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Celiac.com 08/05/2024 - Psoriasis is a prevalent chronic inflammatory skin condition characterized by its autoimmune etiology. Affecting both men and women equally, this disease is often associated with other autoimmune disorders, increasing the complexity of its management. This study aims to explore the prevalence of autoimmune diseases in patients diagnosed with psoriasis at King Abdulaziz Medical City in Riyadh, Saudi Arabia. By identifying these associations, the study provides valuable insights into the interconnected nature of autoimmune conditions. Study Methods and Patient Selection The research was conducted as a retrospective, cross-sectional chart review. Patients with confirmed psoriasis diagnoses were identified through the dermatology clinic's electronic medical records. The charts were meticulously reviewed to document the presence of other autoimmune diseases, including hypothyroidism, hyperthyroidism, alopecia areata, vitiligo, atopic dermatitis, and inflammatory bowel diseases such as Crohn's disease and celiac disease. Ethical approval was granted by King Abdullah International Medical Research Center's Institutional Review Board. Key Findings and Demographic Data A total of 839 patients were included in the study, with a female majority of 56.4%. The age group with the highest prevalence of psoriasis was between 31 and 50 years, comprising 37.1% of the patients. The study found that 6.8% of the patients had hypothyroidism, making it the most common associated autoimmune disease. This was followed by alopecia areata (3.6%) and atopic dermatitis (2.9%). Rheumatoid arthritis, systemic lupus erythematosus, and inflammatory bowel diseases were notably less common in this cohort. Discussion on the Association Between Psoriasis and Autoimmune Diseases The study reveals that a significant number of psoriasis patients also suffer from other autoimmune diseases, with thyroid disorders being the most prevalent. The findings are consistent with other research that suggests a higher susceptibility to autoimmune conditions among psoriasis patients. For instance, autoimmune skin disorders such as alopecia areata and vitiligo were frequently observed. The commonality in immune response mechanisms across these diseases might explain their co-occurrence. In particular, the role of T-cell-mediated processes and cytokine release, such as tumor necrosis factor-alpha and interleukins, is critical in both psoriasis and other autoimmune conditions. Limitations of the Study Despite its valuable findings, the study has several limitations. Being a single-center, retrospective study, the results might not be generalizable to other populations. Additionally, the reliance on documented diagnoses in medical records could lead to underreporting or missing data. A larger, multicenter approach would provide a more comprehensive understanding of the prevalence and association of autoimmune diseases with psoriasis. Implications for Celiac Disease Patients This study underscores the high prevalence of autoimmune diseases among psoriasis patients, with thyroid disorders and skin autoimmune conditions being the most common. For individuals with celiac disease, these findings are particularly relevant. Understanding the interconnected nature of autoimmune disorders can aid in better managing their health and anticipating potential complications. It also highlights the importance of comprehensive care approaches that address multiple autoimmune conditions simultaneously. By recognizing these associations, healthcare providers can improve diagnostic accuracy and treatment plans, ultimately enhancing the quality of life for patients with celiac disease and other autoimmune disorders. Further research in diverse populations and larger settings is necessary to validate these findings and expand our understanding of autoimmune disease interactions. Read more: cureus.com
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Celiac.com 11/29/2019 - In previous issues of The Journal of Gluten Sensitivity, I told the story of how life-long celiac disease had caused me to experience a severe health-crisis rooted in hypothyroidism, and how hard I found it to get a correct diagnosis and treatment. This piece picks up the story at its very end, where I found a serendipitous outcome as a result of doing my own research and taking charge of my own treatment. In fall 2008, my single-minded concentration on my thyroid issues had to take a back seat to another problem I could no longer ignore. Since 1984, I had been having problems with back pains that were sometimes nagging and sometimes intense. The reason for this wasn’t clear; I had never had a severe auto accident or any fall more severe than falling off a bicycle. I had managed to treat this problem with visits to a chiropractor. After a severe pain attack in 2008, I finally decided it was time to thoroughly investigate what the problem was. X-rays from multiple angles, and an MRI, showed a pretty messy situation. I had a herniation at L3-L4, and degeneration at L4-L5 and L5-S1. A visit with an M.D. orthopedist specializing in spinal issues quickly made it obvious that conventional medicine didn’t have much to offer, and the probability of a successful outcome from expensive, life-disruptive surgery was low. I finally elected to do spinal decompression therapy with a reputable chiropractor who has a long record of ethical treatment. Three months of therapy were sufficient to produce improvement, but I still did not feel “cured”. A fall or jolt could cause pain and instability to return. As I lay on the decompression table thinking about what could have caused this problem, the truth was soon obvious. I had already read that celiac patients often have problems related to bone and connective tissue degeneration. It seems obvious now that hypometabolism due to thyroid failure stretching over more than 17 years, multiple endocrine deficiencies, and many years of severe nutritional deficiencies stemming from gluten enteropathy, are the culprits to blame for this problem. Being under constant pressure, it is difficult for the body to repair the lower back; under the conditions caused by gluten poisoning, repair becomes impossible. As 2008 was coming to an end, a net-friend casually asked me if I had considered Wilson’s Temperature Syndrome (or “Reverse T3 Dominance” as it is called outside the USA). I visited the Wilson’s website, ordered the books, and studied the theory carefully. I already knew I had hypometabolism because my body temperature tended to stay rather low, usually just over 97F, and sometimes even as low as 96.3F basal (upon awakening). But, a generation of doctors who had learned to make fun of the late Broda Barnes M.D. and his temperature theory, were in the habit of not noticing sub-normal temperature in their patients; or if they did, stating that it didn’t matter. So, it seemed like the Wilson protocol, with low temperature a primary diagnostic prerequisite, might be worth a try. After all, I had tried (what seems like) almost everything else. In January 2009, I went off T4 completely and began taking a combination of immediate-release and sustained-release T3 (triiodothyronine), along with a daily B-12 lozenge to blunt the “rush” from immediate-release T3. T3 is the thyroid hormone which the body actually requires. The fact that T4 is used successfully with many hypothyroid patients means that they have sufficient quantities of ferritin, cortisol, the deiodinase thyroid conversion enzymes, etc. Patients who don’t have the correct biochemistry, suffer because their bodies convert too much T4 into Reverse T3 in a mis-guided, maladaptive attempt to get rid of excess T4. The result of T3-only therapy on brain function was astounding! Once I had been off T4 10 days, and on T3 doses of 20-25mcg per day for a week, the brain fog and motivation problems I had had for nearly 20 years, simply went away. The conclusion was obvious: in addition to the glandular hypothyroidism I had acquired from the effects of gluten, I had “Reverse T3 Dominance”, a (usually) stress-caused disorder in which the body converts too much of its T4 to rT3. rT3 is a compound which is the chemical mirror-image (reverse) of T3, but has no biological activity, other than to block thyroid receptors from receiving T3. The protocol described by Wilson is difficult; I went though one cycle of loading the body with sustained-release T3 and found it eventually produced hyperthyroid symptoms. It soon became obvious that, in addition to being difficult, there was much about the Wilson Protocol that was simply illogical. Within a couple months after starting T3 therapy using the Wilson protocol, I learned it was possible to use only non-time-release T3 (Cytomel) with equally good results. The leading proponent of this approach is John Lowe, D.C.. I worked my total Cytomel dose up as high as 190 micrograms/day while I was still in the process of clearing rT3. Once rT3 was mostly cleared, I quickly went hyper and began dropping my dose, finally ending up at my current dose of 60 micrograms/day. This dose produces the desired blood FT3 level of 5-8 picograms/ml. On this program, I not only feel energetic during the day and sleep well at night, but my weight dropped to where it should be (165 lbs.). As my treatment progressed during the year 2009, I would discover a totally serendipitous and welcome side-effect of T3 therapy. By June 2009, I became conscious that my back no longer felt as painful and instable as it had. This was proved in Sep 2009, when I was slammed to the ground in a freak mountain-biking accident. My back did not go into spasm, and recovered fairly quickly. By Nov. 2009, I was no longer having any back pain or instability. I still had lingering effects from celiac-caused degeneration, which became obvious in Aug. 2009 when I had an osteoporosis evaluation requested by my regular doctor. He had become suspicious about whether the back problems were related to osteoporosis. The finding of bone density at 0.75 grams/square-centimeter in the neck of my right femur was clearly osteopenic and very close to osteoporosis. This was not a surprising finding; I was expecting a problem. A saliva test of adrenal function, also conducted in August, showed that my adrenals were still awakening in the middle of the night. This is a common effect of previous long-term hypothyroidism, which can be expected to gradually get better, and it has: sleep quality was continuing to improve through the end of 2009. In Nov. 2009, the chiropractor who had been administering my decompression treatments was amazed at my progress. He had thought I was “fragile” when I started treatment with him in Oct 2008, but was now amazed at the increase in leg muscle strength when he tested me on his table. He was definitely interested in what T3 had done to me ... and probably a bit disappointed that I no longer need decompression treatments!
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Celiac.com 12/25/2020 - In Spring 2006, Journal of Gluten Sensitivity Newsletter published an article titled “To HAIT And Back” about my encounter with gluten-induced autoimmune thyroiditis. At the time I wrote that piece, I was confident that the elimination of gluten and proper level of thyroid hormone supplementation had me on a track back to full health. However, little did I know that my illness consisted of two syndromes. Every gluten-induced illness, no matter which of the body’s systems it affects, is accompanied by some degree of intestinal destruction. This is true even in cases of “silent” gluten intolerance/ celiac disease, where there are no obvious digestive symptoms. In fact, my health problems were layered: in addition to thyroid destruction, I also had significant, silent intestinal destruction. In addition to the autoimmune thyroid issue, a second issue of malnutrition had to be corrected before my health would return to a truly high level. As 2005 drew to a close, I realized that, although I was feeling generally much better, my health was not perfect. I was willing, at that point, to attribute this to what Ridha Arem M.D had said in his book, Thyroid Solution: a return to the euthyroid state may not immediately eliminate all symptoms. For that reason, I used a small dose of Mirtazapine to help me feel better. I was able to maintain a fairly level state into spring 2006. By late spring 2006, however, my sleep had begun to deteriorate again in spite of the assistance provided by Mirtazapine and other prescription drugs. In May, I tried acupuncture a few times, and bought a light-box, but still could not get relief. By the time summer rolled around, I was back in the office of the naturopath who had originally convinced me to go gluten-free in June, 2003 due to gliadin antibodies. An adrenal test showed that my adrenal function had gone down to almost nothing. A continual downward trend in adrenal function was shown by tests in 2002, 2004, and 2006. The naturopath contended that I needed to go back on Cortef (hydrocortisone) and DHEA to prop up my adrenals. But that did not provide much symptom relief. By September, I was feeling really bad. The naturopath and her assistant decided that I should be tested for heavy metals. The test came back positive: significantly elevated level of lead, and somewhat elevated level of mercury. Shortly thereafter, I started chelation therapy with the chelating agent DMSA. This continued for eleven 2-week rounds, into Feb. 2007. Although I had periods where the chelation seemed to be making me feel better, the result was not as successful as I expected. Three months after the chelation ended, a follow-up test (non-provoked) showed an undetectable lead level, so it seems unlikely that I have a large amount of lead stored in bone. In spring 2007 I was back in my thyroid doctor’s office, and we discussed other treatment alternatives. Who in the area was likely to come up with new avenues of investigation? The result was a referral to see a “holistic” M.D. in March 2007. Improvement thereafter was rapid. On my second visit to the “holistic” M.D., he recommended that I do a urine test for the stress disorder pyroluria. The results came back positive, although not strongly so. He recommended starting treatment anyway, with a high-dose vitamin and mineral preparation. This preparation contains vitamins B6/P5P, niacin, and pantothenic acid, along with zinc, manganese, and magnesium. I was skeptical, but had no serious objection to trying something that was highly unlikely to be toxic. The result was that I felt almost completely well within three weeks. However, I started feeling worse after about five weeks. Because of my long experience with drugs, I suspected that the very high dose of “pyroluria formula” I was taking might be too high. Cutting back the dose brought me to a state in which I felt clear, calm, collected, and slept well. Because my read-out on the pyroluria test was in the gray zone between no diagnosis and firm diagnosis, it seems sensible that I would not require a mega-dose. I was later to determine that my negative response to large amounts of the preparation was probably due to the high levels of pantothenic acid it contains, and eventually began supplementing the formula with plain B-6 and zinc. To augment my treatment by the “holistic” M.D., I shortly thereafter began seeing a Certified Nutritionist he recommended. On the very first visit, the CN looked over my case history and made a couple recommendations. The first was to add a supplement regimen designed to heal gluten enteropathy. That regimen included large doses of ground flax-seed, Metagenics’ Glutagenics (glutamine/licorice/aloe), probiotics, and minerals. The second recommendation was to do a trial elimination of dairy products, based on her previous observation that people with gluten enteropathy, often cannot digest dairy foods. Going dairy-free turned out to be a positive step. Within a few weeks, I noted that my digestion was working much better. Based on this result, I was ready to follow more of the CN’s advice. At our second visit, she recommended changes to my supplementation plan. She also noted that I am one of a few patients she and the “holistic” M.D. are monitoring to see if pyroluria improves with intestinal healing. The theory is that, when “pyroluria” is actually due to intestinal damage, the pyroluria will recede if the intestine can be healed. These recommendations proved to be good ones. Within about six months, I noticed that I could skip supplement doses without negative effects. I also noticed that my previous sensitivity to dairy foods had disappeared. By the end of 2007, I was finally able to reach the correct, therapeutic dose of thyroxine that would give me a TSH just above 1.0. This ended 17 years of hypothyroidism. Today, I religiously take 118mcg of T4 each night between bedtime and arising. For me, thyroxine acts almost as a sleeping pill. And as before, I am religiously avoiding all traces of gluten grains in my diet, as I have for more than 4 years. This latter bout of illness has taught me an interesting medical fact that I hope I’ll never have to use again: the (relatively) inexpensive test for pyroluria, is an excellent way to diagnose malnutrition caused by destruction of the intestine. Summary In retrospect, the most important things I learned from this last 2 years of illness, on top of the previous 15 years, were: Every gluten-induced illness is going to be accompanied by some degree of intestinal destruction. If you have gluten problems but no obvious digestive symptoms, you probably have the silent form of gluten intolerance/celiac. It is possible to heal gluten-induced destruction, but it can take a very long time. And, you probably cannot do it yourself; you will need a RD or CN who is knowledgeable about gluten-induced destruction, to help you along. Most M.D’s don’t know how to diagnose malnutrition. In fact, most of them are completely unaware of pyroluria. However, the pyroluria test appears to be a fairly reliable way of diagnosing intestinal destruction leading to malnutrition. Of course, genetic pyroluria is a real disorder, but the utility of the test as a diagnostic tool for intestinal destruction, in people who do not have a past history of genetic pyroluria, cannot be denied. The co-existence of HAIT and “pyroluria” (malnutrition) in my case, suggests a hypothesis as to why “Hashimoto’s Anxiety Syndrome”/”Hashimoto’s Encephalopathy” occurs in some people, but not others. Obviously, HAIT by itself causes some anxiety, since ridding myself of HAIT antibodies reduced anxiety related to administration of thyroid hormone. It seems a reasonable hypothesis that any of several biochemical syndromes that are known to cause anxiety, could add anxiety to that caused by HAIT, greatly amplifying overall anxiety. Among the many symptoms of “pyroluria” (in my case, malnutrition), whose functional deficiency of B6 and zinc disproportionately affects the neurological system, are anxiety and atypical/unusual reaction to drugs and hormones. It is known that high oxidative stress can create food allergies (per William Walsh PhD of the Pfeiffer Treatment Center). Since pyroluria (i.e. malnutrition) causes oxidative stress, it is a (unproven at this point) theory that my food allergies may have been worsened by co-existing malnutrition.
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Celiac.com 04/25/2020 - Do you know or suspect that you may have a sensitivity to wheat (or gluten)? According to the European Journal of Endocrinology, 43% of people with gluten sensitivity will manifest a form of thyroid dysfunction. (1) The American Journal of Endocrinology reports 30.3% of people with celiac disease will have thyroid dysfunction. (2) If you have a gluten sensitivity, a common manifestation is that it impacts your thyroid. In fact, thyroid dysfunction is four times higher in people with celiac disease than in the general population. (3) Your thyroid is a butterfly shaped gland located in your neck. The two main hormones produced are triiodothyronine (T3) and thyroxine (T4). The most common types of thyroid dysfunction are related to the levels of hormones. For instance, hyperthyroidism is an overproduction, as seen in conditions such as Graves disease. Hypothyroidism is when you are not producing enough or your thyroid is underactive, as seen in conditions such as Hashimoto’s. Hormones get into the cell through receptor sites specific to that particular hormone. Estrogen goes into an estrogen receptor site. Testosterone goes into the testosterone receptor site. Thyroid hormone will only go into a thyroid receptor site. There is a thyroid receptor site on every single cell of your body. It is an incredibly important hormone. Have you ever turned the thermostat down in your home on a winter night when everyone goes to sleep to save fuel? And in the early morning, turn it up to warm your home before everyone wakes up? Your thyroid is the thermostat that controls the temperature inside every cell of your body, otherwise known as your metabolism. And your metabolism is how fast or slow every function in your body occurs. Because the thyroid regulates the level of function of every cell in your body, any symptom in your body can be the result of thyroid dysfunction. The most commonly recognized symptoms of thyroid dysfunction are: Cold hands and feet Lack of vital energy Brain lacks clarity of thought Difficulty losing weight Depression Hitting snooze multiple times in the am Physical symptoms that may suggest a thyroid condition: Distal third of the eyebrows are thinned out Dry, cracked skin, such as the bottoms of your feet Brittle hair Fatigue Increased sensitivity to cold Constipation Dry skin Weight gain Puffy face Hoarseness Muscle weakness Elevated blood cholesterol level Muscle aches, tenderness and stiffness Pain, stiffness or swelling in your joints Heavier than normal or irregular menstrual periods Thinning hair Slowed heart rate Depression Impaired memory Enlarged thyroid gland (goiter) Medication Warnings for People with Thyroid Dysfunction Of course, if it is determined that you need medication, always follow your doctor’s advice. But at the same time, investigate. ‘WHY’ does my body need medication right now? The FDA warns that some thyroid medications may cause serious consequences, including liver disease, liver dysfunction and death. (4) Although uncommon, if you are taking medications and are not seeing improvement, discuss concerns with your doctor before stopping any medications. Try eliminating gluten from your diet to see if you notice any improvement with your thyroid-related symptoms. People with a sensitivity to gluten who still eat wheat require 49% more thyroid hormone to ‘get the job done’ compared to when they stop eating gluten. (5) That means that IF gluten is a problem for you, when you stop being exposed to gluten, your thyroid begins working better, requires less ‘outside help’ - thus less medication, and less risk of side effects from the medication. If you improve on a thyroid healing protocol, some people find antidepressants are no longer necessary. But before going off any medications, you should first check with your doctor on how to safely do this and confirm it is advisable. Thyroid function is critical to your sense of well being. Whatever it takes to improve its function so you can feel good, keep digging away to discover what may help you. You may be among the many people who have a sensitivity to gluten, and it is triggering an autoantibody response. If so, eliminate gluten from your diet. If gluten is not your trigger, you will need to identify what the trigger(s) are. There is often more than one thing. For example, once BPA, a chemical used to mold plastic found in our food and drinks gets into our bloodstream, it is notorious for binding to thyroid and causing chaos. (6) Removing substances (foods and chemicals) offensive to the thyroid,allows this very important gland to function more normally. Testing is advisable to drill down and uncover the source of the problem. What can impact the thyroid negatively? Chlorine is a common one that binds to the receptor sites. (7) An easy ‘base hit’ is to add a chlorine shower filter to your shower head. It may also improve your skin and hair. Bromine - Overexposure to bromine can cause hypothyroidism. (8) Bromine can be found in baked goods, carbonated soft drinks, hot tubs, and even your car upholstery. Your thyroid relies on iodine for hormone production. Bromine tricks those receptor sites into thinking it is binding with iodine. Ultimately, this results in an iodine deficiency and likely thyroid dysfunction. Fluoride - Some people benefit from choosing fluoride-free toothpaste or fluoride-free water. Fluoride effects appear to be more severe in people with iodine deficiencies and is more closely associated with hypothyroidism. (9) Goitrogenic foods - Goitrogenic means they may inhibit thyroid function. The following are very good foods for you but it is worth seeing if any of them may be inhibiting thyroid function. This would include cruciferous vegetables like broccoli, cabbage, or cauliflower. If you have thyroid problems, screening these foods, keenly observing how you feel and function may be of value. Gluten Sensitivity with or without celiac disease - A recent 2019 study of 34 women with thyroid disease was performed to examine the impact of a gluten-free diet. After six months, the results showed that the group on a gluten-free diet had significantly less antibodies affecting thyroid globulin (TG) and thyroid peroxidase (TPO). (10) Rapid weight loss - When you lose a lot of weight or starve yourself, your thyroid slows down its metabolic activity. Ancestrally, this is your body’s way of protecting you for those times when food is scarce, to prevent death from starvation. When your gas gauge says empty and the nearest station is a few miles away, you slow down to burn less fuel and hopefully you’ll make it to the station for a fillup (your next meal). Responsible weight loss is slow and steady. Estrogen - Yes, estrogen is needed for both men and women, but you can have too much of a good thing. Many studies have been done on the association between estrogen and your thyroid levels. Estrogen dominance produces thyroxine binding globulin (TBG) which binds to that thyroid receptor site, reducing your available thyroid hormone availability. A Case of Mistaken Identity The primary offensive gluten molecule is 33 amino acids long. It’s a long molecule. If your immune system is searching (antibodies) for the food you are sensitive to it may attack other molecules that look like the food. The surface of your thyroid is made up of proteins and fats. The proteins are made up of many amino acids, which can include a section that looks like the gluten molecule. Now the immune system may go after the thyroid damaging your thyroid cell. The ‘geek’ term for this is Molecular Mimicry. Once the immune system goes after the thyroid damaging your thyroid cell because of Molecular Mimicry (in this example), now your body needs to make thyroid antibodies to get rid of that damaged cell. If you have a sensitivity to gluten, every time you eat gluten, your body creates antibodies to gluten. These may also go after the thyroid where it looks like it (if that is your genetic weak link). Eventually, over time, your body develops the mechanism where it starts making antibodies to the thyroid ongoing. Some celiac patients or people with gluten sensitivity find that when they go on a gluten-free diet, the thyroid antibodies also go down. Sometimes dramatically, full remission. Thus, sometimes you can reduce the antibodies to your thyroid just by removing the irritating foods. Foods That Contain Gluten Many foods contain gluten, but the concerning ones (to everyone) stem from wheat, rye, and barley. These are toxic forms of gluten that nobody is able to digest, and it is one of the most common foods people eat. In general, when referring to a gluten-free diet, this means avoidance of foods containing wheat, rye, and barley. Now there is gluten in many other grains, corn, rice, quinoa,... But it’s the toxic family of glutens in wheat, rye and barley we’re talking about here. You may be sensitive to corn. Or rice, or quinoa, or any other food. If you are, stop the food. But it would not be included in the family of gluten sensitivity. That term is allocated to wheat, rye and barley. And remember these grains are used as fillers in many different foods as well as hidden sources, such as sauces, cosmetics and shampoos (which can be inhaled). You want to eliminate all forms of gluten to reap the benefits. A recent study on women with Hashimoto’s showed that a gluten-free diet may offer clinical benefits. (11) And it isn’t just hypothyroidism that seems to show improvement. People with Graves are also reporting improvement. (12) Why? Gluten is a common trigger for a lot of people. You may be one of them and not even realize it. If you are struggling to manage your thyroid symptoms, try a gluten-free diet for a few months. You should notice symptom improvement relatively quickly if gluten is the only trigger making your condition worse. Scientific References Valentino, Rossella & Savastano, Silvia & Maglio, Maria & Paparo, Francesco & Ferrara, Francesco & Dorato, Maurizio & Lombardi, Gaetano & Troncone, Riccardo. (2002). Markers of potential coeliac disease in patients with Hashimoto's thyroiditis. European journal of endocrinology / European Federation of Endocrine Societies. 146. 479-83. 10.1530/eje.0.1460479. Sategna-Guidetti, C & Volta, U & Ciacci, Carolina & Usai, Paolo & Carlino, A & Franceschi, L & Camera, A & Pelli, A & Brossa, C. (2001). Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: An Italian multicenter study. The American journal of gastroenterology. 96. 751-7. 10.1111/j.1572-0241.2001.03617.x. Baharvand P, Hormozi M, Aaliehpour A. Comparison of thyroid disease prevalence in patients with celiac disease and controls. Gastroenterol Hepatol Bed Bench. 2020;13(1):44–49. fda.gov Virili, Camilla & Bassotti, Giulia & Santaguida, Maria & Iuorio, Raffaella & Duca, Susanna & Mercuri, Valeria & Picarelli, Antonio & Gargiulo, Patrizia & Gargano, Lucilla & Centanni, Marco. (2012). Atypical Celiac Disease as Cause of Increased Need for Thyroxine: A Systematic Study. The Journal of clinical endocrinology and metabolism. 97. E419-22. 10.1210/jc.2011-1851. Gore AC, Chappell VA, Fenton SE, et al. EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr Rev. 2015;36(6):E1–E150. doi:10.1210/er.2015-1010 Bercz JP, Jones LL, Harrington RM, Bawa R, Condie L. Mechanistic aspects of ingested chlorine dioxide on thyroid function: impact of oxidants on iodide metabolism. Environ Health Perspect. 1986;69:249–254. doi:10.1289/ehp.8669249 Allain P, Berre S, Krari N, et al. Bromine and thyroid hormone activity. J Clin Pathol. 1993;46(5):456–458. doi:10.1136/jcp.46.5.456 Malin, Ashley & Riddell, Julia & Mccague, Hugh & Till, Christine. (2018). Fluoride exposure and thyroid function among adults living in Canada: Effect modification by iodine status. Environment International. 121. 667-674. 10.1016/j.envint.2018.09.026. Krysiak, Robert & Szkróbka, Witold & Okopien, Boguslaw. (2018). The Effect of Gluten-Free Diet on Thyroid Autoimmunity in Drug-Naïve Women with Hashimoto’s Thyroiditis: A Pilot Study. Experimental and Clinical Endocrinology & Diabetes. 127. 10.1055/a-0653-7108. Gier, Dominika. (2019). EVALUATION OF THE PREVALENCE IgG-DEPENDENT FOOD INTOLERANCE IN WOMEN PATIENTS WITH THYROID DISORDERS. Joshi AS, Varthakavi PK, Bhagwat NM, Thiruvengadam NR. Graves' disease and coeliac disease: screening and treatment dilemmas. BMJ Case Rep. 2014;2014:bcr2013201386. Published 2014 Oct 23. doi:10.1136/bcr-2013-201386
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The following is a list of citations where you can find more information on the relationship between hypothyroidism and celiac disease: The American Family Physician web page (http://www.aafp.org/afp) has an article (March 1, 1998) on detecting Celiac in a patient. It says that autoimmune thryroid diseases were found in 5.4% of celiacs. In the Feb 15,1998 issue there is an article entitled Subclinical Hypothyroidism: Deciding When to Treat. Cole DE, et al. [see Related Articles]. Neonatal severe hyperparathyroidism, secondary hyperparathyroidism, and familial hypocalciuric hypercalcemia: multiple different phenotypes associated with an inactivating Alu insertion mutation of the calcium-sensing receptor gene. Am J Med Genet. 1997 Aug 8; 71(2): 202-210. PMID: 9217223; UI: 97360195. Corazza GR, et al. [see Related Articles] Propeptide of type I procollagen is predictive of posttreatment bone mass gain in adult celiac disease. Gastroenterology. 1997 Jul; 113(1): 67-71. PMID: 9207263; UI: 97350887. Shaker JL, et al. [see Related Articles] Hypocalcemia and skeletal disease as presenting features of celiac disease. Arch Intern Med. 1997 May 12; 157(9): 1013-1016. PMID: 9140273; UI: 97285000. Moran CE, et al. [see Related Articles] Bone mineral density in patients with pancreatic insufficiency and steatorrhea. Am J Gastroenterol. 1997 May; 92(5): 867-871. PMID: 9149203; UI: 97293150. Corazza GR, et al. [see Related Articles] Influence of pattern of clinical presentation and of gluten-free diet on bone mass and metabolism in adult celiac disease. Bone. 1996 Jun; 18(6): 525-530. PMID: 8805992; UI: 96399521. Keaveny AP, et al. [see Related Articles] Bone remodeling indices and secondary hyperparathyroidism in celiac disease. Am J Gastroenterol. 1996 Jun; 91(6): 1226-1231. PMID: 8651176; UI: 96237643. Wrong O. [see Related Articles] A woman with bone pain, fractures, and malabsorption. Lancet. 1996 Mar 23; 347(9004): 829. No abstract available. PMID: 8622356; UI: 96180154. Kumar V, et al. [see Related Articles] Celiac disease and hypoparathyroidism: cross-reaction of endomysial antibodies with parathyroid tissue. Clin Diagn Lab Immunol. 1996 Mar; 3(2): 143-146. PMID: 8991626; UI: 96265434. Bertoli A, et al. [see Related Articles] A woman with bone pain, fractures, and malabsorption. Lancet. 1996 Feb 3; 347(8997): 300. No abstract available. PMID: 8569366; UI: 96158642. Rude RK, et al. [see Related Articles] Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int. 1996; 6(6): 453-461. PMID: 9116391; UI: 97183181. Molteni N, et al. [see Related Articles] Intestinal calcium absorption as shown by stable strontium test in celiac disease before and after gluten-free diet. Am J Gastroenterol. 1995 Nov; 90(11): 2025-2028. PMID: 7485015; UI: 96048763. Pratico G, et al. [see Related Articles] [Calcium-phosphorus metabolism in celiac disease in children]. Pediatr Med Chir. 1995 Sep; 17(5): 403-406. Italian. PMID: 8684993; UI: 96286520. Corazza GR, et al. [see Related Articles] Bone mass and metabolism in patients with celiac disease. Gastroenterology. 1995 Jul; 109(1): 122-128. PMID: 7797010; UI: 95317529. Gonzalez D, et al. [see Related Articles] Body composition and bone mineral density in untreated and treated patients with celiac disease. Bone. 1995 Feb; 16(2): 231-234. PMID: 7756052; UI: 95275602. Mazure R, et al. [see Related Articles] Bone mineral affection in asymptomatic adult patients with celiac disease. Am J Gastroenterol. 1994 Dec; 89(12): 2130-2134. PMID: 7977227; UI: 95067822. Wortsman J, et al. [see Related Articles] Case report: idiopathic hypoparathyroidism co-existing with celiac disease: immunologic studies. Am J Med Sci. 1994 Jun; 307(6): 420-427. PMID: 8198149; UI: 94256518. Bolla G, et al. [see Related Articles] [Tertiary hyperparathyroidism revealing celiac disease in adults]. Presse Med. 1994 Feb 19; 23(7): 346. French. No abstract available. PMID: 8208699; UI: 94269013. Lindh E, et al. [see Related Articles] Screening for antibodies against gliadin in patients with osteoporosis. J Intern Med. 1992 Apr; 231(4): 403-406. PMID: 1588266; UI: 92268780. Caraceni MP, et al. [see Related Articles] Bone and mineral metabolism in adult celiac disease. Am J Gastroenterol. 1988 Mar; 83(3): 274-277. PMID: 3257843; UI: 88147922
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