• Oliver P Kreyden and E Paul Scheidegger.
• Praxis Methininserhof, Muttenz, Switzerland. kreyden@hin.ch
• Clin. Dermatol. 2004 Jan 1; 22 (1): 40-4.

AbstractFor a long period the therapeutic modalities to treat focal hyperhidrosis (HH) were very limited. Due to this the problem of focal HH was delt with stepmotherly. Nowadays we can consider BTX as the therapy of choice for axillary HH after topical treatment with aluminium salts have failed. The amount of successful reports on botulinum toxin (BTX) in the treatment of focal HH brought a change and the interest for this specific disorder grew. This article gives details on anatomy and physiology of sweating and mechanism of BTX. Further distinctive syndromes associated with HH, which all can be treated with BTX like localized unilateral hyperhidrosis (LUH), Ross' Syndrome and Frey' Syndrome are presented. A diagnosis of primary HH is usually based on the patients's history, typical younger age and visible signs of excessive sweating. Before treatment it is important to objectify focal HH with performing sweat tests such like Minor starch test and/or gravimetry. The total number of sweat glands is somewhere between 2 and 4 million and only about 5% are active at the same time, indicating the enormous potential for sweat production. The eccrine sweat gland is a long-branched tubular structure with highly coiled secretory portion and a straight ductular portion. Sweat is produced by clear and dark cells and is a clear hypotonic, odorless fluid. In response to nerve impulses, Acetylcholine (ACh) is released from the presynaptic nerve endings and then binds to postsynaptic cholinergic receptors presumably present in the basolateral membrane of the clear cells. This activates a complex in- and efflux of electrolytes creating the hypotonic sweat. Injection of BTX leads to temporary chemodenervation with the loss or reduction of activity of the target organ. BTX is consisted of a heavy and a light chain. The structural architecture of BTX comprises three domains-L, H(N) and H(C)-each with a specific function in the mechanism of cell intoxication. The heavy chain is responsible for binding to the nerve cell, whereas the light chain catalyzes the proteolysis of one of the three SNARE proteins (Snap-25, Vamp or Syntaxin) depending to the serotype of BTX (7 serotypes A-G). Once cleaved by BTX, the SNARE proteins cannot become part of the complex capable of mediating the vesicle membrane fusion and therefore prevents the release of ACh and hence transmission of the nerve impulse.

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