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Found 6 results

  1. Celiac.com 09/01/2015 - Current medical guidelines recommend routine screening of liver function tests (LFTs) in patients diagnosed with celiac disease. However, there isn't much good data on rates of liver disorders in celiac disease outside of Europe. A team of researchers recently set out to accurately estimate rates of LFT abnormalities in celiac disease in the USA, and to assess the effect of a gluten-free diet on LFTs. The research team included Natalia E Castillo, Rohini R Vanga, Thimmaiah G Theethira, Alberto Rubio-Tapia, Joseph A Murray, Javier Villafuerte, Alan Bonder, Rupa Mukherjee, Joshua Hansen, Melinda Dennis, Ciaran P Kelly and Daniel A Leffler. To identify adult patients with biopsy-proven celiac disease, they used a prospectively maintained database, which they matched with healthy controls. They defined abnormal LFT levels for women and men based on the Third National Health and Nutrition Examination Survey (NHANES III) criteria. The team gathered data on demographics, coexisting liver diseases, and laboratory work-ups including aspartate transaminase (AST) and alanine transaminase (ALT) values at the time of diagnosis and on a gluten-free diet. They later compared data from this group with data from 7,789 individuals participating in the National Health and Nutrition Examination Survey, 2009–2010, and applied univariate logistic regression, Wilcox on signed-ranks, Student's t-test, χ2, and Fischer's exact test for statistical analysis. In 463 celiac disease patients with ALT or AST levels at the time of celiac disease diagnosis, 40.6% had elevated LFTs compared with 24.2% of treated celiac disease patients (P<0.001). Similarly, nearly forty percent of celiac disease patients on the NHANES database showed abnormal ALT values compared with less than twenty percent of non-celiac patients (P=0.03). Just over forty percent of individuals will show elevated LFTs at celiac disease diagnosis, but the vast majority, nearly eighty percent of those patients will show normal LFTs within a year and a half of adopting a gluten-free diet. The team suggests that doctors check all celiac patients for LFTs, and coexisting liver disorder be considered in patients whose LFTs have not improved within a year on a gluten-free diet. Source: The American Journal of Gastroenterology 110, 1216-1222 (August 2015). doi:10.1038/ajg.2015.192
  2. Celiac.com 09/09/2013 - Many people with celiac disease show slightly elevated liver enzymes, though these enzyme levels usually return to normal after gluten-free diet. A team of researchers recently set out to investigate the cause and prevalence of altered liver function tests in celiac patients, basally and after 1 year of gluten-free diet. The research team included Giovanni Casella, Elisabetta Antonelli, Camillo Di Bella, Vincenzo Villanacci, Lucia Fanini, Vittorio Baldini, and Gabrio Bassotti. They are affiliated with the Medical Department, and the Clinical Pathology Department of Desio Hospital in Monza and Brianza, Italy, the Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology Section at the University of Perugia in Perugia, Italy, and with the Department of Laboratory Diagnostics, Pathology Section, Brescia, Italy. The team gathered data from 245 untreated celiac disease patients, 196 women and 49 men, ranging in age from 15 to 80 years. They then analyzed the data, and assessed the results of liver function tests performed before and after diet, as well as associated liver pathologies. They found that 43 (17.5%) of the 245 patients, showed elevated levels of one or both aminotransferases; In 41 patients (95%) the elevation was mild, meaning that it was less than five times the upper reference limit. The remaining two patients (5%) showed marked elevation, meaning levels more than ten times the upper reference limit. After patients eliminated gluten for one year, aminotransferase levels normalized in all but four patients, who had HCV infection or primary biliary cirrhosis. Celiac patients who show hypertransaminaseaemia at diagnosis, and who do not show normalization of liver enzymes after 12 months of gluten-free diet, likely suffer from coexisting liver disease. In such cases, the research team recommends further assessment to assess the possible coexisting liver disease. Spotting and treating coexisting liver disease in celiac patients is important for improving liver function and preventing possible complications. Source: Liver International. 2013;33(7):1128-1131.
  3. After my GI doctor told me nothing was wrong with my blood test, even though i was feeling very ill, i knew it was time for a change. This doctor had recommended me to eat products that had wheat and gave me samplers of probiotics that stated "contained wheat" on the back! The doctor i really wanted to see.... Dr. Crowe at the UCSD celiac clinic. This wonderful place seemed to be the solution to all my gastrointestinal needs. The only problem i faced, my insurance. The battle began with my authorization, who was sent by my primary doctor because i didn't trust the GI doctor to even do it right. Of course as i suspected it got denied. I then call the insurance in a sudden moment of fire, anger, and GI symptoms, demanding to know why they had denied my case. They claimed it was "Not medically necessary". Feeling undeterred i sent in an appeal to prove them wrong, sending in my abnormal blood work, but to no prevail. The next day i got a call saying that it was still ruled "Not medically necessary" because i had other doctors in my group that could handle my case. Unsatisfied with my defeat i sent in a complaint to the CA GOV, who makes sure insurance are doing their job, and opened a case file. 30 days they told me, 30 days till i could have an answer. An answer, the man on the phone said, that would possible be no. Finally feeling defeated by the money loving insurance, and more ill then i could stand i transferred to the highest recommended doctor in the group for patient with celiac. To my surprise and delight my new GI doctors, Dr. Kim not only use to work at the UCSD celiac clinic, but is in close relations with Dr. Crowe. Dr. Kim was immediately intrigued by my test results and about my cluttered family history of autoimmune diseases. My case is so puzzling and abnormal that she is going to share the case with the doctors at the clinic to make sure i get the best treatment possible. I'm still a bit sad that i couldn't go and see the doctor i wanted, but in the end Dr. Kim looks to be the doctor to solve my case. A cause that from my visits with her could be more than anyone ever expected.
  4. My name is Nicole and i am 19 years old. I go to college and work, and have a loving family and boyfriend who have got my back. I have been diagnosed with celiac disease, through blood and scope, for more than 4 years now. I also got diagnosed with DH, eczema, and a large file of allergies. To catch up on what has happened: About 8 months ago i started to feel very ill with the normal GI symptoms, knowing i had celiac i relooked at my diet, only eating simplistic gluten free meals. When that did not help i began to worry and consulted a doctor for advice. He took my blood, and saw nothing unusual in my levels, sending me home feeling ill and disappointed. As the weeks passed my health declined and my skin started to peel off my body in sheets. The skin around my lips became scaly to the point where they would crack and bleed if i smiled, and my legs became riddled with DH. Something was wrong. I them transferred to another doctor who redid my blood test and was shocked by what she found. My levels were extremely high for being on a gluten free diet. These being the numbers they normally diagnose patients with she sent me home to write out a food log, and sent in an authorization to get an MRI done. But before i left her office we had a talk about what this could be. She mentioned that it could just be wheat in my diet, but me having this disease for 4 years, she felt it was highly unlikely. My GI doctor mentioned it could be cancer in my intestines, but the MRI would give us a yes or no answer to that question. The most curious thing she said was that i could be a part of an extremely rare group of people with celiac. This group of people have one very complicated problem..... Our bodies never stop producing antibodies to fight the gluten that is not even there, therefore cause mass destruction throughout our bodies. Shocked by this i though about my sister who has had Chron's for 7 years now, and all the pain she has gone through... Is that my future as well? My doctor went through loads of information on immune suppressors, and the benefits it would have on my body, if it worked. How strong the drug would have to be, and names of prescriptions for me to become informed. Hearing this was a shock. Wasn't this disease suppose to be easy?..... You stop eating gluten and feel better. None of this was making since. All that was going through my head when i left the hospital was; You're prescribing me what?!?!
  5. Celiac.com 09/21/2012 - Refractory celiac disease type II (RCDII) is a severe complication of celiac disease that occurs when symptoms and intestinal damage continue even when the patient adopt a gluten-free diet. Refractory celiac disease marked by abnormal intraepithelial lymphocytes (IELs) of unknown origin that display an atypical CD3(-)CD7(+)icCD3(+) phenotype. About 40% of patients with RCDII lymphocytes develop a dangerous and invasive lymphoma. A team of researchers recently sought to identify possible origins of abnormal intraepithelial lymphocytes in refractory celiac disease type II. The research team included F. Schmitz; T.M. Tjon, Y. Lai; A. Thompson; Y. Kooy-Winkelaar; R.J. Lemmers; H.W. Verspaget; M.L. Mearin; F.J. Staal; M.W. Schreurs; T. Cupedo; A.W. Langerak; C.J. Mulder; J. van Bergen; and F. Koning. In their study, the researches sought to find the physiological counterpart of these abnormal intraepithelial lymphocytes cells. To do so, they used microarray analysis, real-time quantitative PCR and flow cytometry to compare RCDII cell lines with T-cell receptor positive (TCR(+)) IEL (T-IEL) lines. They then used their data to identify cells with an RCDII-associated phenotype in duodenal biopsies from non-refractory individuals by multicolor flow cytometry. They found that RCDII cell lines were distinct from T-IEL lines and showed higher levels of multiple natural killer (NK) cell receptors. In addition to the CD3(-)CD7(+)icCD3(+) phenotype, the RCDII lines showed an absence of CD56, CD127 and CD34, compared with other lymphocyte subsets. Moreover, they found cells matching this surface lineage-negative (Lin(-)) CD7(+)CD127(-)CD34(-) phenotype that showed a functional interleukin-15 (IL-15) receptor and comprised a substantial portion of IELs in duodenal specimens of patients without celiac disease, particularly children. They also found cells of this kind in the thymus. For patients without celiac disease, the Lin(-)CD7(+)CD127(-)CD34(-) subset was one of four subsets within the CD3(-)CD7(+)icCD3(+) population that showed a differential expression of CD56 and/or CD127. The results indicate that the CD3(-)CD7(+)icCD3(+) population is heterogeneous and show the existence of a Lin(-) subset that is different from T, B, NK and lymphoid tissue inducer cells. The team hypothesizes that the IL-15 cells are the counterpart of abnormal cells that are expanded in RCDII and transformed in RCDII-associated lymphoma. Source: Gut. 2012 Jul 6.
  6. Celiac.com 01/17/2010 - A team of researchers based in the Netherlands and in Germany recently found that abnormal T-Lymphocytes in refractory celiac disease may occur beyond small intestinal intraepithelia. The research team was made up of W.H.M. Verbeek, B.M.E. von Blomberg, V.M.H. Coupe, and S. Daum, C.J.J. Mulder, and M.W.J. Schreurs. The team members are associated with the Departments of Gastroenterology, Pathology, Epidemiology and Biostatistics at VU University Medical Centre, Amsterdam, The Netherlands, and with the Department of Medicine I, Gastroenterology, Infectious Diseases & Rheumatology at Charite Universitatsmedizin, Campus Benjamin Franklin, in Berlin, Germany. Refractory celiac disease (RCD) is characterized by persistent mucosal pathology despite a strict gluten free diet. Patients with RCD type II show phenotypically abnormal (CD71CD3-CD4/8-cytoplasmicCD31) T-lymphocytes within the intraepitelial lymphocyte (IEL) population in the small intestine, with 50–60% of these patients developing an enteropathy associated T-cell lymphoma (EATL). The goal of the study was to determine whether abnormal T-lymphocytes in RCD II can be detected in other parts of the small intestinal mucosa besides the intraepithelial compartment. Additionally, the presence of aberrant T-lymphocytes was analyzed in two RCD II patients that developed atypical skin lesions. Researchers conducted multi-parameter flow cytometric immunophenotyping on both IEL and lamina propria lymphocyte (LPL) cell suspensions, isolated from small bowel biopsy specimens of RCD II patients (n 5 14), and on cutaneous lymphocytes isolated from skin-lesion biopsy specimens of RCD II patients (n 5 2). They also carried out immunofluorescence analysis of frozen RCD II derived small intestinal biopsies. The results clearly show that abnormal T-lymphocytes may develop in both the IEL and the LPL compartments of RCD II derived small intestinal biopsies. Indeed, even though the highest percentages are always found in the IEL compartment, abnormal LPL can exceed 20% of total LPL in half of patients with RCD II. Interestingly, cutaneous lymphocytes isolated from atypical skin lesions that developed in some RCD II patients showed a similar abnormal immunophenotype as found in the intestinal mucosa. In RCD II, the abnormal T-lymphocytes may also manifest in the sub-epithelial layer of the small intestinal mucosa, in the lamina propria, or even in locations completely outside the intestine, including the skin. Whether this finding indicates a passive overflow from the intestinal epithelium or active movement towards other anatomical locations remains to be determined. Source: Cytometry Part B (Clinical Cytometry) 76B:367–374 (2009)
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