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Found 7 results

  1. Celiac.com 05/10/2018 - Most people who suffer from inflammatory bowel diseases (IBD) have either Crohn’s disease or ulcerative colitis. Some research has suggested that patients with Crohn's disease have an altered response to vitamin D, among other issues. The exact mechanism behind this is not well understood. To get a better picture of the problem, a team of researchers recently set out to investigate disease-specific gene expression profiles of peripheral blood mononuclear cells (PBMCs) from Crohn’s disease patients in clinical remission. The research team included Holger Schäffler, Maria Rohde, Sarah Rohde, Astrid Huth, Nicole Gittel, Hannes Hollborn, Dirk Koczan, Änne Glass, Georg Lamprecht, and Robert Jaster, with the Department of Medicine II, Division of Gastroenterology, Rostock University Medical Center in Rostock, Germany. The team began by genotyping patients with Crohn's disease in clinical remission or with very low disease activity according to nucleotide-binding oligomerization domain 2 (NOD2), and PBMCs from wild-type (WT)-NOD2 patients, and patients with homozygous or heterozygous NOD2 mutations. Meanwhile the team isolated healthy donors for further analysis. The team then cultured the cells with vitamin D, peptidoglycan (PGN) and lipopolysaccharide (LPS) for defined periods of time before RNA was isolated and subjected to microarray analysis using Clariom S assays and quantitative real-time PCR. They assessed the NOD2- and disease-specific gene expression profiles with repeated measure ANOVA using a general linear model. The team used microarray assays to find 267 genes that were significantly up- or downregulated in PBMCs of WT-NOD2 patients, compared to healthy donors after challenge with vitamin D and/or a combination of LPS and PGN (P < 0.05; threshold: ≥ 2-fold change). For further analysis by real-time PCR, the team selected genes with known impact on inflammation and immunity that fulfilled predefined expression criteria. In a larger group of patients and controls, the team found a disease-associated expression pattern, with higher transcript levels in vitamin D-treated PBMCs from patients, in three of these genes, CLEC5A (P < 0.030), lysozyme (LYZ; P < 0.047) and TREM1 (P < 0.023). The team found six genes that were expressed in a NOD2-dependent manner (Crohn's disease101, P < 0.002; CLEC5A, P < 0.020; CXCL5, P < 0.009; IL-24, P < 0.044; ITGB2, P < 0.041; LYZ, P < 0.042). Interestingly, the team saw the highest transcript levels in patients with heterozygous NOD2 mutations. This study identifies CLEC5A and LYZ as Crohn's disease- and NOD2-associated genes of PBMCs and supports the need for further studies on their pathomechanistic roles. The team found that PBMCs of patients with Crohn's disease display alterations in their response to vitamin D and PAMPs. Disease-associated and NOD2-dependent gene expression profiles are preserved even during clinical remission. The team’s data identifies CLEC5A, LYZ and TREM1 as good candidates for follow-up study. The researchers propose that these genes may act in a common network relevant to celiac disease development. The research team remains committed to the longterm goal of biomarkers to that will accurately predict the clinical course of celiac disease. Source: World J Gastroenterol. 2018 Mar 21; 24(11): 1196–1205. doi: 10.3748/wjg.v24.i11.1196
  2. 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.
  3. Well...after almost two years of just reading the forums, I'm at my wit's end and, making my first post. I'll try to keep this part brief: April of 2011, husband's.celiac diagnosed. Our two daughters blood tested in June of 2011. Like a greek tragedy...one daughter positive, other daughter negative. Daughter with positive blood test was 15 at the time. She was tested by her general practioner, who advised that with father's diagnosis and numbers in her blood work off the charts,(not sure of number but I seem to remember hearing 134), endoscopy was a moot point. She made diagnosis, advised that she join her father on a gluten-free diet, and said she could refer a GI if we wanted. at the same time daughter is diagnosed with scoliosis. So...August of 2011 daugter sees pediatric GI doc. She would advise endoscopy, but agrees with GP that diagnosis is most probably correct. Orders additional bloodwork, and dexa scan (beause of scoliosis daignosis). Test comes back with vitamin D deficiency, calcium deficciency and osteopenia. I should probably throw in here that daughter started gluten-free diet the day she got the results of bloodwork in June. Also she and her dad had little if any symptoms before diagnosis. She has next blood work January of 2012. TTg now 18, other numbers coming down Ped.GI says were doing good keep up the good work. Adds omeprazole for her reflux. Has her taking vitamin d and calcium. May of 2012 both daughters end up with Mononucleosis. but amazingly recover pretty quickly. August 2012, daughter has more bloodwork. Vitamin D normal, TTg now up to 80! Says take multi vitamin, work harder on gluten-free diet, preventing CC etc. Even though we were not a gluten-free household, in August our other daughter left for college, and now there is only VERY LIMITED food containing gluten in the house, and I handle it really carefully. Have separate frying pans, toasters, etc. I work really hard to keep my celiacs safe. So...in January she has another round of bloodwork. This time I'm sure we will see TTg numbers back in the 18 range. Results come back...70!!. Vitamin D at 17. Ped GI nurse calls with results and advises 50,000 i.u. of vitamin D for 8-12 weeks, then retest. Asks if I want to see dietician again. I declined. Nurse calls back two days later and says they want her bloodwork and another dexa scan redone in April, and suggests thaT she may have ssecondary Auto-Immune disease or...Refractory Celiac Sprue. Well that scares the heck out of me,and Ive been searchng ever since for any cases of teenagers with little symptoms of celiac having refractory celiac sprue, and can find nothing. So finally I get to my question... Can a celiac be gluten free and the TTg numbers stay abnormlly high? My daughter has handled this diagnosis and her scoliosis with grace, and I'm really proud of how she's facing it as a teenager. I just can't imagine how she will deal with an additional diagnosis. Her general health is really quite good and the scoliosis hasn't changed. It's hard to comprehend that she could be developing Hashi's or Diabetes or Refratory Celiac Sprue when she seems as healthy as her non-celiac sister. I'm soooo discouraged any ideas will be appreciated So much for being brief
  4. Five months ago I developed symptoms. I felt a tired, low energy, and in the head not feeling all there. A slight sore throat coming on, the feeling you get when you're *about* to get sick. Problem was, I never really got sick (no cough, no runny nose, no fever) and this "almost sickly / tired / foggy feeling continued." For days. Weeks. Months. I went to the doctor. Tests came back normal for things like thyroid checks, vitamin B12, mono, Epstein-Barr, etc. The only thing was my Vitamin D that was insufficient at 23 (30 is normal). I took Vitamin D pills and now my level is 36. The symptoms continue. Some are less and others are more, but the overall feeling is definitely still there. Over the weeks of taking the pills, I'd feel better for a few days, then worse for a few days. Rinse, repeat. The primary symptom during this whole time is what I call brain fog. I see the term thrown around and I don't know if it's the same as what other people say it is but generally I use brain fog because it feels like my experience is clouded in my head. Like having a layer of cloud in your brain fogging things up. Physically it feels almost like a headache, but not quite. It feels almost like being dizzy, but not quite. It feels like tiredness and extreme exhaustion, but that has lessened in recent months and it feels more like a headache. Sleep doesn't change it. There are no noticeable patterns. Even when it's not severe, I feel like it's "always there," my head never feels fully clear. Seems to come in waves. I might go 3-5 days without a severe episode, then it is severe for 3-5 days. Or it might show up in the middle of a day and continue for the rest of that day. Some symptoms came and went: most notably temperature extremes: night sweats, or feeling very cold and shivering. These were quick episodes and stopped after the first month. They happened maybe less than 5 or 8 times. Maybe it's unrelated. The sore throat died down in recent weeks. But I do consistently get cold extremities, which I never used to get. And dry lips, which I also rarely got and only in the winter. And new symptoms appeared in the first month: weakness / feeling of internal 'wobbliness' in my muscles, particularly in my thighs. Not 24/7 but sometimes, kind of like the cycles from before. It wasn't involuntary movement. But I definitely could feel weakness / wobbliness. This has died down in recent weeks. One night I felt tingling on my hands, but that symptom never returned. MRI results are normal. With the exception of something my neurologist described as something about the white matter that is part of normal aging (I'm in my mid-30s), but can appear in people with migraine headaches. I think I will talk with him again to discuss this further because I do not really understand it, but he assured me the MRI was normal. I felt the 'brain fog' prior to and while getting the MRI (symptoms at medium severity). So here I am today, feeling about the same with brain fog / headaches and pretty much always feeling like something's a bit off, like feeling cloudy. I can still do things, exercise, run, go out with friends. But the brain fog / headaches sometimes really kick in sometimes, it seems like in phases. Then I read about gluten sensitivity. I see symptoms like 'brain fog' and headaches and wonder if it might be related. I do think at times after eating heavy meals the fogginess / extreme tiredness came on. But there are days where I eat gluten in cereal and I don't notice an increase in symptoms. Like I said before it comes in waves. 3 days at a time or half a day or 2 days. It's not like after every meal 30 minutes later I feel it then it goes away. But perhaps it's related to *how much* gluten I eat.. My doctor said he does not think it is a gluten issue, but that I can try going gluten free for a few weeks to see if symptoms improve. I'm currently tracking my symptoms and food intake to see if there's a pattern. So I'm just wondering if anyone else here experiences these symptoms and if you think it might be a gluten issue. Thank you for reading.
  5. Hi Everyone, I'm new to the forum. I've been gluten free since 10/26/2013 and am still struggling. I have confirmed celiac's disease from both blood work and biopsies taken during an endoscopy. I didn't have much help in the beginning besides to just stop eating gluten. I did that immediately with no issues and I am not getting cross contamination. It is not in my house. I did replace all necessary kitchen items.. collanders, toaster, etc. Got new butter, jams, etc. I don't lick envelopes and it is not in my toothpaste, lipstick so on and so forth. I'm struggling. Some symptoms have gotten worse. I am still ill in the bathroom every morning. I feel internal inflammation all the time. I'm waiting for appointments with rheumatology (later in March) and endocrinology (beginning of April) because of various symptoms. A neurologist is also working on ruling out MS. I cut out dairy last month (not in the beginning/was told it was not necessary) and now I've pretty much cut out everything else (rice, potato, soy) because I'm desperate to feel better. I've been eating plain fruit, veggies, meat - no seasonings/sauce. Chicken broth. Coffee (yes, it is gluten free) once in the morning and green tea or chamomile. Because of my vitamin D level and ferritin level I am taking the following each day Calcium w vitamin D3 twice a day, a multi vitamin, iron, b-12. Also on 20mg of omeprazole every morning because of my esophagus. I also drink Kefir probiotic smoothie twice a day. (Could that maybe be making me worse?! Just a thought that came to me today) Along with celiac's disease so far I've been diagnosed with Barrett's Esophagus and was told I have osteomalacia. I could share the lifetime of issues (migraines, miscarriages, difficult menstrual cycles, etc, etc) that now seem eye opening but the above are the basics. Should I really still be struggling so much? This has been so difficult. I wish a doctor could tell me that I'm going to be okay. Thank you for any responses that come my way. Looking forward to getting to know you. ~Julie edited to add more: my Celiac diagnosis came after a very long year of many, many doctor appts. I lost 38lbs from Feb until diagnosis, I would fall for no reason, I have neuropathy, terrible periods, mood swings near period and ovulation, not sleeping well, night sweats, anemia, difficulty with things I was able to do before, completely beat all the time, skin issues (don't have DH), joint, muscle, vein issues... I started going to the doctor religiously in the fall of 2012 and by the beginning of Oct 2013 still did not have a diagnosis besides to reduce stress and take care of myself.
  6. Hi! I've been diagnosed for a long time and its well controlled. The last 3.5 years I've been pregnant and/or breastfeeding, 2 c-sections and my body is struggling a little. I'm having trouble with vitamin D levels, my new doctor (like my old doctor) just keep telling me to take 1000iu of vitamin D, but I already do plus good food, however my numbers are about 20 and I want them much higher, especially as my 10 month old still nurses regularly and isn't eating a huge amount yet. Anyone know more about what sort if levels I can take? Thank you!
  7. Hi! I have just joined this forum and it looks great! I have been diagnosed with Celiac for many years and been fairly gluten free since I was a kid. Last Sept I had baby 2 (mid 30s) and as I did with baby 1 struggled with knee pain post partum. I saw my doctor and requested a vitamin D blood test and was low, I went on prescription vitamin Ds and it improved. I retested and was over the minimum amount(35), so she is not concerned (although I am breastfeeding and I have read it should be higher (50)). I am now taking vitamin D and calcium supplements, eating a great diet and still have the following main symptoms: one knee needs cracking often (hurts if I don't), worse in morning. toes hurt a lot in the morning, I need to stretch them/move them for a couple of minutes before trying to walk. groins sometimes fill awkward, every now and then one side will slightly fail me and I nearly fall (not badly just need to readjust). Does anyone know how quickly vitamin D levels can drop again, how often I should get tested? Anything else I should get tested for? My doctor did say it is unlikely to be arthritis at my age, but there is no point testing at this stage anyway as I am breastfeeding and that would involve xrays and then nothing could be done anyway. I used to live in Australia and bone density tests were done every second year on celiacs, my doctor said here it is not done, just calcium blood tests. I do know my bones were slightly fragile (at 30 they looked more like those over a 40 year old) however I haven't had any broken bones or other issues. After writing this, my feeling is I need to find a doctor who knows more about Celiac also! Thank you!