Explore topics related to the Immune Advanced Practice Module:
Clinical Tips: Omega-3 Fatty Acids
By IFM Educator Shilpa Saxena, MD
At IFM’s Immune Advanced Practice Module (APM), the intricacies of inflammation and the major impact of anti-inflammatory therapies are discussed with unique patient categories in mind. Whether autoimmune, immunosuppressed, or lifestyle-inflamed, a patient’s sustained health will likely depend upon an advanced set of solutions to improve the most common driver of their chronic disease(s)—inflammation.
As a practicing clinician for over 15 years, I would be surprised to find providers who are not being asked today’s big health questions by their patients. Is fat good for me? What is bad fat? What is good fat? Why fish oil? Which fish oil? How much fish oil? What I initially thought were acceptable simple recommendations have become more complex as I have learned more about the immune system and the omega-3/6 fatty acid pathways.
While it is a start for a disease-management clinician to recommend eating wild-caught salmon regularly and/or to take a quality fish oil supplement, it behooves the health-promoting provider to know more. Understanding the relative potencies and utilities of ALA, EPA, and DHA can help you provide patients with more personalized prescriptions for anti-inflammatory fish oil benefits.
|Educator Helen Messier, MD, on why the Immune APM can make a difference for so many of your patients.|
Since building my knowledge on inflammation and its relationship with the omega-3/6 pathways, I have been able to counsel patients on fatty acids as a Functional Medicine specialist. Cardiovascular patients can use omega-3s to reduce or eliminate prescription medications; autoimmune patients appreciate the pain reduction aspects; and atopic patients value symptom amelioration.
Join IFM at the Immune APM to learn how to tailor your fatty acid prescription, and the underlying mechanisms by which each type affects immune function. In addition to nutritional information, you’ll walk out the door with a host of new interventions for patients with chronic immune dysfunction.
Shilpa P. Saxena, MD
Sustainable Lifestyle Change to Reduce Inflammation
Elizabeth Board, MD, discusses treating inflammation safely. Sustainable lifestyle change can dramatically improve overall health while decreasing inflammation.
Learn many ways to affect inflammation, improve overall health, and increase immune function at IFM's Immune Advanced Practice Module
Treating Autoimmune Conditions Safely
David Blyweiss, MD, shares his perspective on how the Functional Medicine approach can reduce the use of immunologics with safe, effective treatments. Learn more about treating immune dysfunction at IFM's Immune APM.
Proven Interventions to Reduce Inflammation
Prescriptions for inflammatory conditions are becoming more common. In particular, biologics are increasingly relied upon for patients with a range of such conditions, and soon biosimilars will be as well. Yet the price of these drugs can be quite high, despite their efficacy,1 and they often require a lifetime commitment. One estimate is that by 2020, biologics will be 28% of the pharmacological market.2 Biosimilars may reduce the costs, but many patients are still concerned about taking these drugs. Some patients are too high-risk for these medications, either due to age, comorbidity, or other factors.3,4 Biologic treatment also carries high risks of allergy and may involve very complex treatment plans.5 With the increasing prevalence of autoimmune conditions, clinicians need treatment options that work for all types of patients.
What else can you do to help patients with immune dysfunction and chronic inflammatory conditions? Fortunately, there are ways to reduce or eliminate biologics for some patients while preserving their health, and even help patients with newly diagnosed immune dysfunction without using biologics.
IFM’s Immune Advanced Practice Module (APM) provides the background and tools you need to evaluate and recognize patterns associated with the various underlying causes of immune dysfunction and inflammation. This approach informs your patient assessment and provides a range of treatment options that do not require biologic prescriptions. In the accompanying video, IFM educator Tom Sult, MD, discusses why the Immune APM has such a profound effect on some of his patients:
Join us this February 5-7, in Austin, TX, for techniques to help your patients with autoimmune conditions, inflammatory conditions, and immune dysregulation. You’ll walk out the door ready to help patients with personalized lifestyle treatments and nutritional support. For many patients, you’ll be able to avoid, reduce, or eliminate biologics.References
- Gulácsi L, Brodszky V, Baji P, et al. Biosimilars for the management of rheumatoid arthritis: economic considerations. Expert Rev Clin Immunol. 2015;11(Suppl 1):S43-52. doi: 10.1586/1744666X.2015.1090313.
- Aitken M. Delivering on the potential of biosimilar medicines: the role of functioning competitive markets. IMS Institute for Healthcare Informatics. https://www.imshealth.com/files/web/IMSH%20Institute/Healthcare%20Briefs/Documents/IMS_Institute_Biosimilar_Brief_March_2016.pdf. Published March 2016. Accessed November 16, 2016.
- Sugihara T, Harigai M. Targeting low disease activity in elderly-onset rheumatoid arthritis: current and future roles of biological disease-modifying antirheumatic drugs. Drugs Aging. 2016;33(2):97-107. doi: 10.1007/s40266-015-0341-2.
- Ishchenko A, Lories RJ. Safety and efficacy of biological disease-modifying antirheumatic drugs in older rheumatoid arthritis patients: staying the distance. Drugs Aging. 2016;33(6):387-98. doi: 10.1007/s40266-016-0374-1.
- Committee on Rheumatologic Care. American College of Rheumatology position statement: patient access to biologics. American College of Rheumatology. http://www.rheumatology.org/Portals/0/Files/Patient%20Access%20to%20Biologics%20aka%20Model%20Biologics.pdf. Published August 2015. Accessed November 17, 2016.
The Evolution of Testing for Food Sensitivities
Although estimates vary, approximately 20% of Americans suffer from food intolerance or food allergies.1 Food intolerance can be a difficult diagnosis, particularly as there are many potential physiological mechanisms.2 Environmental triggers, including food substances, are known to affect mucosal immunity. Food antibody testing sometimes results in positive findings for foods the patient has never eaten, which may lead practitioners and patients to question the validity of the test.
Currently, over 15 laboratories in the United States offer food immune reactivity testing using a variety of methods including immunoglobulin E (IgE), immunoglobulin G (IgG), and immunoglobulin A (IgA), with a range of different foods available. While the range of tests may seem impressive, deciding which test is most appropriate for an individual can be a difficult task. Recent research shows that IgG and IgA antibodies for food are not always reproducible from one lab to another.3 Is there still value in these tests or do you just go straight to the elimination diet to uncover food sensitivities?4
Learn more about the current state of food sensitivity testing at IFM’s Immune Advanced Practice Module (APM). Key assessment and intervention tools will be discussed, as well as the underlying biochemistry explaining the range of symptoms for different types of food reactions. Discover important interventions that lead to vastly improved quality of life and reversal of a range of conditions.
This February 5-7, IFM’s Immune Advanced Practice Module (APM) contextualizes the latest research in food reactivity testing to improve clinical outcomes. Update your knowledge on the most important antecedents, triggers, and mediators associated with immune dysfunction and learn how to customize treatment plans for immune sensitivities, autoimmune issues, and other immune dysfunction. Join us either via live stream or onsite in Austin, TX.References
- American Autoimmune Related Diseases Association. Autoimmune disease fact sheet. https://www.aarda.org/autoimmune-information/autoimmune-statistics/. Accessed November 8, 2016.
- Zopf Y, Baenkler HW, Silbermann A, Hahn EG, Raithel M. The differential diagnosis of food intolerance. Dtsch Ärztebl Int. 2009;106(21):359-69. doi: 10.3238/arztebl.2009.0359.
- Vojdani A. The evolution of food immune reactivity testing: why immunoglobulin G or immunoglobulin A antibody for food may not be reproducible from one lab to another. Altern Ther Health Med. 2015;21(Suppl 1):8-22.
- Mullin GE, Swift KM, Lipski L, Turnbull LK, Rampertab SD. Testing for food reactions: the good, the bad, and the ugly. Nutr Clin Pract. 2010;25(2):192-98. doi: 10.1177/0884533610362696.
- Woods CR. False-positive results for immunoglobulin M serologic results: explanations and examples. J Pediatric Infect Dis Soc. 2013;2(1):87-90. doi: 10.1093/jpids/pis133.6. Garcia BE, Lizaso MT. Cross-reactivity syndromes in food allergy. J Investig Allergol Clin Immunol. 2011;21(3):162-70.
- Garcia BE, Lizaso MT. Cross-reactivity syndromes in food allergy. J Investig Allergol Clin Immunol. 2011;21(3):162-70.
- Vojdani A. Reaction of monoclonal and polyclonal antibodies made against infectious agents with various food antigens. J Clin Cell Immunol. 2015;6(5):359. doi: 10.4172/2155-9899.1000359.
Intestinal Permeability and Gluten Sensitivity
The surge of interest in the gluten-free diet as a lifestyle treatment for chronic illness has helped many patients recover from longstanding health issues. Despite some high-profile commentaries to the contrary,1 many clinicians continue to have success when asking their patients to eliminate gluten from their diets. It’s clear why this works for those with frank celiac disease, but the mechanisms are somewhat less clear for patients with gluten sensitivity, as well as for those with no known gluten reactions. A study from the lab of Alessio Fasano, MD, illuminates the impact of gluten on the gut and its role in the development of issues unrelated to celiac.
The study explored the effects of the protein gliadin, a component of gluten that triggers immune responses in some patients, on the integrity of the intestinal barrier. Researchers took duodenal biopsies from four populations: patients with active celiac disease, patients with celiac in remission, patients with gluten sensitivity, and patients with no known gluten reactions. In all of the groups, intestinal permeability was significantly increased by exposure to gliadin. Altered gut barrier function was especially pronounced for those with active celiac disease and those with gluten sensitivity.2 A different study found that a subset of patients who were consuming gluten-containing foods had systemic immune activation correlated with intestinal epithelial damage (measured with FABP2) in both the non-celiac wheat-sensitive group and the celiac group, but not in healthy controls.3
Dr. Fasano has posited that many autoimmune diseases develop in the presence of three factors: genetic predisposition, environmental trigger, and intestinal permeability.4 If this research proves to be correct, eating gluten could increase the risk of autoimmune disease for all patients who have a genetic susceptibility, not just those with gluten intolerance.
Food can be medicine, or it can be toxic. At IFM’s Immune Advanced Practice Module (APM), an expert team of clinicians will present several clinical strategies for assessing and treating leaky gut as a way to prevent or improve autoimmune conditions as well as a host of extra-intestinal issues. Join IFM this February 5-7, 2017, either via live stream or onsite in Austin, TX, and you'll also learn about the state-of-the art in testing for celiac disease as well as gluten sensitivity.References
- Velasquez-Manoff M. The myth of big, bad gluten. New York Times Sunday Review. July 4, 2015. http://www.nytimes.com/2015/07/05/opinion/sunday/the-myth-of-big-bad-gluten.html. Accessed October 17, 2016.
- Hollon J, Puppa EL, Greenwald B, Goldberg E, Guerrerio A, Fasano A. Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity. Nutrients. 2015;7(3):1565-76. doi: 10.3390/nu7031565.
- Uhde M, Ajamian M, Caio G, et al. Intestinal cell damage and systemic immune activation in individuals reporting sensitivity to wheat in the absence of coeliac disease. Gut. 2016 Jul 25. pii: gutjnl-2016-311964. doi: 10.1136/gutjnl-2016-311964. [Epub ahead of print].
- Fasano A. Leaky gut and autoimmune diseases. Clin Rev Allergy Immunol. 2012;42(1):71-78. doi: 10.1007/s12016-011-8291-x.
Obesity and Chronic Inflammation
Worldwide, over a third of adults are estimated to be overweight or obese,1 and the numbers are increasing. We know that these individuals are at increased risk for a number of conditions. One of the mechanisms for this increase is that adipose tissue, specifically visceral adipose tissue (VAT), affects the immune response and may predispose overweight and obese individuals to autoimmune conditions.
How does VAT change the immune response? Adipocytes can increase inflammation in the body by releasing adipokines (a type of cytokine) and inflammatory mediators.2 In addition, a recent study suggests that levels of another cytokine, the T-cell–derived IL-17A, may be affected by different types of fat.3 The study compared IL-17A expression in normal weight versus morbidly obese women in both VAT and subcutaneous adipose tissue (SAT).3 Normal weight women had nearly undetectable levels of IL-17A in either type of adipose tissue, but morbidly obese women showed significantly higher IL-17A expression in their VAT.3 Subcutaneous adipose tissue did not have similarly increased levels of IL-17A, regardless of weight.3
This finding strengthens the biochemical understanding that innate immunity, chronic inflammation, and obesity are all linked—and the mechanism may be that IL-17A induces other cytokines like IL-6, increasing the inflammatory response.3 Because IL-17A is implicated in many autoimmune disorders (like ALS,4 multiple sclerosis,5 asthma,6 and lupus7), increasing VAT may predispose individuals to autoimmunity.
Learn more about antecedent factors for autoimmune conditions at IFM’s Immune Advanced Practice Module, this February 5-7, 2017. Join us either onsite in Austin, TX, or virtually through live stream. IFM’s expert faculty will discuss autoimmune disorders, food allergies and intolerances, immune dysfunction and over-activation, and much more. Join us and return to your practice with new tools for addressing chronic, immune-related diseases. References
- Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384(9945):766-81. doi: 10.1016/S0140-6736(14)60460-8.
- Kwon H, Pessin JE. Adipokines mediate inflammation and insulin resistance. Front Endocrinol (Lausanne). 2013;4:71. doi: 10.3389/fendo.2013.00071.
- Zapata-Gonzalez F, Auguet T, Aragonès G, et al. Interleukin-17A gene expression in morbidly obese women. Int J Mol Sci. 2015;16(8):17469-81. doi: 10.3390/ijms160817469.
- Fiala M, Chattopadhay M, La Cava A, et al. IL-17A is increased in the serum and in spinal cord CD8 and mast cells of ALS patients. J Neuroinflammation. 2010;7:76. doi: http://dx.doi.org/10.1186/1742-2094-7-76.
- Babaloo Z, Yeganeh RK, Farhoodi M, Baradaran B, Bonyadi M, Aghebati L. Increased IL-17A but decreased IL-27 serum levels in patients with multiple sclerosis. Iran J Immunol. 2013;10(1):47-54. doi: IJIv10i1A6.
- Nanzer AM, Chambers ES, Ryanna K, et al. Enhanced production of IL-17A in patients with severe asthma is inhibited by 1alpha,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion. J Allergy Clin Immunol. 2013;132(2):297-304.e3. doi: http://dx.doi.org/10.1016/j.jaci.2013.03.037.
- Chen XQ, Yu YC, Deng HH, et al. Plasma IL-17A is increased in new-onset SLE patients and associated with disease activity. J Clin Immunol. 2010;30(2):221-25. doi: http://dx.doi.org/10.1007/s10875-009-9365-x.
Balancing the Immune System
The idea that infections can trigger autoimmunity isn't new; for instance, antibiotics have been used to treat rheumatoid arthritis since the 1930s.1 Specific bacteria have also been linked to specific types of autoimmune conditions, such as Klebsiella infection and ankylosing spondylitis.2 More recent research has generated a list of infectious agents that are related to autoimmunity, while conversely providing evidence that a lack of infections that used to be common in humans may also contribute to autoimmune conditions.3
Improved sanitation and hygiene in developed countries has led to an unprecedented reduction in the number and species of microbes with which humans interact.7 Evidence suggests this reduction might underlie the huge rise in allergic and autoimmune conditions seen in the past half century.7 The role of tolerance in the immune system may help to explain this connection.
At the same time, epidemiological evidence indicates that people who have ever had certain infections in their lives are more likely to have certain autoimmune conditions, when compared with people who have never been infected.4 Adding to the picture, infection with the Epstein-Barr virus increases the likelihood of Sjögren syndrome, rheumatoid arthritis, and systemic lupus erythematosus, among other autoimmune conditions.5 Evidence also links specific enteroviruses such as coxsackievirus B1 to type 1 diabetes.6
Research has enabled earlier detection of autoimmune conditions, allowing for rapid intervention to halt the progression of the disease. Kara Fitzgerald, ND, an educator at IFM’s Immune Advanced Practice Module (APM) discusses her perspective on these exciting new findings:
How do you uncover information about these potential antecedents and triggers when taking a patient history and use it to help treat patients with autoimmune diseases? When do you test for specific infections or genetic polymorphisms that may predispose your patients to autoimmunity? Will treating these infections help patients with autoimmunity?
At IFM's Immune Advanced Practice Module (APM), you'll discover the many ways in which the immune system can be disrupted, supported, and altered. Learn how to uncover underlying infections as the cause of chronic illness as well as genetic predispositions that can lead to immune dysfunction. Join IFM February 5-7, either onsite in Austin, TX, or online via live stream. You'll come away with practical knowledge about the laboratory tests that can help you pinpoint autoimmune triggers as well as proven techniques for improving immune function.References
- Ogrendik M. Antibiotics for the treatment of rheumatoid arthritis. Intl J Gen Med. 2014;7:43-47. doi: 10.2147/IJGM.S56957.
- Ebringer A. The relationship between Klebsiella infection and ankylosing spondylitis. Baillieres Clin Rheumatol. 1989;3(2):321-38.
- Bach JF. The effect of infections on susceptibility to autoimmune and allergic diseases. N Engl J Med. 2002;347(12):911-20. doi: 10.1056/NEJMra020100.
- Ercolini AM, Miller SD. The role of infections in autoimmune disease. Clin Exp Immunol. 2009;155(1):1-15. doi: 10.1111/j.1365-2249.2008.03834.x.
- Draborg AH, Duus K, Houen G. Epstein-Barr virus in systemic autoimmune diseases. Clin Dev Immunol. 2013;2013:535738. doi: 10.1155/2013/535738.
- Laitinen OH, Honkanen H, Pakkanen O, et al. Coxsackievirus B1 is associated with induction of β-cell autoimmunity that portends type 1 diabetes. Diabetes. 2014;63(2):446-55. doi: 10.2337/db13-0619.
- Rook GA. Hygiene hypothesis and autoimmune diseases. Clin Rev Allergy Immunol. 2012;42(1):5-15. doi: 10.1007/s12016-011-8285-8.
Inflammation, Environment, and Asthma
Asthma and allergy are widespread and increasing in prevalence. The hygiene hypothesis suggests that the modern version of cleanliness may be largely to blame, and a new study suggests two elements that might mediate this effect: endotoxins and genes related to innate immunity.
The study examined the prevalence of asthma and allergy in two communities: the Amish and the Hutterite. These two communities have genetic and environmental overlap, as well as similar lifestyle factors—with one major difference: the Amish still farm in small, family farms, while Hutterites have larger, more industrialized communal farms. The study found that the Amish children displayed significantly lower allergic sensitization and asthma than the Hutterite children.1
When the researchers examined the dust from each environment, they found it contained strikingly different levels of endotoxins. They found that while mice exposed to the dust from Hutterite homes went on to develop asthma or allergy symptoms, those exposed to dust from Amish homes did not. They also found that genes that modulate the innate inflammatory response and genes that depend upon nuclear factor κB (NF-κB) were expressed differently in the Amish versus the Hutterite children.1
Learn more about immune dysfunction and inflammation, as well as the antecedents and triggers for immune conditions, at IFM’s Immune Advanced Practice Module (APM). Join us February 5-7, 2017, either via live stream or onsite in Austin, Texas, where expert clinicians will present on the latest research and clinical tools for diagnosing and treating patients with immune dysfunction. You’ll return to your practice ready to recognize patterns of chronic inflammation or immune dysfunction and improve patient outcomes.References
- Stein MM, Hrusch CL, Gozdz J, et al. Innate immunity and asthma risk in Amish and Hutterite farm children. N Engl J Med. 2016 Aug 4;375(5):411-21. doi: 10.1056/NEJMoa1508749
Helping Patients With Immune Overreactions
Allergic rhinitis currently affects approximately 10-30% of adults and up to 40% of children.1 Allergies are on the rise globally. Based on projected temperatures and seed dispersal patterns, a recent study estimated that ragweed allergies in Europe (the area under study) will double in the next 25-40 years.2 The authors also noted that other species of plants may result in other allergies, and that the changes would not be restricted to Europe.2
You likely see many patients with hay fever and allergies, and while antihistamines may offer some relief, they are not always the best solution. Another approach is to consider the many factors that affect an individual’s predisposition to allergies, such as early-life antibiotics, dust in the home,3 exercise or physical activity,4 atopy,5 mold exposure,5 and parental smoking,5 and provide treatment options that affect the underlying cause.
Join us at IFM’s Immune Advanced Practice Module (APM) to update your knowledge on the most important underlying antecedents, triggers, and mediators associated with immune dysfunction and inflammation, and the treatments that go beyond blocking histamine to address the underlying cause. This February 5-7, expand your clinical approach to common conditions like allergic rhinitis, autoimmune conditions, atopy, and many others. You can attend in person in Austin, Texas, or from the comfort of your own computer via live stream. You’ll walk out the door with key interventions to reduce inflammation and promote healthy immune function in your patients.References
- Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008;122(2 Suppl):S1-84. doi: 10.1016/j.jaci.2008.06.003.
- Lake IR, Jones NR, Agnew M, et al. Climate change and future pollen allergy in Europe. Environ Health Perspect. 2016 Aug 24 [Epub ahead of print]. doi: http://dx.doi.org/10.1289/EHP173.
- Tischer C, Weikl F, Probst AJ, Standl M, Heinrich J, Pritsch K. Urban dust microbiome: impact on later atopy and wheezing. Environ Health Perspect. 2016 May 27 [Epub ahead of print]. doi: http://dx.doi.org/10.1289/EHP158.
- Smith MP, Berdel D, Bauer CP, et al. Asthma and rhinitis are associated with less objectively-measured moderate and vigorous physical activity, but similar sport participation, in adolescent German boys: GINIplus and LISAplus cohorts. PLoS One. 2016 Aug 25;11(8):e0161461. doi: 10.1371/journal.pone.0161461.
- Herr M, Just J, Nikasinovic L, et al. Risk factors and characteristics of respiratory and allergic phenotypes in early childhood. J Allergy Clin Immunol. 2012;130(2):389-96.e4. doi: 10.1016/j.jaci.2012.05.054.
Exploring Obesity and Chronic Inflammation
Worldwide, over a third of adults are estimated to be overweight or obese,1 and the numbers are increasing. We know that these individuals are at increased risk for a number of ailments. One of the mechanisms for this condition is that adipose tissue, specifically visceral adipose tissue (VAT), affects the immune response and may predispose overweight and obese individuals to autoimmune conditions.
How does VAT change the immune response? Adipocytes can increase inflammation in the body by releasing adipokines (a type of cytokine) and inflammatory mediators.2 In addition, a recent study suggests that levels of another cytokine, the T cell derived IL-17A, may be affected by different types of fat.3 The study compared IL-17A expression in normal-weight versus morbidly obese women in both VAT and subcutaneous adipose tissue.3 Normal-weight women had nearly undetectable levels of IL-17A in either of the adipose tissues.3 However, IL-17A expression was higher in the VAT of morbidly obese women than in normal weight women.3 Subcutaneous adipose tissue did not have similarly increased levels of IL-17A, regardless of weight.3
This finding strengthens the biochemical understanding that innate immunity, chronic inflammation, and obesity are all linked - and the mechanism may be that IL-17A induces other cytokines like IL-6, increasing the inflammatory response.3 Because IL-17A is implicated in many autoimmune disorders (e.g., ALS,4; multiple sclerosis,5; asthma,6; and lupus7), increased VAT may predispose individuals to autoimmune problems.
Learn more about antecedent factors for autoimmune conditions at IFM's Immune Advanced Practice Module, February 7-9, 2016. Join us either onsite in Atlanta, Georgia, or virtually through Internet live stream. IFM's educators will discuss autoimmune disorders, food allergies and intolerances, immune dysfunction and over-activation, and much more. Join us and return to your practice with new tools for addressing chronic immune-related diseases.
- Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384(9945): 766-81. doi:10.1016/S0140-6736(14)60460-8.
- Kwon H, Pessin JE. Adipokines mediate inflammation and insulin resistance. Front Endocrinol. 2013;4:71. doi:10.3389/fendo.2013.00071.
- Zapata-Gonzalez F, Auguet T, Aragonès G, et al. Interleukin-17A gene expression in morbidly obese women. Int J Mol Sci. 2015;16(8):17469-81. doi:10.3390/ijms160817469.
- Fiala M, Chattopadhay M, La Cava A, et al. IL-17A is increased in the serum and in spinal cord CD8 and mast cells of ALS patients. J Neuroinflammation. 2010;7:76. doi:10.1186/1742-2094-7-76.
- Babaloo Z, Yeganeh RK, Farhoodi M, Baradaran B, Bonyadi M, Aghebati L. Increased IL-17A but decreased IL-27 serum levels in patients with multiple sclerosis. Iran J Immunol. 2013;10(1):47-54. doi:IJIv10i1A6.
- Nanzer AM, Chambers ES, Ryanna K, et al. Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion. J Allergy Clin Immunol. 2013;132(2):297-304. doi:10.1016/j.jaci.2013.03.037.
- Chen XQ, Yu YC, Deng HH, et al. Plasma IL-17A is increased in new-onset SLE patients and associated with disease activity. J Clin Immunol. 2010;30(2):221-5. doi:10.1007/s10875-009-9365-x.
Persistent, Painful Rash of Unknown Origin
By Kara Fitzgerald, ND
When a patient comes in with severe symptoms that haven't resolved with conventional treatment, the Functional Medicine approach can frequently solve the case. On her Functional Medicine professionals' blog, Kara Fitzgerald, ND
(IFM educator for the Immune Advanced Practice Module
), reported on a recent case of a woman with a severe rash uncontrolled by prednisone:
For the last year-and-a-half, Ellen, a married 39-year-old woman with two young kids, had a total body rash so severe that she'd contemplated suicide, despite an otherwise storybook life. She reacted to virtually everything in her environment. She described her rash as feeling by turns painful/burning/pruritic. Visually, it was red/raised/scaly/crusty with oozing vesicles, sparing only her anterior thighs, hands, and face. It was non-responsive to almost every medication except oral and topical prednisone and about 200 mg of Benadryl per day. And even these were limited in their efficacy, only taking the edge off and enabling her to survive her day. She had previously tried Plaquenil (worsened rash), cyclosporine (couldn't tolerate), and Cellcept (developed severe flu-like symptoms).
Baseline photo taken while on Prednisone.
It turns out that what Ellen described as a rash was actually a collection of different problems, including contact dermatitis of unknown etiology, hives, and dermatographism. She'd seen multiple dermatologists, including a top researcher at a local university. Patch testing was positive for eugenol, nickel, fragrance, Neosporin, Bacitracin, and UVB. The researcher suspected her reaction was caused by sun and sunscreen and advised avoidance. She did, to no avail. She and her husband also gutted and rebuilt their home's interior, sparing no expense to remove all possible antigenic materials. Nothing worked, and after 18 months, it was time for her to taper off the steroid regimen.
Surprisingly, Ellen's personal history wasn't significant for any remarkable allergies beyond seasonal hay fever; nor was there a very compelling family history of allergy. However, skin-prick testing done after the onset of the rash showed positive reactions for almost everything environmental, but no foods.
As I investigated for antecedent and triggering factors, there were two smoking guns. Indeed, Ellen herself knew these were big deals as I now include the FM timeline in my patient intake forms so the patient can start connecting these dots even before we begin talking. First, C. difficile colitis after sushi-triggered food poisoning was a clear antecedent factor in the development of Ellen's rash. She had been hospitalized for a week and was treated with vancomycin. Her gut function has been a problem ever since; she passes up to six loose stools daily. The lasting damage to her microflora and gut wall had to be a piece of her extreme hypersensitivity response. Second, just preceding the onset of the rash in mid-2013, Ellen's year-old infant girl went through a phase where she would not sleep for more than 45 minutes at a stretch. Ellen herself got very little sleep through the night, and as a result of this, her food intake deteriorated. Her diet consisted of "lattes and sugar." After 6 months of this, Ellen woke up with the rash.
When she came to my office, my overriding focus was getting her through the final leg of her steroid taper without the fairly common, but devastating, possibility of rebound dermatitis.
Ellen had started a full Paleo diet prior to our appointment. This dietary change did NOT benefit her skin, although there was mild gut improvement.
Follow up photo 20 days after stopping Prednisone and Benadryl.
As you can imagine, after I removed all the possible foods that she might react to, I was careful in prescribing a simple, traceable starting protocol of hypoallergenic nutrients primarily geared toward dampening the possibility of rebound dermatitis. These included an essential amino acids blend, diamine oxidase (for possible histamine intolerance), and very-low-dose probiotics (lactobacillus and bifido-specific species for allergy). Homeopathic sulfur (for itch), cromolyn sulfate (mast cell stabilizer), and bicarbonate (anti-histamine) were all prescribed as needed. I also added a prescriptive ceramide topical cream and dilute bleach baths.
The sulfur, bleach baths, and ceramide topical cream were reported as useful; the bicarbonate and cromolyn sulfate were never used. Ellen responded to our protocol so rapidly, she stopped steroids before the end of her prescribed taper. She never experienced rebound dermatitis. Not surprisingly, Ellen lost over 40 pounds - her steroid-induced weight gain - over the course of about 10 weeks. Her diet had no calorie restrictions.
Learn more about how to treat complex patients and get to the root cause of immune dysfunction at IFM's Immune Advanced Practice Module
. Learn from Dr. Fitzgerald
as well as Helen Messier, PhD, MD, CCFP
; Linus Pauling Award Winner Robert Rountree, MD
; and Thomas Sult, MD
. Join IFM February 5-7 either in person in Austin, TX, or via live stream.
Article by IFM educator Kara Fitzgerald, ND
Originally published at www.drkarafitzgerald.com
Dr. Fitzgerald received her doctorate of naturopathic medicine from National College of Natural Medicine in Portland, Oregon, and completed postdoctoral training in laboratory science at Metametrix Clinical Laboratory. She is a contributing author to numerous textbooks in Functional Medicine and peer-reviewed journals. An IFM Certified Practitioner, her clinical practice is located in Sandy Hook, Connecticut. Full biography