Idiopathic anaphylaxis (IA): Frequently asked questions
Original question: I started having problems with itchy, dry, bloodshot eyes. My ophthalmologist prescribed Restasis® [brand of cyclosporine ophthalmic emulsion eye drops], which really helped. Could my dry eyes be related to my IA?
Answer: Both allergies (including allergic-like reactions) and dry eye syndrome [also known as keratoconjunctivitis sicca, Sjögren syndrome, or keratitis sicca] can make your eyes miserable. As one specialist [Maskin SL. Reversing Dry Eye Syndrome: Practical Ways to Improve Your Comfort, Vision, and Appearance. 1st ed. New Haven, CT: Yale University Press; 2007] points out, "Not only are ocular [eye-related] allergies and dry eye different, one can cause the other — or at least make the other worse."
He goes on to explain how mast cell disorders and dry eye can influence each other:
If you suffer from an allergy that affects your eyes (hay fever or other seasonal allergy, an allergy to pet dander, a contact allergy to eye makeup), it can turn into dry eye. Here's how: The allergic reaction releases histamine and other inflammatory mediators from the mast cells onto the eyes, which disrupts both the mucin [lubricating and protective glycoproteins] and the lipid [fat-soluble] phases, and directly alters tear film quality, shortening the tear breakup time. The result is dry eye symptoms that may persist for weeks after an allergic episode. If the inflammation becomes chronic, changes may occur, including lid swelling and obstructive meibomian gland [sebaceous glands in each eyelid] dysfunction as well as goblet cell loss with mucin deficiency — in other words, evaporative dry eye. Chronic inflammation numbs the ocular surface, thereby affecting the lacrimal [related to tears] functional unit, which can result in aqueous tear deficient dry eye as well. Reference [Maskin SL. Reversing Dry Eye Syndrome: Practical Ways to Improve Your Comfort, Vision, and Appearance. 1st ed. New Haven, CT: Yale University Press; 2007].
And as if that weren't bad enough:
...Allergies are treated with...antihistamines [which] relieve the allergic symptoms but dry out the mucous membrane and cause or exacerbate dry eye.
Unfortunately, what goes around then comes around:
On the other hand, dry eye can exacerbate, and even create allergies. If you have dry eyes, tears are not washing allergens out of the eye. And the allergens are of higher concentration because they are not being adequately diluted with tears. As a result, if you have dry eye and also suffer from allergies [or mast cell-related problems!], both your dry eye and your allergies can become worse!" Reference [Maskin SL. Reversing Dry Eye Syndrome: Practical Ways to Improve Your Comfort, Vision, and Appearance. 1st ed. New Haven, CT: Yale University Press; 2007.
So, yes, your dry eyes and IA could have a lot to do with one another. And if you need to use artificial tears, remember that some tears contain preservatives that can also cause allergic or hypersensitive reactions!
Oh, and one more thing. Dr. Maskin provides a rule of thumb for deciding whether your eye misery is caused more by an allergic-type reaction or by a dry eye syndrome. Allergies make our eyes feel itchy, whereas dry eye makes our eyes feel gritty — or as though we've got some kind of foreign substance in them. I've found this information useful when deciding whether to use ocular allergy drops or artificial tears to treat my ocular symptoms. ◊
Original question: I was just diagnosed with Hashimoto’s thyroiditis by an endocrinologist. I searched for information on the internet, and since I read about the diet/triggers that cause Hashimoto’s, I feel much better. It seems all of my symptoms are connected with it. For example, gastritis and hives are symptoms of Hashimoto’s, too, and so all of my symptoms could have been that all along. I understand that Hashimoto’s, mastocytosis, and idiopathic anaphylaxis (IA) are all autoimmune diseases. What do you think about that? Can Hashimoto’s thyroiditis cause IA?
Answer: I knew someone who worked for Social Security, evaluating applications for disability determination, and she made this comment about thyroid problems: “Almost everyone who has a serious autoimmune disease has some kind of thyroid involvement. If you walk in and tell your doctor that you have a thyroid problem, the only thing that you’re really telling him is that you have an autoimmune disease.”
Now, this woman was not a doctor, but what she said reflects the frequency with which applications for disability from people who have autoimmune diseases include some component of thyroid involvement.
For example, thyroid problems run in my family. My aunt had a thyroid tumor, my Mom had a goiter, my sister had Hashimoto's thyroiditis, and I have had hypothyroidism for about 20 years. Thyroid peroxidase (TPO) antibodies are produced in response to injury to the thyroid. Between 90 and 100% of the people who have autoimmune thyroiditis (including both Hashimoto’s disease and Grave’s disease, aka hyperthyroidism) have elevated TPO antibodies.
Idiopathic anaphylaxis (IA) is believed to be an autoimmune disease, and it would not surprise me if many of the people who are diagnosed with IA or mast cell activation syndrome (MCAS) have elevated TPO antibodies — even if their thyroid output is within the normal range.
A quote from the 11th edition of Williams Textbook of Endocrinology [Kronenberg HM, Melmed S, Polonsky KS, Larsen R, eds. Williams Textbook of Endocrinology, 11th ed. Philadelphia, PA: Saunders; 2008]:
Hashimoto’s disease is common and may be increasing in frequency. The mean incidence in women is in the order of 3.5 cases per 1000 people per year and in men is 0.8 case per 1000 people per year.... No age group is exempt, although the prevalence increases with age in both women and men.
Also, women may have a transient form of thyroiditis after giving birth. It’s very similar to Hashimoto’s except that it usually tends to resolve itself. However, a woman’s risk of thyroid failure within a few years after pregnancy is increased.
However, while thyroid problems are common, both IA and mastocytosis are not.
The only dietary "trigger" for Hashimoto's Disease is, in a small subset of the population, exposure to iodine. In that case it’s because those people have a genetic inability to handle iodine.
Hashimoto’s is often associated with constipation, whereas many of us with MCAS, IA or mastocytosis have the exact opposite problem. (It was a running joke, for years, between my GP and me that we’d know when my hypothyroidism got really bad, because that’s when the constipation would finally kick in!)
It’s important to understand that classic mastocytosis — whether cutaneous or systemic — is not an autoimmune disease. It is, depending on which specialist you ask, either a blood disease or a neoplastic disease. So, the rate of occurrence of autoimmune thyroiditis among people with mastocytosis should be similar to what you see in the general population. Whereas, people with IA or MCAS may be more likely to have chronic thyroiditis than the average person.
In getting information off the Internet, please be careful about where you get it. As a rule of thumb, any site that also sells supplements, vitamins, or anything else, is not as likely to provide you with well-researched, solid information. Medscape, Mayo, and other doctor-reviewed sites provide much more reliable information. (You probably already know this, but it never hurts to be reminded.) ◊
Original question: “Does it seem to anyone else that the attacks fall at the same time in the day? I used to have attacks late at night. Then, all of a sudden I had one at lunch and now after lunch seems to be the worst time for me.”
Answer: The time of day when attacks occur may provide a clue about what might be setting you off.
For example, on the weekends, are you having after-lunch attacks? Probably not, if the trigger is something that’s in the lunches you eat at work — or the settings where you eat your lunch.
Here are some problems that cause time-of-day-related attacks in some people:
- Our bodies have the naturally highest levels of histamine in the wee hours of the morning [Rehn, 1987] [Rehn D, Reimann HJ, von der Ohe M, Schmidt U, Schmel A, Hennings G. Biorhythmic changes of plasma histamine levels in healthy volunteers. Agents Actions 1987; 22:24–9], which is why some of us will have an attack first thing in the morning (unless we take adequate long-acting meds at bed time to carry us through — a 12-hour time-released Chlor-Trimeton® [chlorpheniramine maleate] works well for this, as do two Zyrtec® [cetirizine] and/or two Ketotifen [also known as Zaditen, which can only be purchased outside the United States]).
- Many pollens are released in the morning, whereas many mold spores are released in the early evening. Depending on which we might react to, either time of day could present a problem.
- Some people are very sensitive to the material produced by dust mites or house pets, which means that they’re most likely to have an attack after they go to bed for the night. If that happens, you may be interested in the advice offered by the Joint Task Force on Practice Parameters, which represents the American Academy of Allergy, Asthma & Immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology [Wallace, 2008] [Wallace DV, Dykewicz MS, et al. The diagnosis and management of rhinitis: An updated practice parameter. J Allergy Clin Immunol 01-AUG-2008; 122(2 Suppl): S1–84]:
“Dust mite exposure can be reduced through measures that kill the mites or degrade and/or prevent their fecal pellets from becoming airborne. This may include HEPA air filtration and vacuum cleaning with a HEPA filter, low humidity, hard surface flooring, hot water laundry, barrier protection on pillows and mattresses, and the use of acaricides [products that kill mites and ticks]. The patient should be encouraged to use multiple interventions because an isolated intervention, such as use of dust mite–impermeable bedding, is unlikely to offer clinical benefit. On the other hand, regular dusting and duct cleaning have not been shown to offer significant benefit. Some of these measures are also helpful for animal and insect allergen reduction, but none are as effective as removing the animal and/or insects.”
Note: This is a revised version of the answer I originally wrote for the TMS Web site anaphylaxis FAQ. ◊
Original question: I'll be going to see my specialist for my yearly appointment next week. If I haven't had to use an epipen in over a year, what do you think are the chances that he'll let me wean off at least some of my medications?
Answer: This question fascinates me because it's one I so often hear from people who have finally managed to stabilize their symptoms. Once they're no longer having daily or weekly attacks, they wonder if they can now get off their IA medications. This puzzles me because it's the meds that are keeping them stable. Reducing the meds is a really great way to de-stabilize yourself and go right back to the way things were a year ago.
I do not mean to suggest that you can never reduce the amount of medication you take. Over time, you may learn that there are times or situations when you are much more or much less prone to have an attack, and then you may be able to titrate the level of your meds in response to changing seasons or situations. For example, I have to add extra meds before I have dental work or a medical procedure done, or when I travel, or when I'm first coming down with a viral infection, or when I'm under extreme emotional stress. And I take less medication in the middle of the winter, when I'm least likely to have a reaction.
But you can't really play with your medication levels until you learn as much as possible about the things you react to. And right now, it sounds like that's what you're doing. As you get the hang of all this, you'll be able to work with your doctor to adjust your medications without getting yourself into trouble. And ultimately, you may become the real expert on your particular flavor of this disease — especially if you learn to listen to your body.
Original question: "My urinalysis showed slightly elevated levels of protein (microalbuminuria), and I'm wondering if this could be related to my IA. I know that histamine creates 'leaky' blood vessels and intestines — maybe this would explain why my kidneys would be leaking small amounts of protein?"
Answer: Microalbuminuria [a slight increase in the urinary excretion of the protein albumin] has been observed in a patient following anaphylaxis during surgery. Reference [Wood PR, Gosling P, Cook MC. Microalbuminuria following anaphylaxis with general anaesthesia. Br J Anaesth. 2000; 84:808–10.]. The authors report:
Microalbuminuria secondary to systemic capillary leak is increasingly recognized in association with a number of acute medical and surgical conditions. We present a case of drug-induced anaphylaxis in which serial measurement of urinary albumin was made during resuscitation and subsequent intensive care. The potential role of microalbuminuria as a sensitive monitor of the systemic inflammatory response is discussed.
A more recent study [Axelsson J, Rippe A, et al. Effects of early endotoxemia and dextran-induced anaphylaxis on the size selectivity of the glomerular filtration barrier in rats. Am J Physiol Renal Physiol. 2009; 296:F242–8.], performed on rats, attempted to further explicate the mechanism involved and concluded, “…There was a transient, immediate increment of glomerular permeability in dextran-induced anaphylaxis, which was completely reversible within 40 min.”
As far as I am aware, no research has investigated the effect of repeated episodes of anaphylaxis. ◊
Please note: This is a corrected answer, posted on 7/15/2011. The original answer incorrectly stated that there it was unlikely that there would be a direct connection between IA and microalbuminuria.
Page last updated: July 15, 2011