Same-Patient Prospective Comparison of Botox Versus Dysport for the Treatment of Primary Axillary Hyperhidrosis and Review of Literature
September 2011 | Volume 10 | Issue 9 | Case Report | 1013 | Copyright © 2011
Irene J. Vergilis-Kalner MD
Background: Botulinum toxin (BTX) is an effective, FDA-approved treatment for primary axillary hyperhidrosis. In this prospective study, two non-bioequivalent toxins: Botox (Allergan, Irvine, CA, USA) and Dysport (Ipsen Ltd., Slough, Berkshire, UK) were compared for the treatment of primary axillary hyperhidrosis. Objective: The objective was to compare the injection site pain, efficacy, safety and tolerability of Botox versus Dysport in the treatment of primary axillary hyperhidrosis using a conversion factor of 1:3, respectively. Methods: A patient with primary axillary hyperhidrosis was treated with 100 units of Botox into the right axilla and 300 units of Dysport into the left axilla. Patient was blinded as to which axilla received treatment and with which of the two toxins. Pain at the injection site of these two toxins was evaluated. The patient was subsequently followed for the next 10 months to evaluate the difference in these two toxins in regards to side effects, time to the onset of reduction of sweating and the duration of action of these two toxins. Results: Significant difference was observed in the onset of action of these two toxins, with dramatic reduction in sweating being observed after one week of injection with Botox and after two weeks of injection with Dysport. At the two-week time point, similar success in eliminating sweating was reported in both axilla. The duration of benefits also differed between the two toxins, with elimination of sweating in the Dysport-treated axilla lasting six months and, in the Botox-treated axilla, nine months. No other differences were observed between these two toxins. Conclusions: Both Botox and Dysport led to a similar perceived reduction of sweating in the treatment of primary axillary hyperhidrosis when a conversion factor of 1:3 was used. However, Botox treatment resulted in a quicker onset of action and longer duration of benefits. J Drugs Dermatol. 2011;10(9):1013-1015.
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Primary hyperhidrosis is characterized by excessive and uncontrollable sweating beyond that which is required to return body temperature to normal in a defined region of the body. Severe focal hyperhidrosis affects 2.8 percent of the population and can have significant psychosocial implications. This condition, which is commonly seen in young people, is often socially, physically, emotionally and professionally debilitating, leading to significant quality of life impairments. First-line therapy traditionally employs topical agents such as aluminum chloride, but efficacy and tolerability vary widely. Other therapies include systemic anticholinergic medications, iontophoresis and surgical interventions such as sympathectomy or surgical removal of axillary skin and sweat glands, which although often effective, are invasive and limited by complications.
Since 1996, intracutaneous injections of botulinum toxin have been used as a minimally invasive treatment for focal hyperhidrosis with numerous studies documenting safety, efficacy and extremely high levels of patient satisfaction. Botulinum toxin A (BTX-A) is one of eight exotixins produced by Clostridium botulinum, a gram-positive, spore-forming anerobe.1 Primary axillary hyperhidrosis is thought to result from localized hyperstimultion of sweat glands by the cholinergic sympathetic fibers.2 Injection of BTX leads to flaccid paralysis which results from the temporary chemodenervation of the muscle fibers at the neuromuscular junctions of the eccrine sweat glands, which utilize acetylcholine as the neurotransmitter.1,3-5 Neurotoxin inhibits the release of the neurotransmitter acetylcholine at the presynaptic axon terminals leading to chemodenervation after BTX-A administration and explains the effectiveness of BTX-A in the treatment of primary axillary hyperhidrosis.1,3-5
Chemodenervation using BTX-A was approved by the US Food and Drug Administration (FDA) in 2004 for the treatment