Updated: May 29, 2009
Hyperhidrosis, which is sweating in excess of that required for normal thermoregulation, is a condition that usually begins in either childhood or adolescence. Although any site on the body can be affected, the sites most commonly affected are the palms, soles, and axillae. This condition may be idiopathic or secondary to other diseases, metabolic disorders, febrile illnesses, or medication use. Hyperhidrosis exists in 3 forms: emotionally induced (in which it affects the palms, soles, and axillae1,2 ), localized, or generalized. The condition often causes great emotional distress and occupational disability for the patient, regardless of the form.
Generalized hyperhidrosis may be the consequence of autonomic dysregulation, or it may develop secondary to a metabolic disorder, febrile illness, or malignancy. In its localized form, hyperhidrosis may result from a disruption followed by abnormal regeneration of sympathetic nerves or a localized abnormality in the number or distribution of the eccrine glands, or it may be associated with other (usually vascular) abnormalities.
Essential hyperhidrosis, a disorder of the eccrine sweat glands, is associated with sympathetic overactivity.3 It does not appear to be a generalized disorder involving vascular endothelium.
In adolescents and young adults, an incidence of 0.6-1.0% is reported.4
Palmoplantar hyperhidrosis occurs 20 times more frequently in the Japanese than in any other ethnic group.5,6
Hyperhidrosis is not associated with mortality. Severe cases of hyperhidrosis may adversely affect the patient's quality of life (see Complications).
All races can be affected; however, Japanese are reportedly affected more than 20 times more frequently than other ethnic groups.5,6
Both sexes can be affected by hyperhidrosis.
Persons of all ages can be affected by hyperhidrosis. Localized hyperhidrosis, unlike generalized hyperhidrosis, usually begins in childhood or adolescence. In a study of 850 patients with palmar, axillary, or facial hyperhidrosis, 62% of patients reported that sweating began since before they could remember; 33%, since puberty; and 5%, during adulthood.7
Hyperhidrosis may be idiopathic or secondary to other diseases, metabolic disorders, febrile illnesses, or medication use.
Blue Rubber Bleb Nevus Syndrome
Glomus Tumor
Pachydermoperiostosis
POEMS Syndrome
Pretibial Myxedema
Burning feet syndrome
Neoplastic diseases
Neurologic diseases
Thyrotoxicosis
Diabetes mellitus
Hypoglycemia
Gout
Pheochromocytoma
Menopause
Febrile illnesses
Use of medications (eg, propranolol, physostigmine, pilocarpine, tricyclic antidepressants, venlafaxine)
Chronic alcoholism
Hodgkin disease
Tuberculosis
Eccrine nevus
Eccrine angiomatous hamartoma
Riley-Day syndrome (familial dysautonomia)
Individuals with hyperhidrosis have morphologically and functionally normal eccrine glands. Localized hyperhidrosis may result from an abnormal number and/or distribution of otherwise normal eccrine glands. Examples of such conditions include eccrine nevus and eccrine angiomatous hamartoma.
Therapy can be challenging for both the patient and the physician. Both topical and systemic medications have been used. Other treatment options include iontophoresis and botulinum toxin injections.
In addition to pharmacologic therapy, other treatments include surgical sympathectomy, surgical excision of the affected areas, and subcutaneous liposuction. Each modality has been used effectively.
Palmar hyperhidrosis is a benign functional disorder that is a psychological and social handicap.33 A survey showed thoracoscopic sympathectomy to be minimally invasive and to improve the patient's quality of life, even if compensatory hyperhidrosis occurs.
Consult a neurosurgeon if sympathectomy is necessary in severe cases of hyperhidrosis that are refractory to all other treatments.
The goals of pharmacotherapy are to reduce morbidity and prevent complications. Control of palmar hyperhidrosis with a new dry-type iontophoretic device has been described.47 Dry-type iontophoresis may reduce palmar sweating more conveniently than other conventional methods.
These agents reduce perspiration by denaturing keratin and thereby occluding the pores of the sweat glands. They have a short-lasting effect. Contact sensitization is increased, especially with formalin. Aldehydes are used to treat the palms and soles; they are not as effective in the axillae.
2% as Cidex. Not as effective but less staining. 20-50% solution can be diluted to 10% (more effective, especially for feet, but still staining occurs).
Apply to affected areas 3 times per wk for 2 wk, then every wk or prn
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid contact with eyes or mucous membranes; produces a temporary brown discoloration; may cause local irritation; thermal decomposition may release harmful fumes according to MSDS
These agents are antiperspirants that are used in the management of hyperhidrosis.
Certin-Dri and Xerac are over-the-counter products at low concentrations. Work best if applied to a dry area and covered with plastic overnight. Should be washed off in the morning. Effect should be noted within 1 mo.
Apply to affected area qhs for 2-7 consecutive days prn; to prevent irritation, completely dry area prior to application
Administer as in adults
None reported
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not for application on irritated, broken, or recently shaved skin
The use of these agents is usually avoided because they are poorly tolerated at the required doses when given systemically. Acetylcholine is the preglandular neurotransmitter for sweat secretion. These drugs inhibit the binding of acetylcholine to the cholinergic receptor. Clinical effects usually occur within days.
Blocks action of acetylcholine at postganglionic parasympathetic receptor sites.
15 mg PO bid/tid 30 min ac initially; gradually titrate to effect
Not established
Concurrent antacids decrease effects; concurrent disopyramide, TCAs, phenothiazides, corticosteroids, atenolol, digoxin, bretylium, or other drugs with anticholinergic activity increase toxicity; may decrease effectiveness of phenothiazides
Documented hypersensitivity to product or related products; ulcerative colitis; narrow-angle glaucoma; obstructive disease of GI tract or urinary tract; intestinal atony of elderly or debilitated patients; myasthenia gravis; toxic megacolon; unstable cardiovascular adjustment in acute hemorrhage
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal, CNS, or hepatic disease; caution in geriatric patients and patients with Down syndrome; may cause urinary retention, arrhythmia, CNS dysfunction, visual changes, xerostomia, constipation, or heat intolerance
Confusion may occur in geriatric patients; diarrhea may be early symptom of incomplete intestinal obstruction (in this instance, treatment with propantheline would be inappropriate and possibly harmful); autonomic neuropathy may occur; caution on concomitant administration of belladonna alkaloids, synthetic/semisynthetic anticholinergic agents, narcotic analgesics, type 1 antiarrhythmics, antihistamines, phenothiazines, TCAs, or other psychoactive drugs; additional adverse effects include congestive heart failure, coronary heart disease, hepatic or renal disease, hiatal hernia associated with reflux esophagitis, hypertension, and hyperthyroidism
Acts in smooth muscle, CNS, and secretory glands to blocks action of acetylcholine at parasympathetic sites.
1-2 mg PO bid/tid initially, then titrate to effective dose; not to exceed 8 mg/d
Topical formulation of extemporaneously formulated 0.5-1% cream or roll-on lotion; 0.1% solution applied using iontophoresis
<16 years: Not established
>16 years: Administer as in adults
Levodopa decreases effects; concurrent antacids decrease effects; concurrent disopyramide, TCAs, phenothiazides, corticosteroids, atenolol, digoxin, bretylium, or other drugs with anticholinergic activity increase activity; may decrease effectiveness of phenothiazides; Slow-K enteric toxicity
Documented hypersensitivity to product or related products; ulcerative colitis; narrow-angle glaucoma; obstructive disease of GI tract or urinary tract; intestinal atony of elderly or debilitated patients; myasthenia gravis; toxic megacolon; unstable cardiovascular adjustment in acute hemorrhage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal, CNS, or hepatic disease; caution in geriatric patients and patients with Down syndrome; may cause urinary retention, arrhythmia, CNS dysfunction, visual changes, xerostomia, constipation, or heat intolerance
Confusion may occur in geriatric patients; diarrhea may be early symptom of incomplete intestinal obstruction (in this instance, treatment with propantheline would be inappropriate and possibly harmful); autonomic neuropathy may occur; caution on concomitant administration of belladonna alkaloids, synthetic/semisynthetic anticholinergic agents, narcotic analgesics, type 1 antiarrhythmics, antihistamines, phenothiazines, TCAs, or other psychoactive drugs; additional adverse effects include congestive heart failure, coronary heart disease, hepatic or renal disease, hiatal hernia associated with reflux esophagitis, hypertension, and hyperthyroidism; contains benzyl alcohol (not for use in patients <1 mo)
Blocks striatal cholinergic receptors; may help balance cholinergic and dopaminergic activity in striatum.
1-2 mg/d PO; not to exceed 6 mg/d
Not recommended
Decreases effects of levodopa; concurrent antacids decrease effects; concurrent disopyramide, TCAs, phenothiazides, corticosteroids, atenolol, digoxin, bretylium, or other drugs with anticholinergic activity increase toxicity; may decrease effectiveness of phenothiazides
Documented hypersensitivity to product or related products; children <3 y; ulcerative colitis; narrow-angle glaucoma; obstructive disease of GI tract or urinary tract; intestinal atony of elderly or debilitated patients; myasthenia gravis; toxic megacolon; unstable cardiovascular adjustment in acute hemorrhage
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal, CNS, or hepatic disease; caution in geriatric patients and patients with Down syndrome; may cause urinary retention, arrhythmia, CNS dysfunction, visual changes, xerostomia, constipation, or heat intolerance
Confusion may occur in geriatric patients; diarrhea may be early symptom of incomplete intestinal obstruction (in this instance, treatment with propantheline would be inappropriate and possibly harmful); autonomic neuropathy may occur; caution on concomitant administration of belladonna alkaloids, synthetic/semisynthetic anticholinergic agents, narcotic analgesics, type 1 antiarrhythmics, antihistamines, phenothiazines, TCAs, or other psychoactive drugs; additional adverse effects include congestive heart failure, coronary heart disease, hepatic or renal disease, hiatal hernia associated with reflux esophagitis, hypertension, and hyperthyroidism
Inhibits action of acetylcholine on smooth muscle and has direct antispasmodic effect on smooth muscles.
Immediate release: 5 mg PO bid/tid; not to exceed 5 mg qid
Extended release: 5 mg or 10 mg PO qd at same time each day; dose may be increased in 5-mg increments qwk, not to exceed 30 mg/d
<5 years: Not established
>5 years: 5 mg (immediate release) PO bid; not to exceed 5 mg tid
>6 years: 5 mg (extended release) PO qd at same time each day; dose may be increased in 5-mg increments, not to exceed 20 mg/d
Effects decrease with concurrent antacids; concurrent disopyramide, TCAs, phenothiazides, corticosteroids, atenolol, digoxin, bretylium, or other drugs with anticholinergic activity increase toxicity; may decrease effectiveness of phenothiazides
Documented hypersensitivity to product or related products; ulcerative colitis; narrow-angle glaucoma; obstructive disease of GI tract or urinary tract; intestinal atony of elderly or debilitated patients; myasthenia gravis; toxic megacolon; unstable cardiovascular adjustment in acute hemorrhage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal, CNS, or hepatic disease; caution in geriatric patients and patients with Down syndrome; may cause urinary retention, arrhythmia, CNS dysfunction, visual changes, xerostomia, constipation, or heat intolerance
Confusion may occur in geriatric patients; diarrhea may be early symptom of incomplete intestinal obstruction (in this instance, treatment with propantheline would be inappropriate and possibly harmful); autonomic neuropathy may occur; caution on concomitant administration of belladonna alkaloids, synthetic/semisynthetic anticholinergic agents, narcotic analgesics, type 1 antiarrhythmics, antihistamines, phenothiazines, TCAs, or other psychoactive drugs; additional adverse effects include congestive heart failure, coronary heart disease, hepatic or renal disease, hiatal hernia associated with reflux esophagitis, hypertension, and hyperthyroidism
These agents inhibit the transmission of nerve impulses at the neuromuscular junction of skeletal muscle and/or autonomic ganglia.
Prevents calcium-dependent release of acetylcholine and produces a state of denervation at the neuromuscular junction and postganglionic sympathetic cholinergic nerves in the sweat glands.
Each injection produces an area of anhydrosis approximately 1.2 cm in diameter. Reportedly results in anhydrosis lasting 4-12 mo.
Injections of botulinum toxin must be repeated at varying intervals to maintain long-term results.
Palmar hyperhidrosis: 50 subepidermal injections of 2 U per palm (total 100 U per palm)
Axillary hyperhidrosis: 50 U/axilla injected intradermally each axilla in 0.1-0.2 mL aliquots to multiple (10 to 15) sites in each axilla
Not established
Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy; mild transient thumb weakness and muscle weakness at toxin-treated sites may occur but resolve within 2-5 wk
Units of biological activity of botulinum toxin type A cannot be compared to nor converted into units of any other botulinum toxin; relative potencies of botulinum A toxin preparations available in United Kingdom and North American differ significantly; reduced blinking as a result of administration of Botox ® Cosmetic may lead to corneal exposure, persistent epithelial defect and corneal ulceration; epinephrine should be available or other precautions taken as necessary should an anaphylactic reaction occur
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hyperhidrosis, excessive sweating, palmoplantar hyperhidrosis, emotionally induced hyperhidrosis, generalized hyperhidrosis, localized hyperhidrosis, palmoplantar sweating, axillary hyperhidrosis, nocturnal hyperhidrosis
Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.
Rachel Altman, MD, Staff Physician, Department of Dermatology, UMDNJ-New Jersey Medical School
Rachel Altman, MD is a member of the following medical societies: Alpha Omega Alpha and Sigma Xi
Disclosure: Nothing to disclose.
George Kihiczak, MD, Clinical Associate Professor, Department of Dermatology, New Jersey Medical School and University Hospital
George Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Medical Society of New Jersey
Disclosure: Nothing to disclose.
Catharine Lisa Kauffman, MD, FACP, Georgetown Dermatology and Georgetown Dermpath
Catharine Lisa Kauffman, MD, FACP is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Royal Society of Medicine, Society for Investigative Dermatology, and Women's Dermatologic Society
Disclosure: Nothing to disclose.
Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Lester F Libow, MD, Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association
Disclosure: Nothing to disclose.
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
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