Sinusitis Case Study: A female USTA Tennis Player in her thirties, who enjoys playing doubles, presented with a history of recurrent sinus and tonsil infections. The subject’s sinusitis frequently required multiple antibiotic doses to clear and some infections appeared unresponsive to therapy. This subject experienced annual colds requiring antibiotic therapy. She also experienced heartburn (gastro esophageal reflux disease (GERD)) which was treated with over the counter medications. This tennis player began a wheat gluten free diet.
Fourteen years post wheat free diet initiation, this subject has experienced no sinus infections nor incidents of heartburn. She has experienced an occasional cold requiring the use of amoxicillin. Upon exposure to wheat, rye, oats, or vegetation she has used over the counter anti-histamine therapy to prevent inflammation of her tonsils. She avoids potatoes as they cause sinus congestion. With continued avoidance of wheat products, her immune response to ingested wheat has become more pronounced. During the past decade, wheat ingestion every two weeks would require antihistamines prior to and post ingestion to avoid inflammation of her tonsils and sinuses. She continues on a wheat free diet with no sinus or tonsil infections.
Sinusitis Discussion:
Normal respiratory epithelium contains cells resembling columns. Many of these cells have brush-like hairs on their borders which are called cilia. Goblet cells which secrete mucous are also present but they are rare. Both the cilia and mucous help to move particles through respiratory structures.
In a pathologic disease process, the structure of this respiratory epithelium changes. When exposed to wheat germ agglutinin (WGA), respiratory epithelial cells with sparce quantities of goblet cells are found to change into epithelium with heavy quantities of goblet cells secreting acid mucin. These are the front line immune response defenders. It is theorized that the increase in mucous secretions could be a host defense mechanism meant to make bacterial adherence to tissue more difficult. Additional sialic and fucose residues are produced to immunologically conceal the mannose sugar and carbohydrate moieties from the wheat germ, presumably disallowing attachment to the tissue. The number of ciliated cells is reduced and the quantity of normal good bacterial flora present in the sinuses is decreased. The resultant disease etiology is sinusitis and allergic rhinitis.
Rhinitis and nasal allergies are frequently associated with Celiac Disease(CD). In a wheat challenge test of 23 bakers with a history of wheat flour induced ocular hypersensitivities, 17 subjects had symptoms of rhinitis within 10-30 minutes of wheat flour exposure (Wittczak, et al., Otori, et al. 1998).
Kaneko, et al. (2000) demonstrated that the use of wheat germ agglutinin showed that this lectin “strongly reacts with cilia and goblet cells”. In a study of 258 baker’s apprentices, 54 developed IgE antibodies against wheat, rye and/or barley. The IgE antibodies developed in response to typical grass and pollen type allergies were found to correlate well with flour sensitization. Radiographs were performed from these subjects and showed “mucosal thickening, opacity, air/fluid levels, and/or polypous shadowing” of the paranasal sinuses (Popp, et al. 1994).
Sinusitis References:
Wittczak, “Challenge testing in diagonsis of occupational allergic conjunctivitis” Occp Med 2007:57:532-534 DOI: 10.1093/occmed/kqm049
Otori N., Carlsoo B., Stierna P., “Changes in Glycoconjugate Expression of the Sinus Mucosa during Experimental Sinusitis: A Lectin Histochemical Study of the Epithelium and Goblet Cell Development”, Acta Otolaryngol (Stockh) 1998; 118: 248-256
Popp W., Wagner C, Kiss D, Zwick, H, Sertl K, “Prediction of sensitization to flour allergens”, Allergy 1994; May; 49(5):376-9
Photograph: Pacific Coast Highway 1 Cambria, California
Disclaimer: The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice. Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist. Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material. We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.
Mountain Bicyclist Asthma Case: A male in his forties, a former NORBA sectionals downhill mountain biking champion, experienced a 40 yearhistory of asthma upon exposure to grass, yard trimmings, or pets. Childhood allergy patch testing showed allergies to most all allergens. His typical medical routine prior to and following allergenexposure included use of antihistamines, corticosteroids, and the use of a nebulizer. This patient experienced a 10 year history of gastro-esophageal reflux disease (GERD). Treatment included use of proton pump inhibitors and histamine H2 receptor antagonists. The acid had inflammed the esophageal stricture, the opening between his esophagus and stomach. To allow for the passage of food, his gastroenterologist had balloon dilated his esophagus and recommended dilation every six months. This athlete frequently experienced gastrointestinal (GI) upsets with diarrhea and vomiting. In 1998, his physician diagnosed him with pneumonia and treated him with antibiotics. To alleviate the long-term asthma, esophagitis and GERD the patient began a wheat gluten free diet (WGFD).
Thirteen years post WGFD initiation this cyclist no longer has asthma nor requires asthma therapy. Anti-histamines are occasionally required upon exposure to wheat, grass or pets. He utilizes Citrus sinesis (orange peel extract containing 98.5% d_limonene, 1000mg) or fresh kumquat to reduce stomach acid. He sleeps on a wedge pillow elevating his chest and head to protect his esophagus from stomach acid. Esophageal balloon dilation was not required at six month intervals for the next ten years. Then the procedure was repeated. Patient has contracted no further cases of pneumonia. He experiences typical cold/flu illnesses less than once each year. Antibiotics are rarely required and amoxicillin is effective. Patient maintains GI bacterial balance with acidophilis and lactobacilli probiotics (more discussion on the Gastrointestinal Post on Wheatfreediseasefree.com). He continues on a WGFD with no ingestion of wheat gluten.
Asthma Discussion:
In the food industry, cross pollinations are utilized to produce high quality wheat (Kuchel et al. 2006). Gluten protein forms a proteinaceous matrix and a viscous elastic network. Three loci (Glu-A1, Glu-B1, Glu-D1) present on the long arm of group 1 wheat chromosomes code for wheat gluten (WG), which determines the functional properties of wheat flour including elasticity and shelf life. (Mondal et al. 2008) Genetic engineering can be utilized to manipulate these subunits to produce a hearty wheat gluten with strong elastic properties which help bread rise and make it soft and chewy.
In manufacturing, the elastic and tensile properties of wheat gluten are utilized as a matrix material for plastic injection molding. The resultant glue-like product is a strong oxygen barrier and produces films which are cytotoxic and restrictive to cell growth (Cho et al. 2011) (Reddy et al. 2010).
Given this genetic modification of wheat, the gastrointestional (GI) system does not digest WG well. Decomposition occurs by an enzyme called a tissue transaminase which produces a gliadin peptide product. This peptide has a lectin, a powerful agglutinin, which causes inflammatory complexes to be formed within the body. Gliadin is a potent stimulator of the immune system, stimulating T lymphocytes which activate both B lymphocytes and secrete harmful chemicals known as cytokines. The B lymphocytes produce the allergy Ig E antibodies which bind gliadin, form gliadin-antibody complexes, and are found crosslinked on collagen sites. The T lymphocyte activated cytokines destroy collagen and activate phagocytes. Thus, the effect of wheat gluten is in initiating a comprehensive immune cascade which damages collagen both physically through immune complex formation and chemically through cytokine secretion and phagocytic actions.
As gliadin-antibody complexes travel through the circulatory system they attach to various tissues containing collagen. Collagen is found in the walls or septum of lung tissue where it supports the oxygen-carbon monoxide exchange sacs called alveoli (Ross & Romrell, 1989). As immune complexes attach septal collagen and damaging chemicals are secreted, the ability of lung tissue to function properly is impaired. Breathing difficulties and a decreased oxygen tissue saturation results.
Gliadin specific IgE antibodies may cause both Baker’s asthma and wheat dependent exercise induced anaphylaxis (Ueno et al. 2010). While the most prevalent upper respiratory allergen is recognized as grass and tree pollens, the cross reactivity of IgE antibodies to wheat flour and grass pollens has been demonstrated (Merget et al. 2011). Given this high cross reactivity and the inhalation of flour dust, there is an increased risk that allergic asthma reactions will occur. Of 25 subjects with mild asthmas and hay fever, given no previous occupational exposure to flour products, each one of these subjects showed sensitization to flour (Merget et al. 2010). Beyond occupational exposure, bronchial activity leading to asthma, can be associated with food allergy to wheat (Salvatori et al. 2008)
Sinus mucosa undergoes modification when exposed to wheat gluten antigen (WGA). Respiratory epithelial cells with low quantities of goblet cells are found to change into epithelium with heavy quantities of acid mucin secreting goblet cells. These are the front line immune response defenders (Otori et al. 1998) Sialic and fucose residues are produced to immunologically conceal the mannose sugar and carbohydrate moieties from the WGA. The resultant disease etiology is sinusitis and allergic rhinitis. In a wheat challenge test of 23 bakers with a history of wheat flour induced ocular hypersensitivities, 17 subjects had symptoms of rhinitis within 10-30 minutes of wheat flour exposure. (Wittczak, et al. 2007)
While conjunctivitis and urticaria are more prevalent wheat manifestations, respiratory problems are more disabling. 30% of workers in a flour mill were found to have chronic bronchitis or chronic productive cough. Chest tightness was an affliction of 22% of the workers, while bronchial asthma developed in 18%. At the end of a work shift three fifths of the workers had a significant drop in Forced Expiratory Volume(FEV) and Forced Vital Capacity(FVC). Flour disease etiologies were found to match those of cotton, hemp and flax milling. (Awad el Karim, et al. 1986)
In addition to asthma, our male bicyclist experienced esophageal and GI problems. Our subject was not tested for Celiac Disease (CD), however, rhinitis and nasal allergies are frequently associated with CD. Gluten peptide inflammation is shown to induce zonulin release in the GI tract opening tight junctions between intestinal cells. The activity is inserted in to the lamina propria of the gut. The immune system responds with CD4+ T helper lymphocytes which are sensitive to gluten and cause damage in the gut and esophagus. (Lucendo, 2011) The release of T cell mediated cytokine interferon remodel the gut tissue , flattening the mucosa and causing malabsorption. This is a cytotoxic attack on the epithelium. (Nova et al. 2010) Motility disorders in celiac subjects have been reported to affect the gastric mucosa, small bowel, gallbladder and colon. GERD can develop in untreated CD which is often associated with esophageal maladies. (Lucendo, 2011)
The cure for this plethora of disease is generally considered to be a gluten free diet (GFD). A GFD is associated with the resolution and improvement of intestinal and esophageal symptoms in celiac subjects. Reflux symptoms are relieved and heartburn, chest or epigastric pain, and regurgitation significantly reduced. With elimination of gluten, the clinical symptoms are reversed. (Lucendo, 2011) With a GFD the CD8+ cytotoxic T lymphocyte counts, TCR antibodies return to normal and the villi recover. (Nova et al. 2010)
REFERENCES:
Awad el Karim MA, Gad el Rab MO, Omer AA, El Haimi YAA, “Respiratory and Allergic Disorders in Workers Exposed to Grain and Flour Dusts”, Archives of Environmental Health, September-October 1986, Vol. 41 No. 5
Cho SW, Gallstedt M, Johansson E, Hedenqvist MS, “Injection –Molded Nanocomposites and Material based on Wheat Gluten”, Int J Biol Macromol 2011 Jan 1;48(1):146-52. Epub 2010 Oct 28
Kuchel H, Langridge P, Mosionek L, Williams K, Jefferies SP, “The Genetic Control of Milling Yield, Dough Rheology and Baking Quality of Wheat”, Theor Appl Genet, 2006 May;112(8);1487-95. Epub 2006 Mar 21
Lucendo AJ, “Esophageal Manifestations of Celiac Disease”, Dis Esophagus 2011 Mar 25. Doi: 10.1111/j.1442-2050.2011.01190.x. [Epub ahead of print]
Merget R, Sander I, van Kampen V, Bechmannn U, Heinze E, Raulf-Heimsoth M, Bruening T, “Allergic Asthma after Flour Inhalation in Subjects without Occupational Exposure to Flours: an Experimental Pilot Study”, Int Arch Occup Environ Health; 2011 Jan 30 [Epub ahead of print]
Mondal S, Tilley M, Alviola JN, Waniska RD, Bean SR, Glover KD, Hays DB, “Use of Near-isogenic Wheat Lines to Determine the Glutenin Composition and Functionality Requirements for Flour Tortillas”, J Agric Food Chem 2008 Jan 9;56(1);179-84. Epub 2007 Dec 12.
Nova E, Pozo T, Sanz, Marcos A, 3rd International Immunonutrition Workshop. Session 4: Dietary Strategies to Prevent and Mitigate Inflammatory Disease. Dietary Strategies of Immunomodulation in Infants at Risk for Celiac Disease, Proceedings of the Nutrition Society (2010), 69, 347-353
Otori N, Carlsoo B, Stierna P, “Changes in Glycoconjugate Expression of the Sinus Mucosa during Experimental Sinusitis: A Lectin Histochemical Study of the Epithelium and Goblet Cell Development”, Acta Otolaryngol (Stockh) 1998; 118: 248-256
Reddy N, Jiang Q, Yang Y, “Novel Wheat Protein Film as Substrates for Tissue Engineering”, J Biomater Sci Polym Ed 2010 Occt 27. [Epub ahead of print]
Ross, Michael H., Romrell, Lynn J., “Histology, A Text and Atlas”, Second Edition, 1989
Salvatori N, Reccardini F, Convento M, Purinan A, Colle R, De Carli S, Garzoni M, Lafiandra D, De Carli M, “Asthma Induced by Inhalation of Flour in Adults with Food Allergy to Wheat”, Clin Exp Allergy, 2008 Aug;38(8):1349-56. Epub 2008 May 28
Ueno M, Adachi A, Fukumoto T, Nishitani N, Fujiwara N, Matsuo H, Kohno K, Morita E, “[Analysis of Causative Allergen of the Patient with Baker’s Asthma and Wheat-Dependent Exercise-Induced Anaphylaxis (WDEIA)]”, Arerugi, 2010 May;59(5):552-7.
Wittczak T, Krakowiak A, Walusiak J, Pas-Wyroslak A, Kowalczyk M, Palczynski C, “Challenge Testing in the Diagnosis of Occupational Allergic Conjunctivitis”, Occupational Medicine 2007;57:532-534
Photograph: Traveling on the Pacific Coast Highway 1 south of Hearst Castle.
Disclaimer: The ERB is a literature research team presenting the findings of other researchers. The ERB is not licensed medical nor dietary clinicians and will not give medical nor dietary advice. Any information presented on this website should not be substituted for the advice of a licensed physician or nutritionist. Users of this website accept the sole responsibility to conduct their own due diligence on topics presented and to consult licensed medical professionals to review their material. We make no warranties or representations on the information presented and should users utilize this research without consulting a professional, they assume all responsibility for their actions and the consequences.
Wheat Free, Disease Free?? 