Primary hyperhidrosis is excessive uncontrollable sweating without any discernible cause. It most commonly involves the axillae, palms, and soles but may also involve the face and groin. 
Secondary hyperhidrosis may be caused by endocrine disorders (eg, hyperthyroidism), secretory tumors (eg, pheochromocytoma), sympathetic nervous system disorders, or primary neurologic or psychiatric disorders. See the image below.
The incidence of hyperhidrosis is uncertain, but Adar's study of a young Israeli population reported a prevalence of 0.6-1% for palmar hyperhidrosis; familial involvement was reported in 25% of patients.  The incidence of axillary hyperhidrosis is believed to be similar.
Etiology of axillary hyperhidrosis is unknown but is related to increased cholinergic sympathetic stimulation of the sweat glands in the axilla. Although the glands invariably become remarkably hypertrophied in this condition, the dramatic glandular growth and oversecretion is believed to be secondary rather than primary; a parallel concept is oxyntic cell hypertrophy in peptic ulcer disease due to vagal hypertonicity.
The observed atrophy of sweat glands in grafted (thus denervated) skin, with reappearance of sweating with reinnervation, led to the conceptual link between sympathetic tone and acinar hypersecretion. Further evidence of the neural control of sweat production comes from the observation that local anesthetic injection transiently stops hypersecretion of sweat as does cholinergic blockade from local injection of botulinum toxin.
While axillary hyperhidrosis almost always begins with puberty, no direct hormonal connection has been suggested.
Several related axillary conditions may be confused with hyperhidrosis.
Axillary bromidrosis (or osmidrosis) is chronic offensive axillary odor; it may be related to apocrine secretions and to chronic bacterial colonization (especially with diphtheroids and micrococci), and antibiotic treatment may be suppressive or curative.
Axillary lymphadenitis is the inflammation and enlargement of underarm lymph nodes.
Axillary hidradenitis is chronic recurring infection of the apocrine sweat glands, manifested by production of repeated boils and sinuses. Once established, the condition may be suppressed, but not cured, by antibiotics. Excision of the involved skin and glands is the only cure; such resections are generally quite disfiguring. The exact cause is unknown, but a hormonal influence appears to be involved.
An axillary breast is the presence in the axilla of subcutaneous breast tissue with or without a nipple.
Bisbal et al have determined that eccrine and apocrine sweat glands are mixed in the axilla, with a proportion of 1:1. 
In patients with axillary hyperhidrosis, Morgan and Hughes demonstrated that the apocrine glands are significantly larger and more numerous than those in axillary hidradenitis and in healthy control subjects. 
Following a thorough resection of the subcutaneous axillary sweat glands (Skoog procedure), a few eccrine glands remain, and practically no apocrine glands can be found.
Thus it seems that a Skoog adenectomy is essentially an apocrinectomy. This is at odds with the observation that the profuse sweat produced in axillary hyperhidrosis (and stopped by Skoog resection) is clear and odorless; classically, apocrine sweat is described as cloudy and odoriferous, while eccrine sweat is labeled clear and without odor. No one has reconciled these seeming inconsistencies, but the inference is that the clear, odorless, profuse sweating observed in axillary hyperhidrosis comes from the hypertrophied and overactive apocrine glands.
Patients with axillary hyperhidrosis usually complain of constant or frequent sweating, with streams of wetness running down their sides. This diathesis wets and ruins clothing and produces social embarrassment or functional problems from skin maceration. Severely affected patients also may have secondary microbial infections. Unlike functional sweating, which may be triggered by exercise, exertion, or high temperature, hyperhidrosis may require no trigger at all or may be stimulated by emotional situations and/or anxiety. Most patients with axillary hyperhidrosis have tried multiple antiperspirants and various medications and often have devised various coping methods involving clothing strategies. Many have consulted various physicians, often to no avail.
Some patients may have unilateral axillary hyperhidrosis or a more severe diathesis on one side than the other. Many patients with axillary hyperhidrosis also are afflicted with palmar, facial, or plantar hyperhidrosis to some degree.
The problem usually begins with puberty but also may present in mid childhood, especially in Asian populations.
A study by Thorlacius et al suggested that with regard to differentiating axillary and palmar hyperhidrosis from physiologically normal sweat production, a gravimetric testing result of 100 mg of sweat/5 min may be an acceptable cut-off point. 
As with any invasive treatment of a non—life-threatening condition, the risks of axillary hyperhidrosis surgery need to be low. Any health condition that substantially increases the surgical risk may make a recommendation for such surgery inappropriate.
Pulmonary or cardiac pathology may make thoracic surgery, even endoscopic thoracic surgery, too dangerous for the nature of the problem. Problems with skin circulation (eg, lupus) or situations known to degrade wound healing (eg, steroid treatment, previous radiation therapy, diabetes) may make the risk of surgery unacceptable.
Patients with only (or predominantly) axillary hyperhidrosis probably should not be steered toward endoscopic transthoracic sympathectomy (ETS). Patients with multiple hyperhidrotic sites should strongly consider ETS before Skoog adenectomy.
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