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Showing results for tags 'severe'.
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Celiac.com 04/18/2022 - Several observational studies have indicated that celiac disease patients do not have higher susceptibility of COVID-19 and the risk of severe COVID-19. However, the the conclusions of such studies can be distorted by reverse causation and confounding, especially for newly-emerged diseases, such as COVID-19. A team of researchers recently set out to further clarify the picture using both observational and Mendelian Randomization analysis. The research team included Jiuling Li, Aowen Tian, Dandan Yang, Miaoran Zhang, Lanlan Chen, Jianping Wen, and Peng Chen. For their observational study, the team used data from the UK Biobank cohort. They conducted both univariate and multivariate logistic regression analysis to identify the risk factors for both COVID-19 susceptibility and severe COVID-19. They also conducted a two-sample Mendelian Randomization analysis to delineate causality between celiac disease and COVID-19 susceptibility and severe COVID-19. The good news is that the team's UK Biobank data revealed that celiac disease patients had a slightly lower overall susceptibility to COVID-19, and that celiac patients did not have higher rates of severe COVID-19. Meanwhile, the Mendelian Randomization study showed that celiac patients had lower susceptibility to both COVID-19 and fewer cases of severe COVID-19, although the lower COVID-19 susceptibility is seen in only in the UK Biobank cohort. These results indicate that people with celiac disease do not face higher risk of getting COVID-19, or of developing severe COVID, than the non-celiac population, and they likely do not need to take any extra COVID-19 precautions. Read more in Clin Transl Gastroenterology The researchers in this study are variously affiliated with the Department of Pathology, College of Basic Medical Sciences, Jilin University in Changchun, Jilin, China; the Experimental Center of Pathogenobiology, Immunology, Cytobiology and Genetics, College of Basic Medical Sciences, Jilin University in Changchun, Jilin, China; the Clinical Medicine of Jilin University in Changchun, Jilin, China; and the Department of Genetics, College of Basic Medical Sciences, Jilin University in Changchun, Jilin, China. -
I have been a diagnosed Celiac for 6 years now. The moment I was diagnosed I have lead a strict gluten free life, I wasn't taking any chances and wanted to feel better. Over the past 6 years I have never intentionally eaten gluten, but there have been times that I have had cross contamination, especially eating out. Yesterday was quite an experience and I've learned from it and upon trying to research it I found nothing....I'm hoping I'm not the only one, although I wouldn't wish this on anyone. About a year ago I found a Chinese restaurant that had an owner who's claim to fame was she had found ways to make just about everything on the menu gluten free. Gluten free Chinese food? Yes please!! I ate there 4 times with no reaction....ahh, life is complete!....until yesterday. I ordered the gluten free potstickers and sweet and sour prawns. About 2 hours later I started feeling really nauseous. The first thing I thought was maybe I got cross contaminated. Then within the hour I told my friend that I needed to go to the emergency room. I had SEVERE middle back pain and upper stomach pain. I was dizzy, extremely nauseous and my lips were burning and tingling. By the time we pulled up to the emergency room I couldn't stop throwing up....it was bad. And the pain was so intense I was told I was whimpering. They got me in right away and started me on an iv and gave me toradol for the pain and zofran for the vomiting. The doctor wanted to do blood work and an ultrasound because he was concerned it was my gallbladder. Well, everything was fine and it was the gluten, although they couldn't test or confirm it. It is day 2 and my lips are still tingly and I still have quite a bit of pain and nausea. I'm extremely tired and weak. I was looking online for people that have had the same or similar reaction and found nothing....am I the only one? Some things I know have helped me and hopefully they can help others....if you've been cross contaminated or "glutenized" as I call it....chew a handful of vitamin c chewables, it helps. Drink LOTS of water. Stick to a bland diet and NO caffeine for a few days to let your stomach heal. Heating pads help and get lots of rest. And there is an amazing product called GI Response, you can buy it on Amazon. It's expensive but you will thank me later. I don't know how long it will take to feel back to "normal", but I have sworn off eating out....I'd swear off eating if I could. Being gluten free sucks. But that's what we've been dealt and so we must deal with it the best we can. I hope that I've helped at least one person.....and if you are unfortunate enough to have the same reaction to gluten as me....know that you aren't alone. -
So I was diagnosed with " Severe Celiacs disease " last year, but I was told nothing was seen in biopsy and I haven't done blood work yet, the only thing that indicated Celiacs was the damage done to my villi.... before I was diagnosed I was very sick I couldn't eat at all, like throwing up, diarrhea, chest pain, neurological problems and headaches, thought I had cancer. Ok skip forward, I've been on this gluten free diet since November of last year and decided to go ahead and cheat my diet, well I've been eating nothing but gluten for over a week and wasn't getting sick but now I'm starting to get chest pain, weird headaches and a little bit of an upset stomach... Is it possible I wasn't getting sick because I'm now I silent celiac even tho before symptoms were obvious, or could I have been misdiagnosed? Still haven't done blood work and nothing was in the biopsy, However my villi is damaged severely, is more positive I'm sensitive to gluten and the damage of the villi is caused by something else? Please help me, I'm so frustrated with my body because of all this and even more frustrated I wasn't getting sick before but now I think I am.
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Celiac diagnosed in 1992. Ate Domino's gluten free pizza (1 small slice every evening for 2 weeks) Experiencing severe bone pain similar to pre-diagnosis. Wondering how long it will last. Anyone else have this following gluten exposure? DebLee
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Celiac.com 09/15/2016 - Some doctors and clinicians have reported cases of severe sprue-like enteropathy associated with olmesartan, but, until now, no clear demonstration of an increased risk has been documented by epidemiological studies. Now, a French nationwide observational cohort study has shown a connection between severe intestinal malabsorption and the drug olmesartan, according to results presented by a team of researchers. Olmesartan is an angiotensin II receptor antagonist which has been used for the treatment of high blood pressure. Olmesartan is also sold commercially under the name Benicar. The research team included Mickael Basson, Myriam Mezzarobba, Alain Weill, Philippe Ricordeau, Hubert Allemand, Francois Alla, and Franck Carbonnel. They are variously affiliated with the French National Health Insurance Fund, Paris, France, and the Université Paris-Sud, Assistance Publique-Hôpitaux de Paris and Gastroenterology unit, Hôpitaux Universitaires Paris Sud, Le Kremlin Bicêtre, France. The team set out to assess, in a nationwide patient cohort, the risk of hospitalization for intestinal malabsorption associated with olmesartan compared with other angiotensin receptor blockers (ARB) and ACE inhibitors (ACEIs). From the French National Health Insurance claim database, they included all adult patients initiating ARB or ACEI between 1 January 2007 and 31 December 2012, with no prior hospitalization for intestinal malabsorption, no serology testing for celiac disease, and no prescription for a gluten-free diet product. Their main endpoint was incidence of hospitalization with a discharge diagnosis of intestinal malabsorption. The team included 4,546,680 patients, for a total of 9,010,303 person-years, and observed 218 events. Compared with ACEI, the adjusted rate ratio of hospitalization with a discharge diagnosis of intestinal malabsorption was 2.49 (95% CI 1.73 to 3.57, p Average length of hospital stay for intestinal malabsorption was longer in the olmesartan group than in the other groups (p=0.02). Compared with ACEI, the adjusted rate ratio of hospitalization for celiac disease was 4.39 (95% CI 2.77 to 6.96, p<0.0001). These results show that olmesartan is assoc qiated with higher rates of hospitalization for intestinal malabsorption and celiac disease. Source: Gut. doi:10.1136/gutjnl-2015-309690 -
Celiac.com 06/17/2015 - Refractory celiac disease type II (RCDII) and EATL (Enteropathy Associated T-cell Lymphoma) are pre-malignant complications of celiac disease. However, there is scant medical literature and data what role malnutrition and intestinal absorption may play in these conditions. With this in mind, a team of researchers set out to conduct a comprehensive assessment of nutritional status and intestinal absorption capacity of patients with RCDII and EATL, and to compare that with data of newly diagnosed celiac disease patients. The research team included N.J. Wierdsma, P. Nijeboer, M.A. de van der Schueren, M. Berkenpas, A.A. van Bodegraven, and C.J. Mulder. They are affiliated with the Department of Nutrition and Dietetics, the Department of Gastroenterology, the Celiac Centre Amsterdam, the Department of Nutrition and Dietetics at VU University Medical Centre in Amsterdam, The Netherlands; and with the Department of Internal Medicine, Gastroenterology and Geriatrics at ATRIUM-ORBIS Medical Centre, Sittard, The Netherlands. They conducted an observational study in tertiary care setting in for 24 RCDII patients, averaging 63.8 ± 8.2 years of age, 25 EATL patients averaging 62.3 ± 5.7 years of age, and 43 celiac disease patients averaging 45.6 ± 14.8 years of age. At diagnosis, the team evaluated anthropometry (BMI, unintentional weight loss, fat-free mass index (FFMI), handgrip strength (HGS), nutritional intake, fecal losses and Resting Energy Expenditure (REE)). They found low BMI (<18.5) more often in RCDII patients than in celiac disease or EATL patients (in 33%, 12% and 12%, respectively, p = 0.029). Also, 58% of EATL patients had unintentional weight loss greater than 10% of total weight, compared to 19% of celiac disease patients, and 39% for RCDII patients (p = 0.005/0.082). The team found energy malabsorption (below 85%) in 44% of RCDII patients, and in 33% of EATL patients, compared with 21.6% in celiac disease (NS). Fecal energy losses were higher in RCDII than in celiac disease patients (589 ± 451 vs 277 ± 137 kcal/d, p = 0.017). REE was lower than predicted, with reulst greater than 10% in 60% of RCDII, 89% of EATL, and 38% of celiac disease patients (p = 0.006). Between one third and two thirds of all patients showed Low FFMI and HGS. Patients with RCDII and EATL show far worse nutritional profiles than untreated naïve celiac disease patients at presentation. This malnutrition is at least partly due to malabsorption as well as hypermetabolism. This study shows the importance of proper diagnosis, and of nutrition in the treatment of these conditions. Source: Clin Nutr. 2015 Apr 30. pii: S0261-5614(15)00124-7. doi: 10.1016/j.clnu.2015.04.014.
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Neurology 2001;56:385-388. Celiac.com 02/15/2001 - According to a new study published in the February issue of Neurology, severe, chronic migraine headaches can be triggered in gluten-sensitive individuals who do not exclude gluten from their diets. The study examined ten patients who had a long history of chronic headaches that had recently worsened, or were resistant to treatment. Some patients had additional symptoms such as lack of balance. Dr. Marios Hadjivassiliou, from the Royal Hallamshire Hospital in Sheffield, UK, and colleagues tested each patient and found that all were sensitive to gluten. . The patients were tested and each was found to be gluten-sensitive. Additionally, MRI scans determined that each had inflammation in their central nervous systems caused by gluten-sensitivity. Results: Nine out of 10 patients went on a gluten-free diet, and seven of them stopped having headaches completely. The patients heightened immune responses, which are triggered by the ingestion of gluten, could be one of the factors causing the headaches. The other two patients who were on a gluten-free diet experienced significant relief, but not complete relief. Conclusion: According to Dr. Hadjivassiliou, removal of the trigger factor by the introduction of a gluten-free diet may be a promising therapeutic intervention for patients with chronic headaches. Further studies are needed to confirm Dr. Hadjivassilious preliminary findings. -
Celiac.com 01/27/2014 - A team of physicians presents the case of a patient who experienced remission of severe aphthous stomatitis of celiac disease with etanercept. The team included Adey Hasan, Hiren Patel, Hana Saleh, George Youngberg, John Litchfield, and Guha Krishnaswamy. They are variously affiliated with the The Department of Internal Medicine, the Division of Allergy, Asthma and Immunology, and the James H. Quillen VA Medical Center at East Tennessee State University in Johnson City, TN, and with the Departments of Medicine and Pathology at Quillen College of Medicine in Johnson City, TN. The team presents a patient with celiac disease complicated by severe aphthous stomatitis that impairs swallowing, chewing and speaking, which have triggered weight loss, psychosocial problems, and impaired her work performance. The woman tried a variety of topical and systemic medications symptoms, but saw little or no improvement in her symptoms. She consented to treatment with etanercept, and experienced complete remission of aphthous stomatitis, decrease in arthralgia and fatigue and considerable improvement in her quality of life. The team points out that newer biological agents, such as etanercept, might be useful in treating certain celiac disease complications, and may even help to improve patient morbidity. They are calling for further study to determine long-term efficacy and safety of these drugs in the mucosal and/or systemic complications of this disease. Source: Clinical and Molecular Allergy 2013, 11:6. doi:10.1186/1476-7961-11-6 -
Celiac.com 09/16/2008 - A team of researchers recently set out to examine the connection between celiac disease and primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis. The research team was made up of Alberto Rubio-Tapia, Ahmad S. Abdulkarim, Patricia K. Krause, S. Breanndan Moore, Joseph A. Murray, and Russell H. Wiesner. The team measured the rates of occurrence for tissue transglutaminase antibodies (tTGAs) and endomysial antibodies (EMAs) in end-stage autoimmune liver disease (ESALD). They then correlated autoantibodies and the human leucocyte antigen (HLA) haplotype. Finally, they assessed the effect of liver transplantation on antibody kinetics. The team tested tTGA levels on blood samples from 488 prior to transplant. 310 of these had ESALD, and 178 had non-autoimmune disease. The team tested positive samples for EMAs, and retested at 6-12 and =24 months after transplant. They then correlated their results with the HLA type of the recipient. The results showed that 3% of ESALD patients showed evidence of celiac disease compared to 0.6% of those with non-autoimmune disease. This represents a five-fold greater risk for those with ESALD. The prevalence of tTGAs was 14.2 for ESALD patients compared to 5.4% for those with non-autoimmune disease (P = 0.0001). The prevalence of EMAs was 4.3 for ESALD patients compared to 0.78% for those with non-autoimmune disease (P = 0.01)—significantly higher for those with HLA-DQ2 or HLA-DQ8 haplotypes. After transplant, tTGAs and EMAs normalized in 94% and 100%, respectively, without gluten elimination. Also, three out of five patients with classical symptoms of celiac disease improved. The research team found two cases of intestinal lymphoma in two cases that showed no clinical signs of celiac disease. Patients with ESALD, particularly those with HLA-DQ2 or HLA-DQ8 gene haplotypes, showed greater occurrances of celiac disease-associated antibodies. Following liver transplants, both tTGA and EMA levels decreased without gluten withdrawal. The team also concluded that symptoms of celiac disease might be improved through immune suppression, but those improvements may not prevent the disease from progressing to intestinal lymphoma. The study doesn’t tell what effect, if any, early detection and treatment of celiac disease might have on rates of ESALD. It would be helpful to know if celiac disease contributes to liver disease, if liver disease contributes to celiac disease, or if some third connection links the two. Until then, we’ll just have to keep a tight eye on developments concerning celiac disease and liver disease. Liver Int. 2008; 28(4): 467-476.
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Dig Dis Sci. 2004 Apr;49(4):546-50 Celiac.com 08/27/2004 – Dr. Peter Green and colleagues at the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, conducted a study designed to determine the sensitivity of the various serological tests used to diagnose celiac disease. To do this they looked at 115 adults with biopsy-proven celiac disease who fulfilled strict criteria which included serological testing at the time of their diagnosis, and a positive response to a gluten-free diet. Out of those studied, 71% had total villous atrophy, and 29% had partial villous atrophy. Serological results indicated that only 77% of those with total and 33% of those with partial villous atrophy actually tested positive for celiac disease, and it did not matter whether the patients presented with classical or silent symptoms. All patients who were positive for anti-tissue transglutaminase had total villous atrophy. The researchers conclude: Seronegative celiac disease occurs. Endomysial antibody positivity correlates with more severe villous atrophy and not mode of presentation of celiac disease. Serologic tests, in clinical practice, lack the sensitivity reported in the literature.
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