| Posted at 9:48 AM on Apr 18, 2008 by concernedcitizen, #29705 |
I think you are becoming over involved in this. I feel you are loosing your credibility. I no longer read your entries. Sometimes, less is more. I think you have some good points, but I question your motives at this point.
It doesn't really matter whether you think that I have any credibility or not. I just post what I find that I think is written clearly enough that others can get something out of it. Most academic work is written as though outsiders need a code book to understand.
There are some very intelligent people here who care about what is happening to their children. I don't have any answers but I see the need to ask many questions. People can read and then make up their minds.
I don't have any agenda. I think that everyone can agree that Merck aggressively marketed Singulair. There is no such thing as a perfectly safe medication for everybody-- for everything.
I for one appreciate the time you have spent and posting the different info you have found. For the people that don't choose to read your entries well isn't it nice they they are able to CHOOSE whether or not they want to! Seems to me that this medication has been out there long enough and people have been complaining over the years. The possible side effects where not given quick enough and made known to the general public so we as parents could make a CHOICE on whether or not to risk effects on our childrens brains. Thanks again for your effort!
If anybody is going to pursue how suppressing the cystLT1 (singulair) receptor affects the normal functioning of the mast cell. There are Harvard researchers who study this.
I am interested in this topic because people who have developed asthma have a different set of immunological problems than people who simply have some seasonal allergies. There are studies that show that high levels of IgE will sustain the mast cell even in the presence of factors that are signally the mast cell that it's time to die. Harvard researchers have shown that the cystLT1 receptor plays a roll in mast cell proliferation. So it's possible that suppressing that receptor is desirable for some people and not desirable for others. I would like to see somebody study whether Singulair works on normal people like an anti-histamine just because it is limiting the number of mast cells available to provide histamine -- that would be a disaster for the immune system leaving the patient wide open to all kinds of bacterial infections in any tissue that should be protected by the mast cells --nasal, lungs, intestines, skin etc.
J Immunol. 2006 Sep 1;177(5):2755-9. Links
Cutting edge: Interleukin 4-dependent mast cell proliferation requires autocrine/intracrine cysteinyl leukotriene-induced signaling.Jiang Y, Kanaoka Y, Feng C, Nocka K, Rao S, Boyce JA.
Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
Reactive mastocytosis (RM) in epithelial surfaces is a consistent Th2-associated feature of allergic disease. RM fails to develop in mice lacking leukotriene (LT) C4 synthase (LTC4S), which is required for cysteinyl leukotriene (cys-LT) production. We now report that IL-4, which induces LTC4S expression by mast cells (MCs), requires cys-LTs, the cys-LT type 1 receptor (CysLT1), and Gi proteins to promote MC proliferation. LTD4 (10-1000 nM) enhanced proliferation of human MCs in a CysLT1-dependent, pertussis toxin-sensitive manner. LTD4-induced phosphorylation of ERK required transactivation of c-kit. IL-4-driven comitogenesis was likewise sensitive to pertussis toxin or a CysLT1-selective antagonist and was attenuated by treatment with leukotriene synthesis inhibitors. Mouse MCs lacking LTC4S or CysLT1 showed substantially diminished IL-4-induced comitogenesis. Thus, IL-4 induces proliferation in part by inducing LTC4S and cys-LT generation, which causes CysLT1 to transactivate c-kit in RM.
Why would doctors be told to prescribe a drug that suppresses the leukotriene receptor for seasonal allergies? Singulair is not an anti-histamine.
leukotriene receptor antagonist mast cell journal of clinical investigation preventing asthma asthma attacks micro organisms cause of asthma montelukast money maker term basis pattern recognition receptors growth and development merck freakin asthma mechanisms medication decisions motives credibility academic work singulair outsiders code book brains parents harvard medical school boston harvard medical school pertussis toxin mast cells interleukin 4 k rao epithelial surfaces harvard researchers cell proliferation anti histamine immunological problems seasonal allergies allergic disease sensitive manner cys bacterial infections th2 intestines