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  • John B. Symes, D.V.M.
    John B. Symes, D.V.M.

    Vitamin D, Antibiotics and the Immune System

    Reviewed and edited by a celiac disease expert.

    Journal of Gluten Sensitivity Summer 2010 Issue. NOTE: This article is from a back issue of our popular subscription-only paper newsletter. Some content may be outdated.

    Vitamin D, Antibiotics and the Immune System - Image: CC by-sa 2.0--keepitsurreal
    Caption: Image: CC by-sa 2.0--keepitsurreal

    Celiac.com 06/28/2019 (originally published 07/12/2010) - The report by R.H. Wasserman titled “Vitamin D and the Dual Processes of Intestinal Calcium Absorption“ is very important.  I have some writing to do (and corrections to make) as a result of reading this.  It helps to explain why dogs don’t suffer from clinical osteoporosis.  It’s obvious that there are processes taking place in the ileum of humans that do not take place in the dog.  

    This came up as I was counseling an Internet acquaintance concerning his osteoporosis.  He was not improving with conventional therapy and was also suffering from chronic lymphocytic colitis.  I knew that the ileum actively absorbs calcium but the numbers in the study above were news to me.  I’ve been telling people for years that one of the biggest difference between a person doing well after gastric bypass vs.  crashing and burning had to be the health of their ileum and now I understand a little more as to why this is the case, especially when it comes to bone density.  So, I’ve turned my attention to the health and wellbeing of the ileum.



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    I have assumed for years that one of the biggest factors in humans is dairy products.  So much points to that.  But…is it the casein and other dietary glycoproteins causing villous atrophy that does it OR is there something IN the milk that is doing it? We know that Mycobacterium paratuberculosis can be involved in Crohn’s and that it can come from milk, even when pasteurized.  Are there other pleomorphs that are doing this?

    I like to point out that, of the “big 4” foods, only dairy is of animal origin and that it is “public enemy number one” for a reason: It not only contains damaging lectins, loads of estrogen, and casomorphins (BCM7) but is a veritable petri dish of microorganisms.  In fact, they now know that the bovine leukemia virus can cause leukemia in primates.  What about mycoplasma, mycobacteria, and the myriad of pleomorphic bacteria is contains, some of which could take up to a year to culture out (e.g.  mycoplasma).  I’m working on a paper that deals with the zoonoses associated with cow’s milk.

    So…I still contend that dairy is one of the biggest culprits in Crohn’s and other chronic diseases of the lower intestine but these are likely to be more examples of “syndromes”, in which resident viruses and bacteria (including those viruses in the DNA) react to chronic insults like gluten, dairy, etc.  and other man-made components of food along with newly acquired viruses and bacteria, some of which are coming from vaccines.  (Gotta wonder about those weaponized versions of mycoplasma floating around.) Also, there is no place like the gut for secondary infections.  

    Here is the application I am wondering about: Could antibiotics help a person with osteoporosis, knowing that pleomorphic bacterial infections are showing up in other areas of “autoimmune” disease, such as rheumatoid arthritis, scleroderma, and sarcoidosis? The process appears to be the same in all cases: The residential viruses and bacteria are all involved in adaptive processes throughout the body.  They are reason for inflammation, as they react to immune challenges being brought against the cell.  Once this process escalates and the immune system crashes, the bacteria become a significant secondary problem requiring specific treatment (see www.bacteriality.com and the “miracles” that are occurring using long-term doxycycline, etc.).  

    As long as the immune system remains competent, these individuals can still be rescued by employing nutritional therapy, holistic approaches and avoidance of the obvious insults (food lectins, preservatives, pollutants, cigarettes, etc.).  Vitamin D3 therapy would be crucial here for both calcium absorption and immune competence.  But the dog, once again, may give us a clue as to which aspect of D3 is the most important in the pathogenesis of osteoporosis.  I believe that the average dog is woefully deficient in D3, with their dismally high incidence of cancer being a leading indicator.  Why wouldn’t they be low? They convert sunlight to D3 much less efficiently than humans, are covered with fur, and spend most of their time indoors.  If and when we start measuring their D3 levels, we will likely be stunned at their low levels.  And yet…they don’t suffer from clinical osteoporosis.  Is it because they don’t live long enough? Hey, they get everything else.  So again, I am wondering more and more about the immune aspects of osteoporosis in humans.

    Once the patient crosses the line and their immune system becomes incompetent (which is when many present initially), bad things happen.  They go from subclinical to clinical, from bad to much worse, or from “stage two” (“autoimmune” diseases) to “stage three” (cancer).  We know now that pleomorphic bacteria are involved in cancer, which makes perfect sense.  They were involved in the adaptive processes from the start (through their influence on the cell’s mitochondria) and play a vital role in determining when the cell (and the viruses it contains) finally decides to form a tumor to escape further insults.  This process is taking place all over the body in every tissue we have.  So…this must be happening in the ileum, where they now say 70-80% of the calcium is absorbed.

    Could antibiotics of the right type be of help when these immune incompetent individuals need rescuing, even in cases of refractory osteoporosis? Certainly, we should try to avoid their use for as long as possible but we have to be realistic sometimes in what the patient or the owner of a pet is willing to do.  Those who are into holistic medicine can avoid this last ditch effort for the longest time, even indefinitely.  But if the last ten years have done anything for me, they’ve made me a realist.  Sadly, most people want a quick fix.

    Source: 

    • Wasserman RH, Vitamin D and the Dual Processes of Intestinal Calcium Absorption,  J.  Nutr.  134:3137-3139, November 2004

     

    Article Corrected 07/01/2019 - The original article was corrected as it referenced a study linking the measles portion of the MMR vaccine with ileum damage in humans, however, this study was retracted.



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    This post is irresponsible. The author is a veterinarian who is taking an anti-vaccination stance here. The measles vaccine is not an “insult” to the body that causes osteoporosis and there is no science to support this idea. Please consider taking it down.

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  • About Me

    John B. Symes, D.V.M.

    John B. Symes, AKA “DogtorJ”, DVM is a veterinarian who has been practicing veterinary medicine for over twenty-five years.  He graduated with honors from Auburn University in 1979 and followed that with an internship at the prestigious Angell Memorial Animal Hospital in Boston.  You can read Dogtor J.'s blog.
     


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  • Related Articles

    Roy Jamron
    This article appeared in the Summer 2008 edition of Celiac.com's Scott-Free Newsletter.
    Celiac.com 06/16/2008 - Do vitamin D deficiency, gut bacteria, and timing of gluten introduction during infancy all combine to initiate the onset of celiac disease? Two recent papers raise the potential that this indeed may be the case. One paper finds that when transgenic mice expressing the human DQ8 heterodimer (a mouse model of celiac disease) are mucosally immunized with gluten co-administered with Lactobacillus casei bacteria, the mice exhibit an enhanced and increased immune response to gluten compared to the administration of gluten alone.[1] A second paper finds that vitamin D receptors expressed by intestinal epithelial cells are involved in the suppression of bacteria-induced intestinal inflammation in a study which involved use of germ-free mice and knockout mice lacking vitamin D receptors exposed to both friendly and pathogenic strains of gut bacteria.[2] Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not.
    If one considers these two papers together, one notices: (1) Certain species of gut bacteria may work in conjunction with gluten to cause an increased immune response which initiates celiac disease; (2) The presence of an adequate level of vitamin D may suppress the immune response to those same gut bacteria in such a way as to reduce or eliminate the enhanced immune response to gluten caused by those gut bacteria, thus preventing the onset of celiac disease.
    Vitamin D has recently been demonstrated to play a role in preserving the intestinal mucosal barrier. A Swedish study found children born in the summer, likely introduced to gluten during winter months with minimal sunlight, have a higher incidence of celiac disease strongly suggesting a relationship to vitamin D deficiency.[3] Recent studies found vitamin D supplementation in infancy and living in world regions with high ultraviolet B irradiance both result in a lower incidence of type 1 diabetes, an autoimmune disease closely linked to celiac disease.[4][5]
    Gut bacteria have long been suspected as having some role in the pathogenesis of celiac disease. In 2004, a study found rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated children with celiac disease, but not to the epithelium of healthy controls.[6][7] Prior to that, a paper published on Celiac.com[8] first proposed that celiac disease might be initiated by a T cell immune response to "undigested" gluten peptides found inside of pathogenic gut bacteria which have "ingested" short chains of gluten peptides resistant to breakdown. The immune system would have no way of determining that the "ingested" gluten peptides were not a part of the pathogenic bacteria and, thus, gluten would be treated as though it were a pathogenic bacteria. The new paper cited above[1] certainly gives credence to this theory.
    Celiac disease begins in infancy. Studies consistently find the incidence of celiac disease in children is the same (approximately 1%) as in adults. The incidence does not increase throughout life, meaning, celiac disease starts early in life. Further, in identical twins, one twin may get celiac disease, and the other twin may never experience celiac disease during an entire lifetime. Something other than genetics differs early on in the childhood development of the twins which initiates celiac disease. Differences in vitamin D levels and the makeup of gut bacteria in the twins offers a reasonable explanation as to why one twin gets celiac disease and the other does not. Early childhood illnesses and antibiotics could also affect vitamin D level and gut bacteria makeup. Pregnant and nursing mothers also need to maintain high levels of vitamin D for healthy babies.
    Sources:
    [1] Immunol Lett. 2008 May 22.
    Adjuvant effect of Lactobacillus casei in a mouse model of gluten sensitivity.
    D'Arienzo R, Maurano F, Luongo D, Mazzarella G, Stefanile R, Troncone R, Auricchio S, Ricca E, David C, Rossi M.
    http://dx.doi.org/10.1016/j.imlet.2008.04.006
    [2] The FASEB Journal. 2008;22:320.10. Meeting Abstracts - April 2008.
    Bacterial Regulation of Vitamin D Receptor in Intestinal Epithelial Inflammation
    Jun Sun, Anne P. Liao, Rick Y. Xia, Juan Kong, Yan Chun Li and Balfour Sartor
    http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/320.10
    [3] Vitamin D Preserves the Intestinal Mucosal Barrier
    Roy S. Jamron
    https://www.celiac.com/articles/21476/
    [4] Arch Dis Child. 2008 Jun;93(6):512-7. Epub 2008 Mar 13.
    Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis.
    Zipitis CS, Akobeng AK.
    http://adc.bmj.com/cgi/content/full/93/6/512
    [5] Diabetologia. 2008 Jun 12. [Epub ahead of print]
    The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide.
    Mohr SB, Garland CF, Gorham ED, Garland FC.
    http://www.springerlink.com/content/32jx3635884xt112/
    [6] Am J Gastroenterol. 2004 May;99(5):905-6.
    A role for bacteria in celiac disease?
    Sollid LM, Gray GM.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04158.x
    [7] Am J Gastroenterol. 2004 May;99(5):894-904.
    Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease.
    Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04157.x
    [8] Are Commensal Bacteria with a Taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease?
    Roy S. Jamron
    https://www.celiac.com/articles/779/


    Alexander R. Shikhman, MD, PhD, FACR
    Celiac.com 05/04/2018 - It has been recognized for several decades that both children and adults with celiac disease have a significantly increased frequency of osteoporosis and increased risk of fractures as compared to the age-matched non-celiac healthy individuals. Based on published data the prevalence of osteoporosis among celiac patients varies from as low as 4% to as high as 70%. The data from our clinic indicate that prevalence of osteoporosis among adults with gluten intolerance and celiac disease is in the vicinity of 30-40%.
    Characteristics and causes of osteoporosis 
    Osteoporosis is a bone disease characterized by the reduced bone mineral density and impaired bone architecture that leads to an increased risk of fracture. The three main mechanisms by which osteoporosis develop include an inadequate peak bone mass, excessive bone resorption and inadequate formation of new bone during remodeling. 
    At a given age, bone mass results from the amount of bone acquired during growth (the peak bone mass) minus the acquired bone loss due to variety of reasons including age-related processes, malabsorption syndromes, chronic steroid use etc.  The rate and magnitude of bone mass gain during the pubertal years may markedly differ from one individual to another. It has been demonstrated that pediatric onset of celiac disease and poor compliance with gluten-free diet during childhood do significantly reduce peak bone mass. 
    One of the main causes of osteoporosis is an alteration in bone remodeling due to imbalance between bone formation and resorption, with a predominance of resorption resulting in a reduction in bone mass and increased risk of fractures. Formation of the new bone is facilitated by specialized cells, osteoblasts, which actively synthesize bone matrix. Bone resorption is mediated by other specialized cells, osteoclasts.
    One of the main regulators of bone remodeling is the RANK/RANKL/OPG system. During bone remodeling, bone marrow cells and osteoblasts produce RANKL(receptor activator for nuclear factor kB ligand), which bonds with a transmembrane receptor of the osteoclast precursor, RANK(receptor activator of nuclear factor kB), causing their differentiation and activation. Osteoprotegerin (OPG) binds to RANKL before it has an opportunity to bind to RANK, and hence suppresses its ability to increase bone resorption.
    Normal bone remodeling is based on the permanent renovation of the skeleton and consists of an initial phase of bone resorption followed by a phase of formation, both of which are regulated by general (endocrine) factors and local (paracrine) factors. The main endocrine factors include parathyroid hormone [PTH] and vitamin D as well as estrogens and, to a lesser extent, testosterone, thyroid hormones, growth hormone and leptin. Local factors include various cytokines (IL-1, IL-6 and TNF-a playing a role) key growth factors that regulate the process.
    There are several well-characterized risk factors which contribute to the development of osteoporosis in celiac patients. These include:
    1. Malabsorption of vitamin D and secondary hyperparathyroidism
    Villous atrophy in celiac patients reduces the active absorption surface and induces steatorrhea (exces fat in feces), which has a chelating effect on calcium and vitamin D, making their absorption difficult. This reduces levels of the vitamin D transporting protein (calbindin and calciumbinding protein) and increases PTH synthesis which, in turn, lead to increased bone resorption causing osteoporosis.
    2. Malabsorption of vitamin K
    Malabsorption of fat soluble vitamins including vitamin K is a common finding in celiac patients. Three vitamin-K dependent proteins have been isolated in the bone: osteocalcin, matrix Gla protein (MGP), and protein S. 
    Osteocalcin is a protein synthesized by osteoblasts. The synthesis of osteocalcin by osteoblasts is regulated by the active form of vitamin D—1,25-dihydroxy-cholecalciferol. The mineral-binding capacity of osteocalcin requires vitamin K-dependent gamma-carboxylation of three glutamic acid residues. 
    MGP has been found in bone, cartilage, and soft tissue, including blood vessels. The results of animal studies suggest MGP facilitates normal bone growth and development. 
    The vitamin K-dependent anticoagulant protein S is also synthesized by osteoblasts, but its role in bone metabolism is unclear. Children with inherited protein S deficiency suffer complications related to increased blood clotting as well as decreased bone density.
    The data on the role of vitamin K in osteoporosis came from the clinical observations indicating that a chronic use of vitamin K antagonists such as warfarin increases risk of vertebral and rib fractures. Accordingly, vitamin K supplementation significantly lowers risk of vertebral and hip fractures. 
    3. Magnesium deficiency
    Magnesium deficiency may be an additional risk factor for celiac-associated osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium. Several human studies have suggested that magnesium supplementation may improve bone mineral density. Magnesium deficiency is easily detected with laboratory tests (eg, low serum magnesium, low serum calcium, resistance to vitamin D) or clinical symptoms (eg, muscle twitching, muscle cramps, high blood pressure, irregular heartbeat). Screening for magnesium deficiency should be routinely included in the screening of celiac patients with osteoporosis.
    4. Chronic diarrhea and metabolic acidosis
    Chronic diarrhea in patients with celiac disease results in significant bicarbonate losses and development of metabolic acidosis. Bone is a major site for the extracellular buffering of the retained acid. Therefore, one of the main compensatory mechanisms maintaining a stable serum bicarbonate level in the face of an uncorrected metabolic acidosis is the dissolution of bone buffers and net efflux of calcium from bone. Bicarbonate supplementation in patients with metabolic acidosis decreases urinary calcium, phosphorus and hydroxyproline wasting supporting the concept of negative effects of acidosis on bone health.
    5. Hypogonadism
    Decline of estrogen production and activity is one of the main events in the development of age-related osteoporosis. It is well known that estrogen deficiency is important in the pathogenesis of osteoporosis not only in women but also in men. Increase in bone mineral density in young men and declines in older men are related to circulating free estrogen, not testosterone. In general, patients with celiac disease are characterized by low levels of circulating estrogens which contributes to the development of premature osteoporosis. 
    6. Chronic use of Proton Pump Inhibitors 
    Proton pump inhibitors (PPIs) are one of the most widely used classes of drugs. The commonly used PPIs include such drugs as Omeprazole (brand name: Prilosec), Lansoprazole (brand name: Prevacid), Dexlansoprazole (brand names: Kapidex, Dexilant), Esomeprazole (brand name: Nexium), Pantoprazole (brand name: Protonix) and Rabeprazole (brand name: AcipHex). Chronic use of PPIs for gastroesophageal reflux disease and other related conditions has been associated with impaired calcium and magnesium absorption and increased risk of vertebral and nonvertebral fractures. 
    7. Chronic use of Selective Serotonin Reuptake Inhibitors 
    Selective Serotonin Reuptake Inhibitors (SSRIs) are frequently used in celiac patients for treatment of depressive disorders. The commonly used SSRIs include such drugs as Citalopram (brand name: Celexa), Escitalopram (brand name: Lexapro), fluoxetine (brand name: Prozac), fluvoxamine (brand name: Luvox), Paroxetine (brand name: Paxil) and Sertraline (brand name: Zoloft). It has been demonstrated that SSRIs increase extracellular 5-HT (5-Hydroxytryptophan) levels that have deleterious skeletal effects. The skeletal serotonergic system consists of 5-HT receptors and the 5-HT transporter (5-HTT) in osteoblasts and osteocytes. 5-HTT is a transmembrane protein targeted by SSRIs. 5-HT restrains osteoblastic activity, thus leading to bone loss. 
    8. Autoimmune mechanisms
    Autoimmune mechanisms have been long suspected as risk factors contributing to development of osteoporosis in celiac patients. Near a decade ago, it was demonstrated that sera from celiac patients with osteoporosis contains significantly high titers of antibodies against bones as compared to non-celiac osteoporotic patients. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. Recently, it has been described that a subset of patients with celiac disease has autoantibodies to osteoprotegerin, which block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-kappaB (RANK), and are associated with severe osteoporosis and high bone turnover. 
    9. Chronic inflammation
    Chronic inflammatory diseases, including celiac disease, are associated with overproduction of proinflammatory cytokines such as TNF-a, interleukin(IL)-1, IL-6, IL-11, IL-15 and IL-17 among others which activate osteoclasts and accelerate bone resorption leading to osteoporosis.
    In conclusion, osteoporosis associated with celiac disease is not a coincidental problem. It is a consequence of disease-specific (autoantibodies to osteoprotegerin), disease-nonspecific (malabsorption of vitamin D, K and magnesium, hypogonadism, chronic inflammation, chronic diarrhea and metabolic acidosis) and jatrogenic (overuse of PPIs and SSRIs) events accelerating resorptive processes in the skeleton. Correction of the aforementioned risk factors in celiac patients can reverse the development of osteoporosis and reduce the risk of osteoporosis-associated fractures.
    Bibliography:
    Bab I, Yirmiya R. Depression, selective serotonin reuptake inhibitors, and osteoporosis. Curr Osteoporos Rep. 2010 Dec;8(4):185-91. Bianchi ML. Inflammatory bowel diseases, celiac disease, and bone. Arch Biochem Biophys. 2010 Nov 1;503(1):54-65. Ito T, Jensen RT.  Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium. Curr Gastroenterol Rep. 2010 Dec;12(6):448-57. Katz S, Weinerman S.  Osteoporosis and gastrointestinal disease. Gastroenterol Hepatol (N Y). 2010 Aug;6(8):506-17. Riches PL, McRorie E, Fraser WD, Determann C, van't Hof R, Ralston SH. Osteoporosis associated with neutralizing autoantibodies against osteoprotegerin. N Engl J Med. 2009 Oct 8;361(15):1459-65. Stazi AV, Trecca A, Trinti B.  Osteoporosis in celiac disease and in endocrine and reproductive disorders. World J Gastroenterol. 2008 Jan 28;14(4):498-505. Sugai E, Cherñavsky A, Pedreira S, Smecuol E, Vazquez H, Niveloni S, Mazure R, Mauriro E, Rabinovich GA, Bai JC.  Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis. J Clin Immunol. 2002 Nov;22(6):353-62. Turner J, Pellerin G, Mager D.  Prevalence of metabolic bone disease in children with celiac disease is independent of symptoms at diagnosis. J Pediatr Gastroenterol Nutr. 2009 Nov;49(5):589-93. Vasquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, Niveloni S, Smecuol E, Mauriño E, Bai JC. Risk of fractures in celiac disease patients: a cross-sectional, case-control study. Am J Gastroenterol. 2000 Jan;95(1):183-9.
     


    Jefferson Adams
    Celiac.com 08/16/2018 - What is the significance of vitamin D serum levels in adult celiac patients? A pair of researchers recently set out to assess the value and significance of 25(OH) and 1,25(OH) vitamin D serum levels in adult celiac patients through a comprehensive review of medical literature.
    Researchers included F Zingone and C Ciacci are affiliated with the Gastroenterology Unit, Department of Surgery, Oncology and Gastroenterology, University of Padua, Padua, Italy; and the Celiac Center, AOU San Giovanni di Dio e Ruggi di Aragona, University of Salerno, Department of Medicine and Surgery, Salerno, Italy. 
    Within the wide spectrum of symptoms and alteration of systems that characterizes celiac disease, several studies indicate a low-level of vitamin D, therefore recent guidelines suggest its evaluation at the time of diagnosis. This review examines the data from existing studies in which vitamin D has been assessed in celiac patients. 
    Our review indicates that most of the studies on vitamin D in adult celiac disease report a 25 (OH) vitamin D deficiency at diagnosis that disappears when the patient goes on a gluten-free diet, independently of any supplementation. Instead, the researchers found that levels of calcitriol, the active 1,25 (OH) form of vitamin D, fell within the normal range at the time of celiac diagnosis. 
    Basically, their study strongly suggests that people with celiac disease can recover normal vitamin D levels through a gluten-free diet, without requiring any supplementation.
    Source:
    Dig Liver Dis. 2018 Aug;50(8):757-760. doi: 10.1016/j.dld.2018.04.005. Epub 2018 Apr 13.  


    Jefferson Adams
    Celiac.com 08/28/2018 - There have been a number of studies that tried to estimate risk levels for celiac disease in patients with osteoporosis, but the data has been highly variable and inconclusive. To address this, a team of researchers recently set out to investigate rates of celiac disease among individuals with osteoporosis.
    The research team included M. Laszkowska, S. Mahadev, J. Sundström, B. Lebwohl, P. H. R. Green, K. Michaelsson, and J. F. Ludvigsson. They are variously affiliated with the Department of Medicine, Celiac Disease Center, Columbia University College of Physicians and Surgeons, New York, NY, USA, the Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University in Uppsala, Sweden, the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet in Stockholm, Sweden, the Department of Paediatrics, Örebro University Hospital in Örebro, Sweden, and with the Division of Epidemiology and Public Health, School of Medicine, University of Nottingham in Nottingham, UK. 
    The team conducted a systematic review of articles that appeared in PubMed, Medline or EMBASE through May 2017 to find studies on rates of celiac disease in patients with osteoporosis. Search terms included “coeliac disease” combined with “fractures”, “bone disease”, “bone density”, “densitometry”, “osteoporos*”, “osteomal*”, “osteodys” or “dexa” or “dxa” or “skelet”. Non‐English papers with English‐language abstracts were included. 
    To confirm their data, the team used fixed‐effects inverse variance‐weighted models, and tested heterogeneity through both subgroup analysis and meta‐regression. They found a total of eight relevant studies, containing data from 3,188 people with osteoporosis. From this group, the team found 59 individuals, or just under 2%, with celiac disease.
    A weighted pooled analysis showed biopsy‐confirmed celiac disease in 1.6% of osteoporosis patients. 
    The team found moderate heterogeneity (I2 = 40.1%), which was influenced by the underlying celiac disease rates in the general population. After adding four studies covering a total of 814 people with celiac disease, based on positive tissue transglutaminase or endomysial antibodies, the pooled rate was comparable (1.6%; 95% CI = 1.2%‐2.0%).
    About 1.6% of people with osteoporosis have biopsy‐verified celiac disease. That’s about the same rate as the general population. Based on this data, the team sees no need to routinely screen osteoporosis patients for celiac disease, contrary to current guidelines. They suggest additional studies to assess the benefits and desirability of such screening programs.
    So, it looks like there’s no reason for people with osteoporosis, or their doctors, to be concerned about celiac disease unless patients shows some physical symptoms or signs.
    Read more in: Alimentary Pharmacology & Therapeutics


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