Mast cell medications: Everything but antihistamines

The following medications listed are available in oral, intramuscular or intravenous formulation. Not all medications are available in the US or Europe. Topical and inhaled medications are not included in these lists.

Mast cell stabilizers interfere structures on the cell membrane required for degranulation and thus prevent the release of granule contents, including histamine.

Mast cell stabilizers
Cromolyn sodium/ Cromoglicic acid/ Nedocromil
*mechanism unclear


Beta-2 adrenergic agonists cause smooth muscles to relax, which allow airways to open. These are used almost exclusively in asthma and pulmonary disease, which a secondary use in controlling uterine contractions in labor.

Beta-2 adrenergic agonists


Leukotriene receptor antagonists work by interfering with the function of leukotrienes by blocking the CysLT1 receptor. Leukotrienes are heavily involved in airway reactivity and inflammation.

Leukotriene receptor antagonists


5-lipoxygenase inhibitors prevent leukotrienes from being made.

5-lipoxygenase inhibitor
St. John’s Wort


Corticosteroids interfere with the activity of mast cells and production of mast cell mediators.

Mast cell stabilizers
*taken orally, with effects local to the GI tract


Proton pump inhibitors reduce the production of gastric acid and treat heartburn, nausea and reflux. This can also be achieved by H2 antihistamines and for this reason, the two classes are often confused. The following medications, which are taken often by mast cell patients, have no known antihistamine effect. They can safely be taken with H2 antihistamines and help many mast cell patients, but it is important to clarify that they are NOT antihistamines.

Proton pump inhibitors

12 Responses

  1. Kristin Elam April 22, 2015 / 8:15 am

    Thank you for this and all that you do here for us!

  2. Yvonne April 23, 2015 / 12:57 pm

    Is there any explanation why the very things that help us seem to trigger us during the first few doses. I reacted to both turmeric and quercetin at first then came back to them and gradually improved. In their activity do they bind to the mast cells (and therefore activate them) but then they become quenched? As a biochemist I am very curious on the mechanisms. I understand that many people also react to sodium chromolin and need a desenitization protocol to start.

    Thanks again so ver much. Love theses posts!

    • Colin May 23, 2016 / 9:55 am

      I’ve been looking around trying to find more information on cromolyn desensitization protocols — getting through the initial reaction has been mentioned a couple of times on this site, and I’d be most grateful for any sources on how to navigate this (as I’ve not been successful finding references to guide my so far unsuccessful attempts to take cromolyn, and my drs don’t seem to know where to look either). (And I’ll take this comment opportunity to thank you for the great reference — I’ve been grateful for awhile!!)

  3. Karen Neill April 28, 2015 / 2:02 pm

    Yvonne, I have exactly the opposite problem with many things. I’m great the first few times, then I gradually start to react to it. With meds, it’s usually to the fillers, coatings etc. If I got a benefit from the med, I will then usually try a form that is as pure as possible.

    Classic example- I’ve been taking Omalizumab/Xolair for two years, never had a problem until last week when I had an anaphylactic reaction! With food, I have gradually sensitized to almost everything, and each reaction is worse than the last. A pretty corner to be painted into, eh?

    I did have one question. It is my understanding that Omalizumab works as an IgE receptor binder, so it’s mechanism is understood. I thought that that was why it worked for some, not others; only working for those who have IgE mediated reactions. Does it have additional mast cell stabilizing properties whose mechanism isn’t understood?

    • Lisa Klimas April 28, 2015 / 2:21 pm

      Xolair binds not to the receptor, but to IgE itself. So it make sense why it works for people with IgE allergies. However, there are now a fair amount of people without IgE allergies (like many with mast cell disease) that see benefit. This is the unclear mechanism I mean. But you’re right, that’s unclear. I will put a note in the post. Thank you!

  4. Mark Beckwith May 1, 2015 / 1:48 pm

    Hi Lisa. Kathy and I are at NIH today with Dr. Melody Carter, participating in the Omalizumab double-blind clinical trial they have going. She describes the mechanism like this: “Omalizumab binds up the serum IgE and takes it out of circulation. The IgE receptors on Mast cells and Basophils then don’t get the IgE they need to get triggered as much as they would have, and are thus effectively downregulated.” Not being a scientist, I can only say I think I understand what she just said. 🙂 Last time around, Kathy’s IgE count was slightly elevated, so this is one reason they feel she could benefit from Omalizumab.

    • Lisa Klimas May 1, 2015 / 2:13 pm

      Yes, but most reactions in mast cell patients are not thought to be mediated by IgE. This is the unclear part I mentioned. Some mast cell patients have no IgE allergies and normal IgE levels but still improve with Xolair.

  5. Wendy August 27, 2015 / 4:58 pm

    Your site is a great resource, thank you. Where does Luteolin complex fit in these lists? I was under the impression that Quercetin was a sacrifice/distraction so that luteolin could be better used by the body. Dr Theoharides says this in a youtube video.

    • Lisa Klimas August 29, 2015 / 1:05 am

      Thanks, I’m glad you find the site helpful. I have not seen that video, but will try to find it. I have not heard of quercetin being described that way, but it is definitely possible that new data has come to light. I will see what I can find and answer back. Thanks again!

  6. Susan April 2, 2016 / 9:35 pm

    Cromolyn sodium is also available in the U.S. as an OTC nasal spray called NasalCrom.
    I’ve not seen it in stores, but have had no difficulty getting it by mail order. For a couple of months now, I’ve been keeping two spray bottles going, one for nasal use and the other for dermatologic use; they’ve helped me reduce both my symptoms and the amount of nasal and topical cortisone spray I need.

  7. Amy Jansen May 16, 2016 / 11:19 am

    It binds free IgE thus preventing mast cells / basophils from becoming active.

    Preventing all IgE’s regardless of the reason. This is what makes the med dangerous.

    • Lisa Klimas May 16, 2016 / 7:32 pm

      There are plenty of ways for mast cells and basophils to become active without IgE, this is the crux of non-IgE mediated mast cell activation. I have written many posts on this topic, touching upon IgG mediated anaphylaxis, C3a activation, C5a activation, toll like receptor activation, and others. I also posted a master table of all the molecules that can activate mast cells. Blocking IgE does not prevent all mast cell activation.

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