Primary focal hyperhidrosis: current treatment options and a

Transcription

JEADV
DOI: 10.1111/j.1468-3083.2011.04173.x
REVIEW ARTICLE
Primary focal hyperhidrosis: current treatment options
and a step-by-step approach
I. Hoorens,* K. Ongenae
Department of Dermatology, University Hospital, Ghent, Belgium
*Correspondence: I. Hoorens. E-mail: [email protected]
Abstract
Primary focal hyperhidrosis is a common disorder for which treatment is often a therapeutic challenge. A systematic
review of current literature on the various treatment modalities for primary focal hyperhidrosis was performed and a
step-by-step approach for the different types of primary focal hyperhidrosis (axillary, palmar, plantar and
craniofacial) was established. Non-surgical treatments (aluminium salts, local and systemic anticholinergics,
botulinum toxin A (BTX-A) injections and iontophoresis) are adequately supported by the current literature. More
invasive surgical procedures (suction curettage and sympathetic denervation) have also been extensively
investigated, and can offer a more definitive solution for cases of hyperhidrosis that are unresponsive to non-surgical
treatments. There is no consensus on specific techniques for sympathetic denervation, and this issue should be
further examined by meta-analysis. There are numerous treatment options available to improve the quality of life
(QOL) of the hyperhidrosis patient. In practice, however, the challenge for the dermatologist remains to evaluate the
severity of hyperhidrosis to achieve the best therapeutic outcome, this can be done most effectively using the
Hyperhidrosis Disease Severity Scale (HDSS).
Received: 9 January 2011; Accepted: 15 June 2011
Conflict of interest
The authors have no conflicts of interest to declare.
Funding sources
The authors have no funding sources to declare.
Introduction
Hyperhidrosis (excessive sweating) can be local, regional or
general. Generalized hyperhidrosis is characterized by sweating
over the entire body with no apparent underlying aetiology. Possible causes can be neurological, infectious, endocrine or pharmacological in nature.1 Local or regional hyperhidrosis, including
primary focal hyperhidrosis, is distinguished by sweating in the
axillae, hands, feet, face or forehead, in addition to the crown or
inguinal region. Exacerbating factors are heat, stress, olfactory and
gustatory stimuli.2 Particularly, a neurological lesion called Frey’s
syndrome gives rise to local hyperhidrosis.3,4 Primary focal hyperhidrosis is idiopathic and occurs in otherwise healthy people.1
Hyperhidrosis has a prevalence of 2.8% in the United States,5
while a prevalence of 1% was reported in a population of Israeli
adolescents.6 Regardless of type, hyperhidrosis often has a major
impact on the social, professional and daily activities of patients.7
The publication of a well-designed Cochrane protocol in 2009
entitled ‘Interventions for localized excess sweating’, by Rzany and
Spinner supported the need for evidence-based guidelines for
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treatment of hyperhidrosis.8 In addition, the need for standardization in the surgical treatment approach for hyperhidrosis was
recently highlighted in an expert consensus report.9 The purpose
of the present review is to give an update and a critical analysis on
the effects of pharmaceutical, physical and surgical therapies in
patients with hyperhidrosis and specifically for the four most
frequently affected body regions (axillar, plantar, palmar and
craniofacial).
Methods
The PUBMED and Cochrane databases were searched using the
following terms: hyperhidrosis, excessive sweating, local treatment,
systemic treatment, aluminium salts, anticholinergics, iontophoresis, botulinum toxin A (BTX-A), surgery, sympathectomy, suction
curettage and clinical outcomes. More than 300 English language
abstracts were analysed; the end-points of interest were patient satisfaction, gravimetric results, adverse reactions, long-term effects
and quality of life (QOL). A step-by-step approach was developed
for the four most frequent forms of primary focal hyperhidrosis
ª 2011 The Authors
Journal of the European Academy of Dermatology and Venereology ª 2011 European Academy of Dermatology and Venereology
Hoorens and Ongenae
2
based on a critical analysis of the reviewed studies according to the
Oxford Centre for Evidence-Based Medicine (OCEBM) Levels of
Evidence Working Group, designated as the Oxford 2011 level of
evidence10 (Table 1).
Results
Pathophysiology
There are four million sweat glands distributed over the human
body. Eccrine sweat glands, associated with hyperhidrosis, are
ubiquitous but are most densely located in the palms, soles, axillae
and forehead. Apoeccrine sweat glands are mixed glands that have
seven times higher output than eccrine sweat glands and were designated by several authors to be instrumental in the pathophysiology of hyperhidrosis.11,12 Eccrine sweat glands are innervated by
cholinergic fibres, while the apocrine sweat glands are innervated
by adrenergic fibres.11 There are no quantitative or qualitative histopathological changes in the eccrine sweat glands of hyperhidrosis
patients. The nature of hyperhidrosis is primarily a complex dysfunction and overstimulation of the sympathetic nervous system13
due to a defect in the hypothalamus, leading to a lack of regulatory
feedback of peripheral thermoreceptors.14 Recently, a role for
nitric oxide (NO) in the pathophysiology of primary focal hyperhidrosis was proposed.15 Hyperhidrosis patients were found to
have higher plasma values of NO when compared to healthy controls. NO synthase is found in eccrine sweat glands, where it may
act as a neurotransmitter or induce local vasodilatation leading to
excessive sweating.15 There is a familial history in 30–50% of
hyperhidrosis cases suggesting genetic involvement.2,16 One study
highlights the specific role of chromosome 14 (Locus 14q11.2q13) in the development of primary focal hyperhidrosis.17 This
genetic factor is autosomal dominant with variable penetrance.18
Importantly, excessive sweating does not occur during sleep indicating the role of emotional factors in the pathophysiology of this
disease.19 However, hyperhidrosis is not generally considered an
emotional disorder, but rather as a physiological disorder, noting
the occasional onset of hyperhidrosis in childhood or infancy as
further evidence.20
hyperhidrosis is made based on the criteria according to Hornberger et al. (Table 2). A strong history and clinical examination are
sufficient for diagnosis, making additional tests unnecessary.7 The
Minor iodine test can be used for localization of the zone of excessive sweating and for treatment evaluation.21 Secondary causes, for
example neuropathies, can be diagnosed by performing the thermoregulatory sweat test.22 Gravimetry is a quantitative tool to
measure sweating, most useful in clinical trials to objectively evaluate the outcome of treatment. The criteria for excessive sweating
depend on location and gender. One study defines a sweat rate of
50–100 mg ⁄ 5 min per axilla as necessary for the diagnosis of axillary hyperhidrosis.23
Impact on the quality of life
Hyperhidrosis has a significant impact on social, professional and
daily activities. QOL can be assessed by the Hyperhidrosis Impact
Questionnaire (HHIQ), Dermatology Life Quality Index (DLQI)
and the Hyperhidrosis Disease Severity Scale (HDSS).24 The HDSS
is a four part questionnaire that provides a quantitative measure
of disease severity and the impact on daily life before and after
treatment. Up to 55.2% of hyperhidrosis patients have an HDSS
score of 42,5 (Table 3).
Conservative treatment
Topical treatment Aluminium salts: Aluminium chloride hexahydrate blocks the epidermal duct of eccrine sweat glands, and
Table 2 Diagnostic criteria of primary focal hyperhidrosis
(adapted from Hornberger et al.7)
The presence of focal, visible sweating for at least 6 months without
any obvious cause, besides the presence of at least two of the
following characteristics:
• Bilateral and relatively symmetrical
• Affects the daily activities of the patient
• A frequency of more than one time per week
• Less than 25 years old at the beginning of hyperhidrosis
• A positive family history
• Absence of night sweats
Diagnosis and clinical presentation
The patient with primary focal hyperhidrosis presents with complaints of excessive (most often bilateral) sweating of the axillae,
hands, soles or face. The diagnosis of primary idiopathic focal
Table 3 Hyperhidrosis Disease Severity Scale (HDSS) (adapted
from Solish et al.26)
‘How would you rate the severity of your hyperhidrosis?’
Table 1 The Oxford 2011 levels of evidence10
Level 1: Systematic review of randomized trials or n-of-1 trials
Level 2: Randomized trial or observational study with dramatic effect
• My sweating is never noticeable and never interferes with my daily
activities: 1
• My sweating is tolerable but sometimes interferes with my daily
activities: 2
Level 3: Non-randomized controlled cohort ⁄ follow-up study
• My sweating is barely tolerable and frequently interferes with my
daily activities: 3
Level 4: Case-series, case–control studies or historically controlled
studies
• My sweating is intolerable and always interferes with my daily
activities: 4
Level 5: Mechanism-based reasoning
Score of 1: mild; Score of 2: moderate; Score of 3–4: severe.
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ª 2011 The Authors
Primary focal hyperhidrosis
3
Table 4 Current surgical and non-surgical treatment options in a step-by-step approach for the four most frequent forms of primary
focal hyperhidrosis (axillary, palmar, plantar, craniofacial hyperhidrosis)
Step 1
Step 2
Step 3
Step 4
Step 5
Axillary
hyperhidrosis
Topical aluminium
chloride
hexahydrate
15–20% (to 35%)
in ethyl alcohol (L2),
salicylic acid gel
(L3) or thermophobic
foam (L3)
BTX-A injections (L2)
Systemic
anticholinergics
(L2)
Suction curettage
(L2) or excision
of the sweat
glands (L3)
Repeat suction curettage
(L3) or sympathetic
denervation (L2)
Palmar
hyperhidrosis
Topical aluminium
chloride
hexahydrate
15–20% (35%) in
ethyl alcohol (L2),
salicylic acid gel
(L3) or thermophobic
foam (L3)
Iontophoresis,15–20 mA,
20–30 min, TWI (L2),
Anticholinergics (L2),
BTX-A (L3),
Dry-type (L3)
BTX-A
injections (L2)
Systemic
anticholinergics
(L4)
Sympathetic
denervation (L2)
Plantar
hyperhidrosis
Topical aluminium chloride
hexahydrate 15–20%
(35%) in ethyl alcohol (L2)
or salicylic acid gel (L3)
Iontophoresis, 15–20 mA,
20–30 min, TWI (L2),
Anticholinergics (L2)
BTX-A
injections (L4)
Systemic
anticholinergics
(L4)
Craniofacial
hyperhidrosis
Topical aluminium chloride
hexahydrate 15–20%
(35%) in ethyl alcohol (L2),
Topical glycopyrrolate
(2%) (L3)
Systemic
anticholinergics (L4)
BTX-A
injections (L4)
Sympathetic
denervation (L2)
BTX-A = botulinum toxin A; L = level of evidence; TWI = tap water iontophoresis.
induces atrophy and vacuolization at the level of the glandular
secretory cells. Necrosis of the epidermal cells of the duct delineation is also induced25 (Fig. 1). The initial dose is a 10–12% solution which can be increased to a 35% solution dissolved in ethyl
alcohol or a 2–4% salicylic acid gel.26 The keratolytic properties of
salicylic acid gel improve the absorption of aluminium chloride
hexahydrate in the hyperkeratotic skin. In addition, salicylic acid
has antiperspirant qualities and maintains a normal level of skin
hydration unlike ethyl alcohol.27,28 A recent study described the
use of 20% aluminium sesqui-chlorhydrate thermophobic foam.
This vehicle allows a more practical use on the hairy skin leading
to increased patient compliance. Thermophobic foam is also less
irritating than alcohol solutions and produces similar efficacy.29
The main side effects of aluminium chloride hexahydrate are
skin irritation accompanied by a burning or painful sensation.
Concomitant use of a local hydrocortisone 1% is suggested to
relieve pain.30 A notable disadvantage of aluminium salt treatment
is the short duration of the effect (within one week the condition
reverts to the level of the untreated stage).31 Nevertheless, due to
efficacy, low cost and convenience, topical treatment with aluminium salts should be the first line treatment for all mild forms of
primary focal hyperhidrosis. The vehicle can be adjusted depending on localization of the condition (Table 4).
Topical anticholinergics: Topical anticholinergics are used
mostly in the treatment of craniofacial hyperhidrosis. Two casereports describe successful topical treatment with 0.5% topical
glycopyrrolate for craniofacial hyperhidrosis.32,33 A clinical trial
of 25 patients confirmed these results, showing a significant
reduction in craniofacial sweating with 2% topical glycopyrronium solution applied to one side of the face compared to
AlCl
Figure 1 The eccrine sweat gland and the
different targets for hyperhidrosis treatment.
M = inhibition muscarinic receptors;
? = mechanism of iontophoresis unknown;
x = inhibition of acetylcholine release;
⁄ ⁄ ⁄ ⁄ ⁄ ⁄ = mechanical destruction; AlCl =
aluminium chloride.
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?
M
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Hoorens and Ongenae
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placebo on the other side. However, the effect lasted for only
one to two days.34
Iontophoresis Tap water iontophoresis (TWI): While the mechanism of action of TWI is not yet entirely clear, it is an effective
treatment in the inhibition of sweat secretion (Fig. 1). TWI treatment consists of 20–30 min treatments, three to four times per
week. Each palm or sole is placed in a small tray filled with tap
water with a current of 15–20 mA.26 Upon euhidrosis, maintenance treatment consisting of one session per week or even one
session per month can be effective. Favourable results are attained
in 81.2% of patients with palmoplantar hyperhidrosis after eight
initial treatments. The main side effects are erythema, burning sensation and temporary vesicle formation on the palms and soles.35
Most iontophoretic systems use direct current (DC) although
alternating current (AC) can also be used or even AC with DC offset (AC ⁄ DC). Lesser side effects are associated with devices that
use AC ⁄ DC.36 TWI is a safe, cost-effective and efficient treatment
for the motivated patient with palmar or plantar hyperhidrosis
and should be considered when topical treatment fails (Table 4).
Administration of anticholinergics through iontophoresis: Glycopyrronium or hexopyrronium bromide (0.1%) administration
through iontophoresis has significantly prolonged effectiveness
compared to TWI.37 However, all 26 patients enrolled in this study
experienced varying degrees of systemic effects (dry mouth,
accommodation disturbances, abdominal pain and bladder dysfunction). Another study described the use of a 0.5% solution of
poldine methosulphate with similar systemic side effects.38 A
recent controlled clinical trial found a significantly greater effect of
iontophoresis with administration of a 0.05% glycopyrrolate solution compared to TWI in the treatment of palmoplantar hyperhidrosis with only one patient experiencing dry mouth and throat.39
If TWI fails, administration of low dose anticholinergic agents
through iontophoresis may be considered. However, this treatment option is not recommended by the Canadian Hyperhidrosis
Advisory Committee (Table 4).
Administration of botulinum toxin A through iontophoresis: A
recent study found efficacy in the treatment of palmar hyperhidrosis with the BTX-A, Dysport (n = 8). Patients were treated with
250 units of Dysport dissolved in 3 mL saline on one hand and
TWI on the other hand. Hyperhidrosis was significantly improved
with Dysport iontophoresis treatment compared to TWI. In addition, there were no typical BTX-A side effects, such as loss of muscle strength, observed.40 Moreover, iontophoresis administration of
BTX-A is preferable since injections are often painful. Another
study (n = 8) found similar results with the application of 100
units of Botox dissolved in 2.7 mL saline to one hand. However,
this study reported compensatory hyperhidrosis of the control
palm treated with TWI.41 A case report describes similar positive
results with BTX-A iontophoresis in two patients with needle phobia.42 The current role of BTX-A iontophoresis in treating hyperhidrosis is not entirely clear, but appears to be a promising technique.
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Dry-type iontophoretic device: The dry-type iontophoretic
device uses patient sweat for conduction. The patient holds a cylinder during treatment. Effects similar to TWI have been
described with the advantage of this method being that it can be
administered while performing daily activities such as reading,
watching TV or even jogging.43 One study confirms the effectiveness of dry-type iontophoresis for palmar hyperhidrosis using
conductive pads applied to the patients’ palmar side of the lower
forearm.44 This system induces an immediate reduction in sweat
production confirmed by the Minor iodine test. Further studies
should be performed directly comparing dry-type iontophoresis
and TWI.
BTX-A The BTX-A binds to presynaptic cholinergic neuromuscular junction receptors and autonomic cholinergic neurons.
Upon entering the cytosol, BTX-A breaks down polypeptides necessary for exocytosis of acetylcholine (Fig. 1) resulting in flaccid
paralysis and autonomic dysfunction. Neural activity of eccrine
sweat secretion is regulated by acetylcholine, and therefore, BTX-A
injections decrease sweat secretion.45 Several randomized control
trials (RCTs) have demonstrated the effectiveness of BTX-A in the
treatment of axillary hyperhidrosis.46–49 One study showed an
81.4% reduction in sweat production as measured by gravimetry
after injection of 200 units Dysport. BTX-A, however, has a temporary effect ranging from 4 to 17 months.46 BTX-A injections for
axillary hyperhidrosis results in a drastic improvement of the QOL
(measured by the HHIQ).48 A major drawback of BTX-A treatment is the cost. Complications include headache, myalgia, itching
and increased compensatory sweating of the face.46 Compensatory
sweating is seen in 5% of the patients treated with BTX-A for axillary hyperhidrosis.49 BTX-A is also an option in the treatment of
palmar hyperhidrosis. BTX-A affects acetylcholine secretion at the
level of the neuromuscular junction, and thus could lead to
adverse effects on hand motor function. However, there is no significant difference in grip strength (measured by hydraulic dynamometer) between palms receiving BTX-A and palms receiving
placebo.50,51 In contrast, thumb-index pinch strength decreased
after injections of BTX-A, and 77% of the patients who received
100 units of BTX-A reported hand weakness.51
Three studies have shown BTX-A treatment to be effective and
safe for plantar hyperhidrosis.52–54 The role of BTX-A in the treatment of craniofacial hyperhidrosis55 is investigated and is an alternative to tackle the problem. Indeed the Canadian Hyperhidrosis
Advisory Committee recommends BTX-A injections as a treatment option for axillary, palmar, plantar and craniofacial hyperhidrosis26 (Table 4). Pain during axillary injections can be reduced
through cryotherapy (cold air systems, ice or gel packs)56 while a
peripheral nerve block has been shown to be useful during palmar
injections.57 A recent RCT found that BTX-A reconstituted with
lidocaine significantly reduces pain while providing similar efficacy
on sweat reduction compared to BTX-A dissolved in a salt
solution.58
ª 2011 The Authors
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Systemic anticholinergics Systemic anticholinergics inhibit
sweating by competitive blocking of muscarinic receptors near the
eccrine sweat glands (Fig. 1). The use of anticholinergic drugs,
however, is greatly limited due to well-known side effects. An
RCT described efficacy of methanthelinium bromide (Vagantin)
in a dose of 50 mg, twice daily for axillary hyperhidrosis with
acceptable tolerance.59 A retrospective study reported effective
treatment with glycopyrronium bromide (2 mg, two to three
times daily over 4 years) for both generalized and local hyperhidrosis in 75% of patients. However, 79% of patients complained
of dry mouth, causing a 50% dropout rate.60 Systemic anticholinergics are recommended by the Canadian Hyperhidrosis Advisory
Committee only if other non-surgical treatments fail26 (Table 4).
A case report described the use of Paroxetine (10 mg per day) as
a successful treatment in palmoplantar hyperhidrosis. The most
likely mechanisms of action are anticholinergic and anxiolytic
effects.61 Indeed, the role of anxiety and stress as precipitating factors in the exacerbation of hyperhidrosis is reported in epidemiological studies.2 The possible contribution of psychotropic drugs
in the treatment of primary focal hyperhidrosis should be further
investigated.
Surgical treatment
Local surgery Excision of the sweat glands: A euhidrotic state
can be induced by local surgical removal of sweat glands (Fig. 1).
The first reports of surgical excision of axillary sweat glands
described high complication rates (less arm movement, unaesthetic scars, infection and haematomas).62–64 A clinical trial in
2006 reported a 65% success rate by Shelley’s procedure.65 A
recent study reported that suction curettage was as successful as
radical excision with Y-plasty and a skin conserving operation
while achieving a lower complication rate.66
Suction curettage: Curettage and tumescent liposuction have
been used separately and in combination in the treatment of axillary hyperhidrosis. A cannula is placed at the junction between the
dermis and hypodermis where most sweat glands are located.67
The major advantage of tumescent liposuction is the absence of
unaesthetic scar formation. The success rate varies; one study of
10 patients describes a relapse of 40%.68 Tumescent liposuction
has been found to be particularly effective in the treatment of axillary bromhidrosis.69 Possible complications are bleeding, pain,
haematoma, secondary infection, seroma and damage to the
brachial plexus.67–69
Jemec70 was the first to describe the use of curettage in the
treatment of axillary hyperhidrosis. This technique requires two
1.5 cm skin incisions in the armpit under either local or general
anaesthesia. A curette is used to remove the entire subcutaneous
tissue. A study of 161 patients found 36% of patients dissatisfied
with the outcome, reporting significant side effects such as
haematomas, abscesses and severe necrosis with the need for skin
grafting.71
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Successful results of suction curettage, as evaluated by gravimetry, have been reported with a 12 month follow-up.72 These results
were only significant for patients with a high pre-operative sweat
rate (25 mg ⁄ min). A hypertrophic scar was reported in 1 out of
28 patients, which required skin grafting.72 Other side effects
described were local bruising, skin erosion, bridle formation, seroma, local alopecia and dysesthesia.73
A recent study of 163 patients compared subcutaneous curettage with tumescent suction curettage. Patient satisfaction was
97% vs. 89.2% (subcutaneous curettage vs. tumescent suction
curettage respectively). However, there were greater number of
side effects and a prolonged hospital stay in patients undergoing
subcutaneous curettage.74 Another study reported a 79% success
rate with suction curettage, but in some cases there was a need
for reoperation after 6 months due to persistent high sweat
secretion75 which according to Bechara et al.76 was due to insufficiently aggressive treatment. A comparative study using a aggressive cannula confirmed this theory but reported a higher
complication rate. However, the authors considered the gain in
sweat reduction (66.1% vs. 44.6%) to outweigh the complications.77 In cases where suction curettage is insufficient, reoperation with a more aggressive method can be an option. A study
examining the safety and efficacy of repeating suction curettage
reported that 89% of patients showed a significant decrease in
sweat secretion, with acceptable complications.78 In conclusion,
suction curettage appears to be an effective and relatively safe
treatment for axillary hyperhidrosis after attempting non-surgical
treatments and before stepping up to sympathetic denervation
(Table 4).
Sympathetic denervation There are three different techniques
for the treatment of hyperhidrosis by sympathetic denervation.
(Fig. 1). The first method is sympathectomy or ganglionectomy
(for example of the T2 ganglion) and is performed by a transection above and below the T2 ganglion or by resection or ablation
of the actual ganglion. The second method is a sympathotomy or
sympathicotomy which is performed by interrupting the rami
interganglionares between the stellate ganglion and the T2 ganglion. Finally, a ramectomy results in the interruption of the rami
communicantes.79,80 The terms sympathectomy, sympathotomy
and ramectomy are often used interchangeably without a proper
definition and therefore need clarification. Clipping is the analogue of sympathotomy but uses a clip to interrupt the sympathic
chain instead of ablation or resection. Blocking is the analogue of
sympathectomy by using a clip. The post-operative results of
sympathectomy, sympathotomy and clipping or blocking are
similar.81,82 The advantage of the clip is that it can be removed if
excessive compensatory sweating occurs.83,84
Sympathetic denervation is the last step in treating severe palmar, craniofacial and axillary hyperhidrosis (Table 4). Studies
in the treatment of plantar hyperhidrosis by lumbar sympathectomy have reported good results at follow-up.85–87 The major
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complication described is sexual dysfunction87,88 and therefore,
fine tuning of the technique is necessary to introduce it as a standard approach.
The most common side effect of sympathetic denervation in the
treatment of primary axillary, palmar and craniofacial hyperhidrosis is compensatory sweating, with incidence ranging from 14% to
90% for mild compensatory sweating and 1.2% to 30.9% for
severe compensatory sweating.89 The large range in results may
partly rely on a lack of objective methodology for defining compensatory sweating, as well as the wide variety of techniques of
sympathetic denervation. Compensatory sweating was originally
thought to be a mechanism of excessive sweating (in an anatomical region with an intact sympathetic nervous system) to maintain
a constant rate of total sweat secretion.90 However, this theory was
not confirmed by other studies, demonstrating that compensatory
sweating represented a reflex action by an altered feedback mechanism at the level of the hypothalamus which is dependent on the
level at which sympathetic denervation occurs. Sympathectomy at
the level of the T2 ganglion leads to decreased negative feedback
to the hypothalamus. When performing a sympathectomy at a
lower level, the negative feedback to the hypothalamus is less
inhibited, leading to a decrease in compensatory sweating. Chou
et al.91 have proposed the term ‘reflex sweating’ to replace compensatory sweating. Other side effects described in a review article
by Dumont89 are gustatory sweating, cardiac effects, phantom
sweating, lung function changes, dry hands and altered taste.
Besides these side effects there are significant risks of complications
during and after surgery (arterial or venous vascular injury, pneumothorax, infection, Horner syndrome etc.).
Discussion
Together, the literature on the severity and procentual risk of side
effects associated with each treatment for hyperhidrosis suggests
that disease severity (as measured by the HDSS) and affected
body region must be considered when deciding on treatment.
Table 4 summarizes the various effective surgical and non-surgical
treatments for the four most frequent forms of primary focal
hyperhidrosis. Table 1 reveals that no systematic reviews of RCTs
(level 1) have been conducted to date. However, a protocol has
been designed for such a review.8 There is a high level of evidence
to support most therapeutic options in the step-by-step guidelines
(level 2). Notably, the level of evidence for BTX-A injections
depends on the treated region; with a high level of evidence for
axillar and palmar hyperhidrosis, while a lower level of evidence
(level 4) was found for craniofacial and plantar regions. Likewise,
for systemic anticholinergics the level of evidence is high only for
the axillar region (level 2), and low for all other locations (level
4). Finally, a higher level of evidence was found for aluminium
hexahydrate formulation in ethyl alcohol (level 2) than the formulations in salicylic acid gel or thermophobic foam (level 3).
The HDDS is useful in the assessment of severity of hyperhidrosis. However, in addition to the HDDS score and localization,
JEADV 2012, 26, 1–8
factors such as the duration of effect, side effects, complications,
cost, local level of availability of health care and patient wishes
must be considered when deciding on treatment options. Since
hyperhidrosis is not a life-threatening condition, but rather a condition which significantly interferes with social, professional and
daily activities, the patient must make an informed decision concerning the best management strategy. The precise pathogenesis of
hyperhidrosis is not yet fully understood and as such current treatments are focused on symptoms instead of underlying cause. The
use of BTX-A and anticholinergics through iontophoresis, and the
new dry-type iontophoresis may offer new treatment possibilities.
To find a more causal therapeutic approach, clinical trials should
examine the effect of psychotropic drugs on excessive sweating. In
the case of more aggressive therapy, the level at which sympathetic
denervation should be performed to insure optimal outcome and
reduce compensatory sweating for the different types of hyperhidrosis remains unclear. Future studies should focus on the specific
neurophysiological dysregulation of the autonomic nervous system, the role of specific neurotransmitters and the genetic basis of
primary focal hyperhidrosis to support the development of more
specific causal therapies.
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ª 2011 The Authors

Primary focal hyperhidrosis: current treatment options and a

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