Internal body temperature
 Nine times more efficient
 Central and peripheral changes in temperature
influence the thermal receptors in the preoptic area
and anterior hypothalamus.
 Osmotic factors
 Mental stimuli

13.  Local control
 From the sympathetic ganglia non‐myelinated C
fibres pass to eccrine sweat glands ending at many
cholinergic terminals and a few adrenergic
terminals
 Sweat coils contain androgen receptors

14. composition of sweat
 varies greatly from person to person, time to time
and site to site.
 Sweat duct is largely responsible for the
modification in sweat constituent concentration
 Sodium, chloride, potassium, urea and lactate.
 Normal sodium concentration is between 10 and 20
mmol/L at low sweat rates, and up to 100 mmol/L at
high rates.
 Lactate is found in a concentration of 4–40 mmol/L.
 Glucose

15. DISORDERS OF ECCRINE SWEAT GLANDS
 Hyperhidrosis
 Hyperhidrosis is defined as excessive
production of sweat, that is, more than is
required for thermoregulation
 It can be defined gravimetrically as greater
than 2 standard deviations above mean
values of sweat secretion for a normal
population in various sites (palmar 50
mg/min/m2, plantar 50 mg/min/m2, axillary
150 mg/min/m2 and facial 50 mg/min/m2).

16.  • Generalized.
 • Focal – palmar, plantar, axillary and cranio‐facial.
 • Localized naevoid.
 • Compensatory.
 • Hyperhidrosis with extensive anhidrosis (Ross
syndrome).

17. GENERALIZED HYPERHIDROSIS
 • Febrile infective illnesses: tuberculosis, malaria, brucellosis,
 endocarditis, etc.
 • Metabolic diseases: diabetes, hyperthyroidism,
 hyperpituitarism, hypoglycaemia, phaeochromocytoma
 • Menopause
 • Underlying solid malignancy and lymphoma
 • Congestive heart failure
 • Neurological disorders:
 • Brain disease:
 • Parkinson disease
 • episodic hypothermia with hyperhidrosis
 • generalized hyperhidrosis without hypothermia
 • Peripheral neuropathies:
 • familial dysautonomia (Riley–Day)
 • congenital autonomic dysfunction with universal pain loss
 • cold‐induced sweating syndrome
 • Drugs: fluoxetine

18. FOCAL HYPERHIDROSIS
 Palmoplantar hyperhidrosis.
 Axillary hyperhidrosis.
 Cranio‐facial hyperhidrosis.

19. PALMOPLANTAR HYPERHIDROSIS
 Begins in childhood or around puberty.
 Continuous or phasic
 When continuous, it is worse in the summer, and
not so clearly precipitated by mental factors.
 When phasic, it is usually precipitated by minor
emotional or mental activity, and is not markedly
different in summer and winter.
 Hands may be cold and show a tendency to
acrocyanosis.
 Symmetrical lividity (vasomotor changes, so that
the sodden skin is also cold and cyanotic)

21. AXILLARY HYPERHIDROSIS
 Continuous, or more commonly phasic
 Uncommon before puberty
 Axillary sweating on undressing is very common
 Overactivity of the eccrine glands, unlike axillary
odour, which is mainly apocrine in origin.
 Cranio‐facial hyperhidrosis
 Often phasic
 Middle age

24. COMPLICATIONS AND CO‐MORBIDITIES
 Palmoplantar hyperhidrosis predisposes to
vesicular eczema (pompholyx) and allergic
sensitization to footwear constituents;
 Dermatophyte and bacterial infection.
 Pitted keratolysis of the feet, due to infection with
Kytococcus sedentarius.
 Hyperhidrosis may persist for some years, but there
is a tendency to spontaneous improvement of
axillary and palmar hyperhidrosis after the age of
25 years.

25. CAUSES OF LOCALIZED HYPERHIDROSIS
 Spinal cord injury:
 • Hyperhidrosis associated with autonomic dysreflexia
 • Hyperhidrosis due to orthostatic hypotension
 • Intrathoracic neoplasia
 • Gustatory hyperhidrosis
 • Frey syndrome
 • Granulosis rubra nasi
 • Functional and true sweat gland naevi
 • Sweating associated with local skin disorders:
 • Glomangioma
 • Blue rubber bleb naevi
 • Pachydermoperiostosis
 • Pretibial myxoedema
 • POEMS syndrome
 • Burning feet syndrome
 • Compensatory: after sympathectomy, or with partial anhidrosis
 • Idiopathic unilateral circumscribed hyperhidrosis

27. COLD‐INDUCED SWEATING SYNDROME
 Presents in infancy with poor feeding and difficulty
in suckling, followed in adulthood by paradoxically
cold‐induced hyperhidrosis and anhidrosis in heat
 Mild neuropathy, kyphoscoliosis, valgus deformity
of the elbows, high arched palate and digital
syndactyly.
 Inactivation of a cardiotropin‐like cytokine, a second
ligand for ciliary neurotrophic factor receptor

28. GUSTATORY HYPERHIDROSIS
 Hyperhidrosis precipitated by eating specific foods
 Also occurs in pathological conditions involving the
autonomic nervous system.
 Damage to the sympathetic nerves around the head and
neck (abnormal connections are made during
regeneration)
 very rare, usually start in childhood and are not
progressive
 Face and knees
 The commonest site is within the distribution of the
auriculotemporal nerve, which may be injured by
trauma, abscess or surgery in the parotid region
(auriculotemporal or von Frey syndrome)

29.  • Idiopathic
 • Central
 • Post‐herpetic
 • Post‐peripheral nerve injury:
 • Parotid surgery, injury and abscess
 • Auriculotemporal
 • Chorda tympani
 • Greater auricular
 • Cervical sympathectomy
 • Peripheral autonomic neuropathy:
 • Diabetes

30.  Occurs in 50–80% of patients subjected to
operations on the parotid gland.
 Usually the symptoms appear 4–7 months after the
operation, and either persist indefinitely or wane
after 3–5 years.
 The stimuli required to initiate the reflex vary, as
does the severity.
 Sometimes chewing, without taste sensation, is the
most important stimulus.
 Injury to fibres from the vagus may cause gustatory
sweating localized to the upper arm after cervical
sympathectomy.

32. MANAGEMENT
 Surgical interruption of the parasympathetic
pathway.
 Excision of the auriculotemporal nerve is usually
followed by recurrence.
 Topical therapy with aluminium chloride
 Topical glycopyrronium bromide
 Botulinum toxin injections

33. MANAGEMENT OF HYPERHIDROSIS
 First line
 • Eccrine duct‐blocking agents (aluminium chloride hexahydrate)
 • Topical anticholinergics (glycopyrrolate)
 Second line
 • Iontophoresis with tap water or anticholinergics (hands,
 feet and axillae)
 • Intradermal botulinum toxin (axillae, hands and face)
 • Oral anticholinergics: propanthelene, methanthelene
oxybutynin,
 glycopyrollate
 • Oral clonidine
 • Oral β‐blockers and anxiolytics
 Third line
 • Removal or ablation of eccrine glands (axillary)
 • Sympathectomy (thoracic or lumbar)

34. GRANULOSIS RUBRA NASI
 A rare disorder characterized by hyperhidrosis of
the nose and associated skin changes
 Symptoms develop from as early as 6 months but
can occur at any age in childhood and occasionally
in adults.
 Initial presentation is with excess sweating localized
over the tip of the nose.
 Droplets of sweat are usually visible.
 With time erythema, papules, vesicles and
telangiectasia may develop over the nose, cheeks
and upper lips

35.  Resolution occurs around puberty but persistent
cases are recognized.
 Peripheral acrocyanosis and palmoplantar
hyperhidrosis.
 Chronic inflammatory cell infiltrate with dilatation of
vascular spaces on histopathology.
 Reassurance
 Botulinum toxin

37. ANHIDROSIS AND HYPOHIDROSIS
 Diminished sweat production may be partial
(hypohidrosis) or complete (anhidrosis)
 Disturbance of any part of the physiological
pathway of sweat production may decrease
sweating.
 Heat intolerance, fatigue, drowsiness and pyrexia.

38.  Organic brain lesions of hypothalamus, pons and medulla
 • Spinal cord lesions:
 • Syringomyelia
 • Sympathectomy
 • Congenital insensitivity to pain with anhidrosis
 • Degenerative syndromes:
 • Shy–Drager syndrome
 • Ross syndrome
 • Peripheral neuropathy:
 • Diabetes
 • Alcohol
 • Leprosy
 • Autonomic neuropathy
 • Drug‐induced blockade of neurotransmission:
 • Ganglion‐blocking agents
 • Anticholinergic agents
 • Calcium channel‐blocking agents
 • α‐adrenergic blockers

39.  Genetic disorders:
 • Bazex syndrome
 • Ectodermal dysplasia
 • Fabry disease
 • Incontinentia pigmenti
 • Atrophy or destruction of eccrine
glands:
 • Scleroderma
 • Burns
 • Sjögren syndrome
 • Lymphoma
 • Acrodermatitis chronica atrophicans
 • Obstruction of sweat ducts:
 • Miliaria
 • Eczema
 • Psoriasis
 • Lichen planus
 • Ichthyosis
 • Porokeratosis
 • Drugs affecting eccrine gland
function:
 • Topical aluminium salts
 • 5‐Fluorouracil
 • Mepacrine
 • Topiramate
 • Idiopathic:
 • Acquired idiopathic generalized
anhidrosis

40. ROSS SYNDROME
 Characterized by a triad of segmental anhidrosis,
tonic pupils and absent deep tendon reflexes
 A progressive degenerative disorder of sensory and
autonomic nerves
 The main symptoms are those of heat intolerance
and socially disabling compensatory hyperhidrosis
 Asymmetrical, patchy or unilateral.
 Iontophoresis and botulinum toxin

42. MILIARIA
 This is a common acute or subacute skin condition
that arises due to the occlusion or disruption of
eccrine sweat ducts in hot humid conditions,
resulting in a leakage of sweat into the epidermis
(miliaria crystallina and miliaria rubra) or dermis
(miliaria profunda)

43.  Miliaria crystallina.
 Clear, thin‐walled vesicles, 1–2 mm in diameter
without an inflammatory areola, are usually
symptomless and develop in crops, mainly on the
trunk.
 In persistent febrile illnesses, recurrent crops may
occur.
 The vesicles soon rupture, and are followed by
superficial, branny desquamation.
 Commonly in infants due to a delay in patency
developing in the sweat ducts.

45.  Miliaria rubra.
 Typical lesions develop on the body, especially in
areas of friction with clothing, and in flexures.
 Uniformly minute erythematous papules, which may
be present in very large numbers
 Characteristically, the lesions produce intense
discomfort in the form of an unbearable pricking
sensation.
 Relief is often instantaneous when the stimulus to
sweating is abolished by a cool shower.
 In infants, lesions commonly appear on the
occluded skin of the neck, groins and axillae, but
also occur elsewhere.

47.  Miliaria profunda.
 This nearly always follows repeated attacks of
miliaria rubra, and is uncommon except in the
tropics.
 The affected skin is covered with pale, firm papules
1–3 mm across, especially on the body, but
sometimes also on the limbs.
 There is no itching or discomfort from the lesions.

48.  Disease course and prognosis
 If continued sweating occurs, recurrent episodes
lasting a few days are usual, but discomfort may be
continuous.
 Secondary infection and disturbance of heat
regulation.
 Permanent damage to the sweat duct may occur,
especially after miliaria profunda.

49. MANAGEMENT
 First line
 • Control local environment (remove excess bedding,
fans, air
 conditioning)
 • Cool the skin (damp compresses, cool showers)
 • Avoid tight or excessive clothing
 Second line
 • Menthol (e.g. 0.5% menthol in aqueous cream)
 • Topical antibiotics if there is secondary infection
 • Mild topical steroids
 Third line
 • Removal to cooler climate
 • Prophylactic oral vitamin C

50. NEUTROPHILIC ECCRINE HIDRADENITIS
 Refers to a rare clinical condition with non‐specific
features but characteristic acute inflammation of the
eccrine sweat glands, seen on skin biopsy.
 • Chemotherapy‐induced neutrophilic eccrine
hidradenitis.
 • Infectious neutrophilic eccrine hidradenitis.
 • Palmoplantar neutrophilic eccrine hidradenitis.
 • Neutrophilic eccrine hidradenitis with HIV
infection.
 • Neutrophilic eccrine hidradenitis with Behçet
disease.

51. PATHOPHYSIOLOGY
 Necrosis of the eccrine epithelium in association
with a dense neutrophilic infiltrate
 In drug‐induced NEH this is most commonly
reported with the use of cytotoxic chemotherapeutic
agents.
 Childhood NEH is not associated with underlying
disease.
 Infectious NEH is most frequently encountered in
immunosuppressed individuals.

52.  Drug‐associated NEH typically occurs 8–10 days
after starting chemotherapy.
 Painful erythematous papules and plaques develop
on the limbs, neck and face
 Facial erythema and swelling may be severe
enough to mimic cellulitis
 The condition typically resolves within 2 weeks of
treatment ending.

53.  Childhood NEH has a particular predilection for the
soles and less frequently the palms.
 Typically, tender plaques and nodules are seen.
 Attacks resolve spontaneously in 3 weeks but the
condition may be recurrent
 Skin biopsy
 Associated neutropenia

56.  Resolves without any treatment.
 In adult NEH systemic corticosteroids, dapsone and
colchicine have all been recommended
 Dapsone may also be helpful in preventing
recurrent disease

57. APOCRINE MILIARIA
 Apocrine miliaria is a disorder of the apocrine
glands comparable to prickly heat of the eccrine
glands, and caused by obliteration of the apocrine
duct at the infundibulum.
 It usually presents with an itchy papular eruption in
the axillae, ano‐genital area or on the areolae of the
nipple.

58.  The earliest pathological sign is a small vesicle in
the apocrine duct.
 Later, the apocrine glands are seen to be enlarged,
and as a consequence of repeated inflammatory
events, perifollicular xanthomatosis with
perifollicular foam cells expressing CD68 may
develop

59.  Mainly in women soon after puberty, but can be
postmenopausal
 Reported after laser axillary hair epilation
 Itching
 Skin‐coloured or slightly pigmented, dome‐shaped,
follicular papules develop
 Hair loss in the axillae usually ensues
 Very prolonged course
 Some remission may occur in pregnancy

60.  First line
 • Topical or intralesional steroids
 • Topical clindamycin lotion
 • Topical retinoids
 Second line
 • Ultraviolet light
 • Oral retinoids
 Third line
 • Surgery

63.  Eccrine Angiomatous hamartoma
 Cluster of painful pink–violet papules and plaques
on the thigh and knee that had been present since
one year of age. There was associated
hyperhidrosis, but not hypertrichosis. Histologically,
an increased number of both eccrine glands and
small blood vessels is seen.