hi joan this is the best ??? on this site and it needs to be ansawed
antihistamines and mast cell stablizers only block the
symptoms thay do not stop the damage
one is ostoprosis and there are a lot moore
peter

I think it's very important that we are working with two different disease entities and no longer one that of mastocytosis and mast cell activation.  

In the case of mastocytosis, so much of the damage incurred is not just the damage the activation of the mast cells cause but also the damage caused by the invasion of the aberrant mast cells into tissues.  When those neoplastic mast cells don't die off as they should, they are going to take up space.  The more they are degranulated, the more they are called into action and thus more invastion of the tissues there.  Because they don't die off when they should, they end up taking up the space and crowding the tissues there and this causes damage, not only in that they need more room, but also with the concentrated mediator release they will cause the problems within the bone marrow and spleen and pancreas, etc.  So, you have two major problems going on, not just one.

Yet, with the Activation syndrome, this may be limited to only the damage that the mediators themselves cause and if this is so, then the use of the medications may indeed be very beneficial, but in both cases it is beneficial.  You see, according to research, mast cell stabilizers do help to prevent more damage and they think that the leukotreine blockers and anithistamines may help as well in that if you can stop the mast cell from releasing their mediators, that's a big step towards preventing more damage because it keeps them from degranulating as much.  The degranulation of mast cells creates an inflammatory process of calling in other inflammatory cells to that site of degranulation.  If you can limit this degranulation with the use of mast cell stabilizers, then you interfere with the inflammatory process going on.  This is very important.  However, by using the blockers, you also calm down the effects of the mediators systemically which means that you help to cut down on some of the degranuation - it's a matter of a chain of events and one thing connects to the next.  Reverting the process helps to decrease the damage.  It may not make is so that no damage occurrs, but at least you may diminish or prevent some and that's very important.

Here is an abstract of an article on the use of these medications and the conclusions that researchers have come to regarding mast cells within the artery walls of aneuyrsms.  

If this is so for aneurysms, then it is also so for other areas where the mast cells cause inflammation due to their deganulation.




Mast Cells: Important Players in the Orchestrated Pathogenesis of Abdominal Aortic Aneurysms.
Swedenborg J, Mäyränpää MI, Kovanen PT.

Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; Department of Vascular Surgery, Karolinska University Hospital, Stockholm, Sweden; Wihuri Research Institute, Helsinki, Finland; Department of Pathology, Haartman Institute, University of Helsinki, Finlind; and HUSLAB, Division of Pathology, Meilahti Laboratories of Pathology, Helsinki University Central Hospital, Finland.


Abstract
Mast cells (MCs) regulate inflammation and immunity. Their granular content includes heparin, histamine, and several enzymes (tryptase, chymase, carboxypeptidase, and cathepsin G). In addition, activated MCs synthesize and release eicosanoids and a large number of cytokines and chemokines. Recent findings suggest a role of MCs in abdominal aortic aneurysms (AAAs) in humans, where they are found in the media and adventitia. Experimentally induced AAA in MC-deficient animals and animals treated with MC inhibitors demonstrate that MCs are involved in the pathogenesis of AAA via several different mechanisms. MC-dependent activation of metalloproteinases and the renin-angiotensin system, contribution to smooth muscle cell apoptosis, and release of proteolytic enzymes are some key examples. Human studies indicate that MCs are the main source of cathepsin G in AAAs and contribute to activation of the renin-angiotensin system via chymase and cathepsin G. Activated MCs also contribute to neovascularization, inflammation, and atherosclerosis, all hallmarks of AAA. Thus, we may envision that MC stabilizing agents, as well as leukotriene receptor antagonists and histamine receptor blockers already in clinical use for treatment of other diseases, could also be tested for their efficacy in preventing development and growth of AAA.

Hi Debbie,

If you're out there, I was just wondering if you'd heard back from Dr. Akin on the subject of antihistamines and mast cell stabilizers.

Thanks!

Hi Josie,

I've actually been off the gastrocrom for more than 2 months, and the digestive symptoms have not come back.  I don't know if that means it worked, or whether it didn't help but the supplements I took did help (l-glutamine, bromelain, quercetin, probiotics).  I now still take the bromelain and quercetin daily, but the probiotics only a few times/week.  Whatever it was, this has been one of the most stressful months in my life (my father died), and yet my digestive system has done well, and a really long flare seems to have subsided.  My GI doc who treats people for mastocytic enterocolitis told me that 6 weeks on the gastrocrom would make a huge difference, and he was right.

One reason I'm concerned about whether I should be using gastrocrom as a primary medicine, even though my symptoms are minimal now, is that a side effect of ear ringing (tinnitus) has been reported, and my ears have been ringing more often and a lot louder since a few weeks into taking it.  The ENT couldn't say (and neither could the manufacturer) whether the gastrocrom might have caused it.  Still, would rather have some hearing problems than ruin my internal organs!  So, will be curious to see if Dr. Akin gets back to Debbie on this topic.

Everything is so individual with these disorders.  I think it's difficult to treat us!