I think I've pretty much used up all available conventional (and unconventional) means to better my IBS. After reading this BB for several months I'm seeing the same things come up again and again. NOTE: I'm not saying that's bad or there's anything wrong with the BB, just that there isn't much in terms of treatments that is new to me. I've gotten a good deal better from trying different things, but I'm just wondering what is on the horizon in terms of new treatments, drugs and studies. I'd appreciate it if anyone (flux? Kmottus?) could tell me what they see happening in the not so distant future... say the next 2 years. I realize there's a lot of guessing involved.1) What do you think will happen with Zelnorm and what does the time line look for that?2) Are there any other IBS drugs in the pipeline, and if so what do you think the time line would be for them?3) Are there any major studies/investigations of IBS underway that you think might lead to some sort of breakthrough?4) Anything else you can think of? I guess I'm wondering if you think 2 or even 5 years from now the treatments available will be the same as today.I appreciate your response!
What's on the Horizon?
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I think it's difficult to answer. The FDA has become increasingly conservative lately. I think the chances of the drugs being re-released under marketing doesn't look all that great given the recent NYT article...search.nytimes.com:80/plweb-cgi/fastweb?state_id=998922515&view=site&docrank=1&numhitsfound=4&query=%28fda%29%20AND%20%2820010729%3C%3Dpdate%29&query_rule=%28$query%29&qu ery1=thedbs%3Dpast30days%26section%3DALL%26fields%3DALL%26thequery%3Dfda&query2=sorting%3DBYFIELD%3A-skey_pdate&query7=fda&query8=from%20the%20past%2030%20days&docid=70984&docdb=20 01arc&dbname=unify&numresults=10&sorting=BYFIELD%3A-skey_pdate&operator=AND&TemplateName=abs_MPoff.tmpl&setCookie=1
I think pain will continue to be a target for IBS and new drugs may come from the pain management arena (e.g, nmda antagonists). IBS in general doesn't appear to involve motility in a significant way, but a few may have a true motility disorder and for them, a few motility drugs being looked at which include CCK antagonists and motilin agonists (similar to erythromycin). It should all shake out this decade.
If the idea holds up that the brain talks to the gut via histamine, we might see H3 antagonists. There will almost certainly be better classification (Rome III).------------------I am not a doctor, nor do I work for profit in the medical/pharmacological field, but I have read scientific and medical texts, and have access to numerous sources of medical information that are not readily available to others. One should always consult a medical professional regarding advice received.[This message has been edited by flux (edited 08-27-2001).]
I think it's difficult to answer. The FDA has become increasingly conservative lately. I think the chances of the drugs being re-released under marketing doesn't look all that great given the recent NYT article...search.nytimes.com:80/plweb-cgi/fastweb?state_id=998922515&view=site&docrank=1&numhitsfound=4&query=%28fda%29%20AND%20%2820010729%3C%3Dpdate%29&query_rule=%28$query%29&qu ery1=thedbs%3Dpast30days%26section%3DALL%26fields%3DALL%26thequery%3Dfda&query2=sorting%3DBYFIELD%3A-skey_pdate&query7=fda&query8=from%20the%20past%2030%20days&docid=70984&docdb=20 01arc&dbname=unify&numresults=10&sorting=BYFIELD%3A-skey_pdate&operator=AND&TemplateName=abs_MPoff.tmpl&setCookie=1
I think pain will continue to be a target for IBS and new drugs may come from the pain management arena (e.g, nmda antagonists). IBS in general doesn't appear to involve motility in a significant way, but a few may have a true motility disorder and for them, a few motility drugs being looked at which include CCK antagonists and motilin agonists (similar to erythromycin). It should all shake out this decade.
If the idea holds up that the brain talks to the gut via histamine, we might see H3 antagonists. There will almost certainly be better classification (Rome III).------------------I am not a doctor, nor do I work for profit in the medical/pharmacological field, but I have read scientific and medical texts, and have access to numerous sources of medical information that are not readily available to others. One should always consult a medical professional regarding advice received.[This message has been edited by flux (edited 08-27-2001).]
Ugh, Check this out for more drug info. http://www.ibsgroup.org/ubb/Forum10/HTML/000428.html BQ
Ugh, Check this out for more drug info. http://www.ibsgroup.org/ubb/Forum10/HTML/000428.html BQ
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·They're also working on a way of dealing with the visceral hypersensitivity (pain) that may be started in the neural gut fibers that run to the spinal cord (afferents) and relay this information. Some work has shown the presence of a specific serotonin receptor on these neural inputs (the 5-HT3 receptor). Although it remains to be unequivolcally demonstrated in the GI tract, the presence of these receptors on the spinal "afferents" may expain the ability of certain 5-HT receptor antagonists to provide pain relief in certain cases of IBS (Even though the defined role of these receptors appears to be peristaltic reflex, and results in marked constipation).Other spinal afferents fall under the category of "silent or sleeping" and are only awakened under conditions of inflammation or injury - resulting in a "gain" in the stimulus-response relationship. If this gain can be reduced, pain may be lessened. Proinflammatory agents that are currently being looked at include: Bradykinin, prostaglandinins and leukotrienes, ATP, serotonin and capsaicin, among others. If their mechanisms can be deduced and found to increase gain, antagonists may be able to reduce the sensory signal transduction mechanisms. Christian
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·They're also working on a way of dealing with the visceral hypersensitivity (pain) that may be started in the neural gut fibers that run to the spinal cord (afferents) and relay this information. Some work has shown the presence of a specific serotonin receptor on these neural inputs (the 5-HT3 receptor). Although it remains to be unequivolcally demonstrated in the GI tract, the presence of these receptors on the spinal "afferents" may expain the ability of certain 5-HT receptor antagonists to provide pain relief in certain cases of IBS (Even though the defined role of these receptors appears to be peristaltic reflex, and results in marked constipation).Other spinal afferents fall under the category of "silent or sleeping" and are only awakened under conditions of inflammation or injury - resulting in a "gain" in the stimulus-response relationship. If this gain can be reduced, pain may be lessened. Proinflammatory agents that are currently being looked at include: Bradykinin, prostaglandinins and leukotrienes, ATP, serotonin and capsaicin, among others. If their mechanisms can be deduced and found to increase gain, antagonists may be able to reduce the sensory signal transduction mechanisms. Christian
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Guest
·Ugh, You might want to check the news forum or join the zelnorm action group. Patients can have some impact here.tom
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Guest
·Ugh, You might want to check the news forum or join the zelnorm action group. Patients can have some impact here.tom
The nature of IBS has been debated for decades. At one point, its being a primary motility disorder was a big idea, but the data never showed that and that led the emergence of other ideas, namely visceral hypersensitivity. Today, the thinking is that it is multifactorial. Motility sometimes plays a role (for example there may be rapid transit present), but in general it is usually a minor role. If the role is clear, the disorder it is no longer considered IBS (e.g, slow-transit constipation.------------------I am not a doctor, nor do I work for profit in the medical/pharmacological field, but I have read scientific and medical texts, and have access to numerous sources of medical information that are not readily available to others. One should always consult a medical professional regarding advice received.quoteerhaps a dumb one but here goes anyway: Is a rapid transit diagnosis referring to motility? And could you explain why motility isn't playing a significant role in IBS. I always thought it did. Educate me,
The nature of IBS has been debated for decades. At one point, its being a primary motility disorder was a big idea, but the data never showed that and that led the emergence of other ideas, namely visceral hypersensitivity. Today, the thinking is that it is multifactorial. Motility sometimes plays a role (for example there may be rapid transit present), but in general it is usually a minor role. If the role is clear, the disorder it is no longer considered IBS (e.g, slow-transit constipation.------------------I am not a doctor, nor do I work for profit in the medical/pharmacological field, but I have read scientific and medical texts, and have access to numerous sources of medical information that are not readily available to others. One should always consult a medical professional regarding advice received.quote
There must be some confusion over semantics here. Motility is an important enough factor for those of us suffering from IBS to identify ourselves as IBS-C or IBS-D. I have slow gut transit, but it has been diagnosed as IBS-C. Tegaserod is the only medicine that helps me and it is designed for IBS-C. Tegaserod promotes motility, as well as reduce bloating and visceral sensitivity.
There must be some confusion over semantics here. Motility is an important enough factor for those of us suffering from IBS to identify ourselves as IBS-C or IBS-D. I have slow gut transit, but it has been diagnosed as IBS-C. Tegaserod is the only medicine that helps me and it is designed for IBS-C. Tegaserod promotes motility, as well as reduce bloating and visceral sensitivity.
Actually, there is no C and D classification. The Rome criteria define IBS as a separate entity simply requiring that bowel movements be "altered". Functional constipation is a separate classification from IBS. Pain is not a symptom of functional constipation.Either way it doesn't say anything about whether abnormal motility is present. It may or may not be. Generally, if it is, the diagnosis can (and should) be changed since it is based on an abnormal finding and not symptoms.
All of the conditions are formally defined by their symptoms. In some persons with "functional constipation", slow or delayed transit is found. At that point, the diagnosis should be changed to say "slow or delayed transit". So then to be clinically accurate, you do not have IBS.(Just consider that every few years, a bunch of doctors trek out to Rome, Italy to argue the above points while they take in the sights and sample the fine cuisine.)
Actually, there is no C and D classification. The Rome criteria define IBS as a separate entity simply requiring that bowel movements be "altered". Functional constipation is a separate classification from IBS. Pain is not a symptom of functional constipation.Either way it doesn't say anything about whether abnormal motility is present. It may or may not be. Generally, if it is, the diagnosis can (and should) be changed since it is based on an abnormal finding and not symptoms.
All of the conditions are formally defined by their symptoms. In some persons with "functional constipation", slow or delayed transit is found. At that point, the diagnosis should be changed to say "slow or delayed transit". So then to be clinically accurate, you do not have IBS.(Just consider that every few years, a bunch of doctors trek out to Rome, Italy to argue the above points while they take in the sights and sample the fine cuisine.)
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