Oral Presentation Abstracts: 50


[50]

SUCCESSFUL LONG-TERM TREATMENT OF PAIN IN POST-HERPETIC NEURALGIA WITH THE VENOM OF APIS MELLIFERA

*Andrew Kochan, M.D.

The treatment of post-herpetic neuralgia (PHN) is unsatisfactory to most sufferers and strictly palliative in nature. Current treatments involve tedious repetitive procedures, or the taking of medications that may have serious side effects. None of these interventions alter the natural history of the condition.
Treating pain with the venom of the European honeybee, Apis mellifera, dates back several thousand years. Eleven PHN patients, who suffered pain for an average of 45.5 months (range 6 to 131), were injected at multiple sites (range 3 to 30) with 100 micrograms of dried bee venom in 0.1 cc of 0.5% lidocaine. These sites corresponded to the location of the greatest pain, origins of shooting pain and to areas of cutaneous scarring. Patients received an average of 15 treatments.
The mean Visual Analog Scale (VAS) pain score at the beginning of treatment was 7.8 ± 1.4 and at the end was 2.7 ± 2.3, representing a mean decrease of 4.8 ± 3.3 (p < 0.005). Within 3 days of beginning treatment five patients noted significant improvement (>50% decrease in pain). At follow-up, which averaged 18 months from completion of treatment, the group had a mean VAS score of 2.8 ± 2.8, with 3 of the patients pain-free. Initially, 9 patients were taking antidepressants and 3 were taking opioids. By the end of treatment, 5 patients stopped antidepressants and 1 stopped opioids. Those remaining on medication were on lower dosages.
There are over 20 biologically active peptides in Apis mellifera venom, some of which are anti-inflammatory and others neurotoxic in nature. The results of treatment in these patients suggest that one or more components of honeybee venom are able to decrease the pain of PHN by more than 66%. The results are maintained long-term. Relief of pain using bee venom may involve retrograde transport of one or more of these peptides in the axon of the affected nerve cell to the DRG, thereby modifying transmission of the pain signal to the CNS.

Corresponding Author: Andrew Kochan M.D., 8744 Paso Robles Ave., Northridge, CA 91325, USA ©