1274: Botulinum Toxin Type a Inhibits the Release of Calcitonin Gene-Related Peptide in an Acute Inflammatory Rat Bladder Model

Background: Botulinum toxin type A (BoNT-A) is widely employed for cosmetic purposes and in the treatment of certain diseases such as strabismus, hemifacial spasm and focal dystonia among others. BoNT-A effect mainly acts at the muscular level by inhibiting the release of acetylcholine at presynaptic levels consequently blocking the action potential in the neuromuscular junction. Despite the great progress in approval and pharmaceutical usage, improvement in displacing BoNT-A to other pathologies has remained short. Patients under diagnosis of several types of cancer experience pain in a myriad of ways; it can be experienced as hyperalgesia or allodynia, and the severity of the pain depends, in some degree, on the place that the tumor is located. Pain relief in patients diagnosed with cancer is not always optimal, and as the disease progresses, transition to more aggressive drugs, like opioids is sometimes unavoidable. In recent years BoNT-A employment in cancer has been explored, as well as an antinociceptive drug; experiments in neuropathic, inflammatory and acute pain have been carried out in animal models and humans. Although its mechanism has not been fully cleared evidence has shown that BoNT-A inhibits the secretion of pain mediators (substance P, Glutamate, and calcitonin gene related protein) from the nerve endings and dorsal root ganglion, impacting directly on the nociceptive transmission through the anterolateral and trigeminothalamic systems. Aim: Collect available literature regarding molecular, physiological and neurobiological evidence of the BoNT-A in cancer patients suffering from acute, neuropathic and inflammatory pain in order to identify possible mechanisms of action in which the BoNT-A could impact positively in pain treatment. Conclusion: BoNT-A could be an important neo-adjuvant and coadjuvant in the treatment of several types of cancer, diminish pro-tumor activity and secondary pain.

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Improvement in Both Raynaud Disease and Hyperhidrosis in Response to Botulinum Toxin Type a Treatment.

Journal of Cutaneous Medicine and Surgery ◽

10.2310/7750.2008.07044 ◽

2008 ◽

Vol 12 (4) ◽

pp. 189-193 ◽

Cited By ~ 16

Author(s):

Irèn Kossintseva ◽

Benjamin Barankin

Keyword(s):

Botulinum Toxin ◽

Color Change ◽

Glutamate Release ◽

Botulinum Toxin Type A ◽

Type A ◽

Botulinum Toxin Type ◽

Negative Control ◽

Palmar Hyperhidrosis ◽

Calcitonin Gene ◽

Positive Results

Background: A patient with concurrent Raynaud disease presented for Hyperhidrosis of the axillae and palms. After a positive response to botulinum toxin type A (BoNTA) for axillary hyperhidrosis, she returned requesting palmar treatment. Objectives: Our goal was to investigate the effect of BoNTA on Raynaud disease in concurrent hyperhidrosis with respect to color change, swelling, and digital pain. Methods: The patient had treatment with 100 units of BoNTA to one hand at first, with the other being a negative control, followed by treatment of the second hand 1 week later. Results: After the injection into the first palm, the patient demonstrated an 85% reduction in palmar hyperhidrosis and a significant improvement in her Raynaud symptoms. Specifically, the BoNTA-treated hand had reduced swelling, color change, and pain, whereas the untreated control hand remained affected. After the second hand was treated, it, too, demonstrated the same positive results. Conclusions: Our case report of concurrent Raynaud disease and palmar hyperhidrosis shows significant improvement in both conditions to BoNTA administration. The physiology is multifactorial and relates to BoNTA's effect on acetylcholine, noradrenaline, substance P, calcitonin gene-related peptide, and glutamate release from nerve terminals. These results present an encouraging novel treatment option in dermatology for patients with Raynaud disease.

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