Rx: New Therapies And Medications For Crohn's Disease
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From: zumone2002 on 8 Jul 2008 22:28 http://www.medicalnewstoday.com/articles/114150.php New Therapies And Medications For Crohn's Disease 08 Jul 2008 A New Drug Class article released on July 4, 2008 in The Lancet seeks to highlight a new group of drugs intended to treat Crohn's disease. Most current drugs seek to control the autoimmune response via the tumor necrosis factor alpha (TNF-alpha), but many new classes attempt to control other aspects of the immune response or even to reinforce the intestinal barrier itself. Crohn's Disease (CD) is a gastrointestinal disorder which is indicated by chronic inflammation of the wall of the digestive tract. Usually, regions of inflammation are separated by regions of normal lining, called skip lesions. The disease involves constant cycles of flare-ups and remission throughout the life of the patient, and is an inflammatory bowel disease (IBD), similar to ulcerative colitis. The primary gastrointestinal symptoms are abdominal pain, blood in the stool, diarrhea,constipation, vomiting, weight loss, or weight gain. Presently, the standard drug treatment of Crohn's disease attempt to inhibit tumor necrosis factor alpha, which would normally amplify the immune response. However, some novel therapies instead target other biochemical factors that initiate or participate in the immune response, often by controlling T-cells, an instrumental part of the immune response. Drugs such as visilizumab, daclizumab and basiliximab blockade specific T-cells from responding, and tocilizumab and fontolizumab actually prevent the formation or activation of T-cells. In another experimental therapeutic technique, T-cells are "reset" through bone-marrow transplants, which can bring extended remission. In addition to modulation of T-cell response, other approaches are being explored A new class of drugs hopes to modulate T-cell response while additionally attempting to reinforce the intestinal barrier by encouraging the repair processes in the intestinal lining. Additionally, a tolerance against the instigators of the immune response can be built orally by ingesting protein extracts, thus reducing the overall immune response in inflammatory bowel diseases. The authors, including Professor Jean-Frederic Colombel, Hopital Claude Huriez, Centre Hospitalier Universitaire de Lille, France, and colleagues, discuss the mechanisms and merits of all of these strategies. They conclude with a statement of hope for future therapies for this disease: "As a result of decades of intensive research, treatment for inflammatory bowel disease is undergoing a transition from the era of TNF antagonists to an era of new biological agents, including those that are able to stimulate the innate immune system. In parallel, clinicians are working on new strategies aimed at modification of the natural history of Crohn's disease, including an early aggressive therapeutic approach." -- Luke
From: jinhale on 13 Jul 2008 16:28 On Jul 8, 10:28 pm, zumone2002 <zumone2...(a)yahoo.com> wrote: > http://www.medicalnewstoday.com/articles/114150.php > > New Therapies And Medications For Crohn's Disease > 08 Jul 2008 > > A New Drug Class article released on July 4, 2008 in The Lancet seeks > to highlight a new group of drugs intended to treat Crohn's disease. > Most current drugs seek to control the autoimmune response via the > tumor necrosis factor alpha (TNF-alpha), but many new classes attempt > to control other aspects of the immune response or even to reinforce > the intestinal barrier itself. > > Crohn's Disease (CD) is a gastrointestinal disorder which is indicated > by chronic inflammation of the wall of the digestive tract. Usually, > regions of inflammation are separated by regions of normal lining, > called skip lesions. The disease involves constant cycles of flare-ups > and remission throughout the life of the patient, and is an > inflammatory bowel disease (IBD), similar to ulcerative colitis. The > primary gastrointestinal symptoms are abdominal pain, blood in the > stool, diarrhea,constipation, vomiting, weight loss, or weight gain. > > Presently, the standard drug treatment of Crohn's disease attempt to > inhibit tumor necrosis factor alpha, which would normally amplify the > immune response. However, some novel therapies instead target other > biochemical factors that initiate or participate in the immune > response, often by controlling T-cells, an instrumental part of the > immune response. Drugs such as visilizumab, daclizumab and basiliximab > blockade specific T-cells from responding, and tocilizumab and > fontolizumab actually prevent the formation or activation of T-cells. > In another experimental therapeutic technique, T-cells are "reset" > through bone-marrow transplants, which can bring extended remission. > > In addition to modulation of T-cell response, other approaches are > being explored A new class of drugs hopes to modulate T-cell response > while additionally attempting to reinforce the intestinal barrier by > encouraging the repair processes in the intestinal lining. > Additionally, a tolerance against the instigators of the immune > response can be built orally by ingesting protein extracts, thus > reducing the overall immune response in inflammatory bowel diseases. > > The authors, including Professor Jean-Frederic Colombel, Hopital > Claude Huriez, Centre Hospitalier Universitaire de Lille, France, and > colleagues, discuss the mechanisms and merits of all of these > strategies. They conclude with a statement of hope for future > therapies for this disease: "As a result of decades of intensive > research, treatment for inflammatory bowel disease is undergoing a > transition from the era of TNF antagonists to an era of new biological > agents, including those that are able to stimulate the innate immune > system. In parallel, clinicians are working on new strategies aimed at > modification of the natural history of Crohn's disease, including an > early aggressive therapeutic approach." > > -- > Luke Another novel therapy, low dose Naltrexone, has done quite well by STIMULATING the immune system. 2/3 of CD patients went into full remission. 89% experienced a reduction in symptoms. http://en.wikipedia.org/wiki/Low_dose_naltrexone Also I want to point out Crohn's can be caused by MAP (Mycobacterium avium subspecies paratuberculosis) in at least some individuals. Also Crohn's appears treatable/curable in at least the majority of patients using RMAT (special antibiotics specific to MAP) appropriately. http://alan.kennedy.name/crohns/research/chemo/htfull.htm http://www.bmj.com/cgi/content/full/316/7129/449 http://www.mad-cow.org/00/paraTB.html
From: Kofi on 14 Jul 2008 07:10
> Another novel therapy, low dose Naltrexone, has done quite well by > STIMULATING the immune system. 2/3 of CD patients went into full > remission. 89% experienced a reduction in symptoms. > > http://en.wikipedia.org/wiki/Low_dose_naltrexone > > Also I want to point out Crohn's can be caused by MAP (Mycobacterium > avium subspecies paratuberculosis) in at least some individuals. Also > Crohn's appears treatable/curable in at least the majority of patients > using RMAT (special antibiotics specific to MAP) appropriately. > > http://alan.kennedy.name/crohns/research/chemo/htfull.htm > http://www.bmj.com/cgi/content/full/316/7129/449 > http://www.mad-cow.org/00/paraTB.html I'm not sure these sites captured the entirety of why LDN may work. Dropping an antagonist on a receptor in low doses tends to have the opposite effect of upregulating it, hence the body becomes more sensitive to opiates. This also enhances natural cannabinoid signaling, which is tied into the mu opioid network. It's possible the mu opioid receptor loss occurs, at least in part, due to a drop of intestinal butyrate uptake - either for genetic reasons or gut bacteria death via antibiotic overuse. The mu opioid receptor, along with metallothionein, requires proper histone acetylation to work and butyrate is an HDAC inhibitor. Metallothionein is part of the recently discovered gut protective HIF-1a/EPO/MT pathway. The cannabinoid signaling matters not only for pain relief but it also seems to affect B-cell behavior - something that hasn't been closely examined yet in the LDN literature. I've written multiple posts over the last few years on these topics if you're interested. low-dose naltrexone in some rats can inhibit tolerance of opioids like morphine and enhance antinociception [PMID 16527399; see also PMID 16409995] low-dose naltrexone in a trial of humans lowers the effective therapeutic dose of oxycodone (oxytrex) and reduces dependency on it; patients reported 55% less dependency than on oxycodone alone, less constipation, somnolence, and pruritus; one cellular mechanism of action is the prevention of aberrant G protein signaling by mu opioid receptors caused by chronic opioid administration [PMID 17157780] LDN (low dose naltrexone) enhances cannabinoid-induced analgesia [PMID 16286810] low-dose naltrexone enhances cannabinoid-induced antinociception (i.e., raised the pain threshold in rats); a high dose has no effect; a cannabanoid antagonist stopped the combination from working; this suggests a mechanism of cannabinoid-opioid interaction where activated opioid receptors couple to Gs-proteins and attenuate cannabinoid-induced antinociception and/or motor functioning; LDN also enhances the effects of morphine and other mu opioid agonists [PMID 16286810] friendly gut bacteria - lactobacillus acidophilus - found in yoghurt and probiotics boosts the synthesis of receptors for mu opioids and cannabinoids (CB1 and CB2) - our natural painkillers - in human and rodent gut cells; rats given probiotics experienced a 20% increase in their pain threshold or twice that if they had irritable bowel syndrome; the analgesic effect was similar to morphine and suggests the microbiology of the intestinal tract influences our visceral perception <http://www.newscientist.com/article/dn10808.html>, [PMID 17159985] |