Effects of hormones in adult-onset allergies.
Article Type: Report
Subject: Estrogen (Health aspects)
Estrogen (Physiological aspects)
Allergic reaction (Risk factors)
Allergic reaction (Genetic aspects)
Allergic reaction (Environmental aspects)
Allergic reaction (Identification and classification)
Allergic reaction (Care and treatment)
Allergy (Risk factors)
Allergy (Genetic aspects)
Allergy (Environmental aspects)
Allergy (Identification and classification)
Allergy (Care and treatment)
Author: Tano, Benoit
Pub Date: 12/01/2012
Publication: Name: Townsend Letter Publisher: The Townsend Letter Group Audience: General; Professional Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2012 The Townsend Letter Group ISSN: 1940-5464
Issue: Date: Dec, 2012 Source Issue: 353
Product: Product Code: 2834122 Estrogen & Progestogen Preps NAICS Code: 325412 Pharmaceutical Preparation Manufacturing SIC Code: 2834 Pharmaceutical preparations
Geographic: Geographic Scope: United States Geographic Code: 1USA United States
Accession Number: 310884657
Full Text: In my practice, I see more and more patients who present in adulthood with complaints of allergic rhinitis, asthma symptoms, severe urticaria (hives), angioedema, and even newly acquired food allergies. Recent CDC reports on atopic diseases indicate a growing allergy problem, particularly in women.

Estrogens have been discussed as possible causal factors in atopic diseases, and several articles listed on the website of the American Academy of Allergy, Asthma and Immunology (AAAAI) have touched on the role of hormone imbalance in the etiology of this allergy epidemic. As an allergist who sees the manifestations of allergic diseases in pediatric and adult patients, I have also come to conclude that the growing incidence of atopy in American adults is due to an estrogen epidemic, which has been neither fully investigated nor understood. In the next ten years, the evidence supporting these conclusions may become clearer. These atopic diseases can be regarded as windows to the entire body, which reveal the estrogen connection to many of the disorders frequently seen by allergists and other physicians.

Research on Estrogens as Allergy Triggers

Data from the Healthcare Cost and Utilization Project (HCUP) indicate higher levels of adult-onset allergic rhinitis, asthma, and urticaria in women than in men. Why are women so vulnerable to this allergy epidemic? The following analysis will attempt to provide some answers to this question.

Recent research conducted by Professor Midoro-Horiuti and colleagues at the University of Texas Medical Branch (UTMB) in Galveston, Texas,' has demonstrated that estradiol can trigger mast cell and basophil activity. Research on an animal model demonstrated that estradiol can induce mast cells to release preformed granular protein 13-hexosaminidase (a mediator that serves as a useful clinical indicator of histamine and leukotriene release). Researchers concluded that binding of physiological concentrations of estradiol to membrane estrogen receptors (ER-a) initiates a rapid onset and progressive influx of extracellular calcium, which supports the synthesis and release of allergic mediators. Estradiol also enhances IgE-dependent mast cell activation, resulting in a shift of the allergen dose response.

Primary mast cell cultures were derived from bone marrow of knockout wild-type mice that were deficient in estrogen receptor-a (ER-[alpha]). Mast cells in knockout mice that lacked ER-[alpha] did not induce [beta]-hexosaminidase release when they were exposed to estrogen. A human mast cell line was also incubated, and a similar process was shown to occur in cultured human mast cells (HMC-1).

The presence of estradiol triggered the release of the newly synthesized leukotriene C4 (LTC4) from RBL-2H3, a leukemia cell line cloned from Wistar rat basophilic cells. Estradiol was found to enhance IgE-induced degranulation and potentiation of LTC4 production and to trigger increased concentration of intracellular calcium prior to and in parallel with mediator release. Both estrogen receptor antagonists and calcium chelation inhibited these estrogenic effects.

In a subsequent study, this UTMB research group examined the allergenic effects of environmental estrogen pollutants with estrogen-like activities, including DDT, endosulfan, and atrazine. The goal of this second study was to identify possible pathogenic roles for environmental estrogens in the development of allergic diseases. Thousands of agricultural pesticides and herbicides function as environmental estrogens. These pollutants tend to degrade slowly in the environment, bioaccumulating and bioconcentrating in the food chain; environmental estrogens also have long biological half-lives.

Researchers screened a number of pollutants with estrogenic effects for their ability to modulate the release of allergic mediators from mast cells. Mast cell cultures were then exposed to these environmental estrogens in vitro, and degranulation of mast cells was assessed by quantifying the release of [beta]-hexosaminidase. Results showed that all the environmental estrogens tested caused rapid, dose-related release of [beta]-hexosaminidase from mast cells and enhanced IgE-mediated release. The combination of physiologic concentrations of 17[beta]-estradiol and several concentrations of environmental estrogens had additive effects on mast cell degranulation. Comparison of bone marrow mast cells from ER-[alpha]-sufficient and ER-[alpha]-deficient mice indicated that much of the effect of environmental estrogens was mediated by these receptors (ER-[alpha]). Based on these findings, researchers concluded that estrogenic environmental pollutants might promote allergic symptoms by inducing and enhancing mast cell degranulation via physiologic estrogens, in conjunction with exposure to allergens.

Subsequent research has confirmed that mast cells have a high affinity for ER-[alpha]. Mast cell degranulation, with the release of histamine, leukotrienes (LTC4), and prostaglandins, and the subsequent development of allergy symptoms, has been associated with the binding of both human estradiol and estrone. These same effects are documented for exposure to environmental estrogens in agrichemicals, common household chemicals, cosmetics, and cosmeceuticals. Estrogen-dominant reactivity has been implicated in respiratory allergies including asthma, in skin conditions such as hives and eczema, and in food allergies.


Symptom Patterns

Some allergic individuals inherit genes predisposing them to allergies from one or both of their parents. If one parent has allergies, the child has approximately a 40% chance of developing allergies; if both parents have allergies, the child has about a 70010 to 90010 chance; if neither parent has allergies, the child still has a 10% to 15% chance of developing allergic sensitivity. The allergy gene alone does not cause allergic reactions. To react, the individual must have the gene and be in an environment that stimulates the expression of the gene. Hence, gene-environmental interactions lead to allergic reactions.

Predominant symptoms. Many of the female patients 1 see in my practice suffer from adult-onset asthma, steroid-dependent dermatitis (such as hives), or perennial nonallergic rhinitis (chemical sensitivity). Frequently these patients also have important comorbidities, such as obesity, hypothyroidism, hyperlipidemia, hypertension, insulin resistance, or female menstrual disturbances such as menstrual irregularity, fibroid tumors (with menorrhagia, metrorrhagia, or menometrorrhagia), fibrocystic breast disease, ovarian cysts, cervical dysplasia, or endometriosis. Often, patients with these symptom patterns have seen numerous physicians for these conditions. Some have had a hysterectomy, while others have had breast biopsies that revealed fibrocystic breast disease. Many of these women take birth control pills to control their menstrual problems; many others are on antidepressants for depression, panic attacks, nervousness, or anxiety. Chronic chest pain due to anxiety is often reported in these patients, who have been evaluated by cardiologists and, in some cases, have undergone cardiac catheterization (usually without significant findings). Frequently, women with this profile have high cholesterol levels and high blood pressure and are therefore on cholesterol- and blood-pressure-lowering medications. I have seen this symptom pattern in patients as young as 13.

Estrogen dominance. In most cases, these women have estrogen dominance which, by definition, involves normal or high estrogen in the presence of deficient progesterone. Excess endogenous estrogens, coupled with exposure to environmental estrogens and plant-based estrogens (such as soy, hops in beer, barley, rye, wheat, etc.), can cause allergic symptoms by stimulating estrogen receptors on mast cells and basophils, and by potentiating the effect of IgE antibodies on mast cells and basophils. When I suspect a hormone-related allergic response in patients with adult-onset-allergies, I make it a point to inform them that their allergy symptoms do not conform to patterns discussed in the conventional allergy literature and may not be caused by typical environmental allergens.

Case history--phytoestrogen triggers. The worst allergic reactivity is seen in recurrent anaphylactic reactions to foods and to allergen immunotherapy. During a fellowship training program at the Johns Hopkins Asthma and Allergy Center in Baltimore, we evaluated a patient who presented with the symptoms of anaphylaxis after ingesting crabs prepared with Old Bay seasoning, a popular dish in that region. The woman, who was postmenopausal (age 60), had a negative skin test and passed a food challenge for crab meat with flying colors. Her reaction was not due to the protein in the crab, which she had eaten and tolerated for years, but rather was due to her estrogen dominance, triggered by the Old Bay seasoning, which contains five phytoestrogens: cinnamon, cloves, and nutmeg, as well as bay leaves and celery. This patient had also ingested beer, which contains hops, another phytoestrogen. These plant-based estrogens, coupled with her already high endogenous estrogens, caused an intense histamine and LTC4 release that led to the anaphylactoid reaction. A food challenge with only the crab meat (but not the seasoning) therefore caused no reaction. I refer to this type of reactivity, which is not caused by food proteins, as pseudo-allergies.

Case history--urticaria. Recently, I saw a patient in my office who presented with urticaria. She was clear that the allergenic trigger was soy protein. She and her husband had recently gone on a high protein diet, and she was eating a great deal of soy. She then developed severe urticaria eruptions that improved when she stopped the soy protein diet. At that point she resumed eating soy, and the urticaria returned. When she saw me, I confirmed with her that the soy protein, a phytoestrogen, was indeed causing her urticaria lesions by adding to her own estrogen production, which was already known to be high because she had polycystic ovarian syndrome (PCOS). Another patient recently presented with similar episodes of urticaria after eating shrimp seasoned with thyme and rosemary, both phytoestrogens.

Allergists who are not aware of these estrogen reactions will do a standard workup for urticaria (CBC with differential, complete metabolic panel, thyroid function test including thyroid antibodies, ANA, complement C3/ C4, and ESR), and the results will be within normal limits. The patient is then labeled as suffering from "idiopathic" urticaria. The progression of treatment is usually something like this: first, antihistamines; then, when the case is desperate, steroids. The following testing and protocol for estrogen-dominant allergies can significantly improve patient outcomes.


Skin and Blood Tests

Skin testing is performed to characterize the allergens involved in the patient's atopic symptoms. Blood testing, also known as RAST (RadioAllergoSorbent Test), is often performed for food allergens and occasionally for environmental allergens. The RAST measures specific IgE markers for the foods, but the case has been made for measuring specific IgG markers as well. Both skin tests and blood tests have two additional purposes: to determine the timing of the treatment and to develop a patient-specific allergy vaccine.

Coordinating allergy testing and treatment. Patients with spring or fall allergies should preempt their seasonal allergies by getting tested so they can start the medication therapy two weeks prior to the beginning of the season, rather than waiting to be treated once they develop full-blown symptoms. Patients with year-round allergies should be treated on an ongoing basis. Symptoms generally fall into the following patterns:

* Spring symptoms are typically due to tree pollens

* Summer symptoms are due to grass pollens

* Fall symptoms are usually triggered by weed pollens

* Year-round (perennial) symptoms can be due to sensitivity to molds, dust mites, or cockroaches, as well as a broad range of animals including cats, dogs, rabbits, guinea pigs, horses, or other species

Note that these symptom patterns can overlap; for example, in late summer, patients may develop reactivity to both grass and weed pollens simultaneously.

Skin testing in adult-onset allergy patients. Since these patients are convinced that they have seasonal/perennial allergic rhinitis, I always offer them the option of a skin test procedure. Patients with skewed hormone levels are frequently surprised to see that their skin-testing results are negative. Some patients are in disbelief, with the impression that the skin test is faulty.

When you are performing skin testing, antihistamine medications must be discontinued, since histamine serves as the positive control and saline the negative control. Antihistamines blunt the positive control, and if the patient continues to use them, there will be no reactions (anergy).

For premenopausal women, skin test reactivity also tends to vary in parallel with the phases of the patient's menstrual cycle, (3), (4) and premenstrual asthma (late luteal phase asthma exacerbations) in women is well documented in the allergy literature. (5) However, allergists do not routinely take this into account in their practices when performing skin testing or when women react to allergen immunotherapy.

Hormone Testing

I couple the skin test with a measure of the patient's endogenous hormones. Frequently the estrogen level is too high and progesterone too low. In the majority of cases, the prescription of bioidentical progesterone balances the hormone levels of these patients, and their allergy symptoms often improve. Several methods exist today for evaluation of hormones, including saliva and blood tests.

Measuring Nutrient Levels

While measuring hormones, do not forget to include vitamin D in the basic hormone panel. Vitamin D deficiency is rampant and is associated not only with heart disease, but also with allergic diseases such as asthma, allergic rhinitis, urticaria, and angioedema.

Therapy for Atopic Diseases

The medications used to treat allergic rhinitis, asthma, and recurrent sinusitis are palliatives and will not cure the root cause of the symptoms. Therefore my ongoing strategy is allergen immunotherapy (AIT), provided subcutaneously or sublingually. Although AIT offers the most effective long-term relief for the treatment of lgE-mediated allergic reactivity, it does not reduce symptoms immediately. To provide patients with more immediate relief, I selectively use medication during the four to six weeks before AIT takes effect. Efficacy of the AIT is measured by the reduction of symptoms and success in reducing the medication therapy.

Clinical Strategies

The choice of treatment depends on the severity of symptoms. If the patient presents with postnasal drainage and sore throat, chronic seasonal allergies, or chronic sinus infection, then combination therapy is optimal. In these cases a single medication is often not sufficient to resolve the symptoms. Combination therapy typically involves antihistamines to block the histamine released from mast cells and basophils, LTRAs (leukotriene receptor antagonists) to block leukotrienes, and nasal corticosteroids to block the various inflammatory mediators that participate in allergic reactions.

Histamine-mediated symptoms. Symptoms that are histamine-related include itchy eyes, nose, or throat; sneezing; and runny nose. When histamine is the only chemical released by mast cells and basophils, the allergy solution is simple: antihistamines alone are sufficient to resolve all the symptoms. Effective antihistamines include Benadryl, Claritin, Clarinex, Allegra, and Zyrtec (one of the most efficacious of the over-the-counter antihistamines). Unfortunately, histamine is not usually the only mediator released by mast cells and basophils.

Leukotriene-mediated symptoms. Leukotrienes (LTC4) and prostaglandins tend to cause late-phase allergic reactions: stuffy nose, postnasal drip, coughing, or difficulty clearing phlegm in the throat. Leukotrienes are also implicated in asthma, causing airway constriction, and therefore shortness of breath and wheezing. Those symptoms tend to occur at night for most allergy and asthma sufferers because that is when leukotrienes are produced. Leukotriene receptor antagonists were conceived to block the leukotrienes. Montelukast, marketed under the brand name Singulair, and zafirlukast (Accolate) are the most popular of the LTRAs. Children and adults who have allergic rhinitis and asthma symptoms tend to do best using a combination of a good antihistamine such as Zyrtec and a good LTRA such as Singulair.

Steroid therapy for atopic conditions. Corticosteroids are highly effective in treating atopic diseases. They inhibit many mechanisms that contribute to chronic Th2-driven inflammation, inhibit cytokine production, and induce eosinophil death, which reduces the level of inflammation. Inhibitors of the Th2 inflammatory response (blocking IL-4, IL-5, or leukotriene antagonists) are not as effective in atopic diseases as corticosteroids. However, long-term use of steroids has undesirable effects.

Brittle asthma or severe atopic inflammation. Steroids are the master blocker of all the chemicals released by mast cells and basophils, which is why many physicians inject cortisone or give prednisone to patients when they present with allergy symptoms. These systemic steroids, however, have multiple undesirable effects in both adults and children and should be reserved only for short-term bursts for brittle asthma or other forms of severe atopic inflammation.

Allergic rhinitis. For the treatment of allergic rhinitis, nasal corticosteroids that act locally are desirable They include Flonase, Veramyst, Nasonex, Nasacort, and Rhinocort. For children, Nasonex, which has the same potency as Flonase, is most desirable and is approved for kids two years old and above. Medications approved for those four years of age and older include Flonase, Veramyst, and Omnaris (ciclesonide). A corticosteroid approved for pregnant women with allergies is budesonide (Rhinocort Aqua).

Adult-onset rhinitis and chemical sensitivities. Independent of environmental allergens, rhinitis can take the form of perennial non-allergic rhinitis (PNAR), sometimes described as vasomotor rhinitis. Patients with these conditions have sensitivities to irritants such as cigarette smoke, petrochemicals, household cleaning agents, perfumes, scented candles, and sometimes even natural flower scents such as rose, lilac, and others. Although some patients with these conditions respond to the usual rhinitis medications, most will respond best to Astelin or Patanase, the only two antihistamine nasal sprays that, ironically, work well on non-allergic rhinitis. Astelin and Patanase work because most of these PNAR cases are due to histamine release from mast cells secondary to non-genomic processes such as estrogens binding to receptor-[alpha] on mast cells.

Usefulness of saline nasal sprays. With all treatment modalities listed above, saline nasal spray, particularly Ocean nasal spray, is an effective adjuvant. If used three to four times daily, the spray can prevent dry nasal mucus membranes and the postnasal drainage that often leads to a cough, as well as colds and sinus infections. This nasal spray may even prevent snoring due to postnasal drip.

Hormone-Related Therapies

Avoiding xenoestrogens and phytoestrogens. Given the evidence that xenoestrogens and phytoestrogens play a major role in adult-onset allergic processes, I provide patients with a list of substances to be avoided that includes xenoestrogens in the environment and the home and phytoestrogens that are ubiquitous in the diet.

Bioidentical hormones. For patients with hormone imbalance, bioidentical hormone replacement therapy has been a useful addition to treatment.

Premenstrual asthma treatment. In the case of premenstrual asthma, Nakasato et al. recommended Singulair as an effective treatment. It is clear that in the late luteal phase, progesterone levels fall below those of estrogen (see Figure 1). That transient estrogen dominance is responsible for priming mast cells and basophils and for triggering premenstrual asthma or premenstrual exacerbations of allergy symptoms. In these cases, LTC4 is released in addition to histamine, and therefore a combination of antihistamines and Singulair (LTRA) is most optimal.


Complementary Therapies

Supportive nutrients. I recommend nutritional supplements to enhance the patient's immune system and for overall wellbeing. One supplement I have found useful in an allergy treatment protocol is Nutrient 950 by Pure Encapsulations, a multivitamin that contains NAC (N-acetyl-L-cysteine), B-complex vitamins, ascorbic acid, vitamin D3, minerals (calcium, magnesium, zinc, manganese, molybdenum, chromium, selenium), and other nutrients.

For patients with estrogen dominance, I recommend CDG EstroDIM (I3C, DIM, Calcium D-glucarate) by Ortho Molecular, which helps to modulate excess or harmful forms of estrogens. Other nutritional supplements to consider for allergy patients include:

* Omega-3 fish oil (EPA 900 mg/DHA 600 mg)

* Additional buffered ascorbic acid (1000 to 3000 mg)

* Additional vitamin D3 (2000 to 5000 IU per day)

* Aller-Essentials by Pure Encapsulations, which contains quercetin, vitamin C, tinospora cordifolia, hesperidin methyl chalcone, nettles (urtica dioica), apple polyphenols, beta-glucan (1,3/1,6 glucan), and ubiquinol CoQl0

Digestive support protocol. For patients with food allergies or food sensitivities, I recommend probiotics, fermented foods (organic kefir seems to work well), and digestive enzymes.

New Therapies

Humanized anti-IgE antibodies. The efficacy of humanized anti-IgE antibody therapy (Xolair) in atopic disease is now well recognized by allergists. Additional studies of other forms of monoclonal antibody therapy are currently under way.

Allergen-Specific Immunotherapy

Allergen immunotherapy (AIT), conceived as long-term relief, is designed to specifically restore normal immunity against allergens. The response to AIT is primarily mediated by T regulatory cells and B cells. This treatment takes two forms: subcutaneous immunotherapy (SCIT) provided by injection, and sublingual immunotherapy (SLIT) taken orally in liquid form. Both methods stimulate T regulatory cells and B cells equally well and are effective in the treatment of atopic diseases. SLIT is most popular in Europe, but it is making its way into allergy practice in the US. Beneficial effects of allergen-specific immunotherapy include:

* Decrease in IL-4 and IL-5 production by C04+ T cells

* A shift from Th2 cytokine pattern towards increased interferon-[gamma] (IFN-[gamma]) production

* Rise in allergen-blocking IgG antibodies, particularly of the IgG4 class, which supposedly block allergen- and IgE-facilitated antigen presentation

* Generation of IgE-modulating CD8+ T cells

* Reduction in the number of mast cells and eosinophils, including the release of mediators

* Induction of a tolerant state in peripheral T cells, an essential step in allergen-specific immunotherapy

Effects of AIT on T regulatory cells and B cells. Peripheral T cell tolerance is characterized mainly by suppressed proliferative and cytokine responses against major allergens. The T cell tolerance is initiated by autocrine action of IL-10, which is increasingly produced by antigen-specific T cells. Tolerized T cells can be reactivated to produce either of the distinct Thi or Th2 cytokine patterns depending on the cytokines present in the tissue microenvironment. The response to allergen immunotherapy is primarily mediated by T regulatory cells and B cells. T regulatory cells produce IL-10 and TGF-[beta], and B cells produce IgG4 and IgA in the presence of allergen immunotherapy. In response to allergen-specific immunotherapy, the effects of IL-10 and TGF-[beta] released by the T regulatory cells include:

* Decreased IgE production by B cells and increased production of IgA and IgG4

* Decreased IgE-dependent activation of mast cells and basophi Is

* Decreased activation and survival of eosinophils

* Suppressed mucus production by the epithelial cells and reduced airway hyperreactivity

* Decreased antigen presentation activity of dendritic cells

* Decreased Th2 cytokine production and suppression of their proliferation

SCIT and SLIT are good, cost-effective, long-term treatment choices for patients with atopic diseases. However, sublingual SCIT carries a higher risk of anaphylactic reaction than SLIT. AIT-related anaphylactic reactions are more common in women than men.

Case history - anaphylaxis in allergen immunotherapy. The following protocol has proven beneficial in reducing the incidence of anaphylactic reactions to AIT. I recently saw a woman on AIT who could not progress to a maintenance protocol due to anaphylactic reactions. Consequently, I reformulated her AIT extracts and started her on a slower injection schedule. She was able to successfully complete phase 1 of the therapy. However, with her second dose of the concentrate antigen (the red vial), she experienced another anaphylactic reaction. This time, instead of simply reformulating her AIT extracts or changing her injection schedule, I measured her hormones and, not surprisingly, found that her estrogen level was very high and progesterone level very low. I started her on progesterone 25 mg/m1 cream, 1 ml daily, and continued the AIT. She was also having unexplained syncope episodes, and all these symptoms resolved when she started the progesterone therapy. In this case, the high endogenous estrogen had caused a synergistic effect with the IgE on her mast cells and basophils, which led to her recurrent anaphylactic reactions.

Since this case, I have seen several more young women who experienced similar episodes. In the most recent case of anaphylaxis, the young woman experienced an anaphylactic reaction to her AIT injection in day 12 or 13 of her pre-ovulation menstrual phase, which is usually characterized by high estrogen levels (see Figure 1). I recommended that she skip her AIT injections during her pre-ovulatory phase and three to five days before onset of her menstrual period, which also corresponds to a transient estrogen-dominant state. I also started her on low-dose progesterone because her measured estrogen was elevated and her progesterone was low, resulting in mast cell and basophil degranulation with corresponding release of histamines and leukotrienes, which in turn results in allergic reactions. Subsequently, she has not had any more episodes, and she has tolerated AIT injections and reached maintenance.

Health care providers will want to take into account estrogen dominance, as well as phytoestrogen and xenoestrogen effects, when evaluating patients suspected of adult-onset anaphylactic/anaphylactoid reactions and AIT-induced anaphylactic reactions. Using this approach, when the actual cause of allergy symptoms is discovered and treated, both the patient and the allergist are rewarded. However, if a patient reacts several times to the AIT injections, to avoid any potential liability the allergist is advised to stop the AIT until the patient's estrogen-progesterone balance can be achieved.

In summary, allergic diseases are on the rise. Recent allergy literature indicates that adult-onset atopy is more prevalent in women and the obese, and women with increased estrogen dominance tend to have the highest rates of asthma and other atopic diseases. Endogenous estrogens, xenoestrogens, and phytoestrogens are ubiquitous and induce significant morbidity and mortality, primarily in women. Hence, estrogen status should be evaluated in diseases that have a predilection for women. An effective integrative approach to allergic disorders includes testing and balancing hormones, short-term relief for allergy symptoms, allergen immunotherapy for more permanent remediation, and nutritional supplementation.

Benoit Tano, MD, PhD

Dr. Tano is board-certified in internal medicine and in allergy and immunology. He serves as Clinical Associate Professor of Medicine at the University of North Dakota School of Medicine and has also taught at the University of Texas School of Medicine. Originally from COte d'Ivoire, Dr. Tano holds a PhD in economics from the State University of New York at Albany (1988), with specialization in econometrics, and taught economics at the University of Toledo in Ohio for eight years. At that point in his career, he entered medical school and completed his MD degree at the Medical College of Ohio, followed by a three-year residency in internal medicine at Ohio State University. In 2002, he engaged in a two-year research fellowship at Ohio State, followed by a two-year clinical fellowship in allergy and immunology at the Johns Hopkins Asthma and Allergy Center.

Preceptorships with Allergy Associates

As an allergist and immunologist with Allergy Associates of La Crosse, Wisconsin, located near Minneapolis, Dr. Tano sees patients and also provides training to health care professionals in sublingual immunotherapy (SLIT). Allergy Associates' protocols cover not only environmental allergens, but also a broad range of food allergies. Dr. Tano may be contacted at 608-782-2027 or by e-mail at btano@allergy-solutions.com. For more information on the preceptorship or Allergy Associates, see www.allergy-solutions.com.

Editorial. Nancy Faass, MSW, MPH, is a writer and editor in San Francisco who has worked on more than 40 books for publishers that include Elsevier, Harper, McGraw-Hill, Mosby, and others. Director of the Writers' Group, she also provides articles, white papers, and writing for the Web. For more information, see www.HealthWritersGroup.com.


(1.) This article was adapted from Tano B. The Allergy Detective: Allergic Rhinitis Treatment Secrets Your Doctor May Not Tell You. Integrative Medical Press, 2011.

(2.) Narita S. et al. Environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators. Environ Health Perspect. 2007 Jan;115(1):48-52.

(3.) Nelson HS. Subcutaneous injection immunotherapy for optimal effectiveness. Immunol Allergy Clin North Am. 2011 May; 31(2): 211-26, viii.

(4.) Kalogeromitros D, Katsarou A, Armenaka M, Rigopoulos D, Zapanti M, Stratigos I. Influence of the menstrual cycle on skin-prick test reactions to histamine, morphine, and allergen. Clin Exp Allergy. 1995 May; 25(5): 461-6.

(5.) Nakasato H, et al. Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist. J Allergy Clin Immunol. 1999 Sep; 104(3 Pt 1): 585-8.
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