Botulinum toxin type B: where do we stand?

Accessible online at: www.karger.com/journals/ene Therapeutic use of botulinum toxin type A (BT-A) has dramatically increased after its introduction by Scott [1] in 1980. It now provides help for patients suffering from muscle hyperactivity disorders in neurology, rehabilitation medicine, pediatrics, otorhinolaryngology, ophthalmology, urology and many other areas. Recently, it has been recognised that its cholinergic blockade can also be used to reduce exocrine gland hyperactivity: the longsearched-for remedy for hyperhidrosis. With some evidence suggesting an analgetic effect in tension headache and migraine and with extension of its indications into the fashion world for removal of wrinkles, BT might look almost like a 19th century patent medicine. It certainly sells like one: worldwide BT-A sales soared to mind-boggling US$ 300 millions or so. Obviously, such a market attracts manufacturers. A new one has just arrived. With his product using botulinum toxin type B (BT-B) botulinum toxin therapy has now taken a new step. Do we need a new botulinum toxin product? Competition keeps the markets in good shape. With costs of around US$ 3,000 per year to treat a single torticollis patient vigorous competition is more than welcomed by the health economists. Do we need a new type of BT? So far, there has been no reason to believe that BT-B will work better than BT-A. With one exception: conventional BT preparations can induce antibody formation. This is a rare phenomenon, occurring in around 5% of torticollis patients. Not a large number, but, up to now, for most of those patients BT therapy was over. This is where BT-B comes in. Robust studies have demonstrated that BT-A antibodies do not inactivate BT-B [2]. This offers new hope to those patients. But questions remain to be answered: although statistical risk factors have been identified [3], therapy failure cannot be predicted. As a matter of fact, the activity of the individual patient’s immune system may well be the key factor. If this is true, antibody formation against BT-B would be imminent, especially given the high structural similarity between BT-B and BT-A. Whether these considerations will transform into a clinical problem we do not know. Only time will tell. When botulinum toxin therapy failure is unrelated to BT-A antibodies BT-B will not help. Reasons for unrelated therapy failure are numerous and considerable clinical experience is needed to identify them. BT-B cleaves the intracellular transport protein chain at a site different from BT-A [4]. It is not clear whether this matters therapeutically. Studies indicate that in torticollis patients between 7,500 and 10,000 mouse units of BT-B are needed to produce a reasonable therapeutic effect [5]. Similar therapeutic effects are seen after about 150–200 mouse units of Botox® [6] or about 500–750 mouse units of Dysport® [7]. This indicates a conversion factor for Botox® to BT-B in the order of 40–70 and for