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Celiac.com 11/25/2024 - The relationship between intestinal diseases and anal diseases has long been observed in clinical settings. Many patients with intestinal diseases, such as Crohn's disease or ulcerative colitis, also suffer from anal complications like hemorrhoids or fissures. However, the exact causal connection between these conditions is still unclear, due to limitations in previous observational studies. This study sought to clarify these relationships using Mendelian randomization, a method that uses genetic data to help determine causal effects and reduce bias caused by other variables. Methodology and Data Collection In order to explore the link between different types of intestinal diseases and anal diseases, researchers used genome-wide association study data. Seven types of intestinal diseases were examined, including inflammatory bowel disease, Crohn's disease, ulcerative colitis, irritable bowel syndrome, colorectal cancer, celiac disease, and constipation. Five types of anal diseases were also investigated: anorectal abscess, hemorrhoidal disease, fissures and fistulas of the anal and rectal regions, benign neoplasm of the anus, and malignant neoplasm of the anus. Using the Mendelian randomization technique, genetic variations were analyzed to determine whether these intestinal diseases have a direct influence on the development of anal diseases. This approach allowed researchers to control for confounding factors and focus on potential causal relationships. Key Findings The results of the analysis showed a significant link between several intestinal diseases and anal conditions. Inflammatory bowel disease, Crohn's disease, and ulcerative colitis were all found to increase the risk of three anal conditions: anorectal abscess, fissures and fistulas, and hemorrhoidal disease. These findings reinforce what has been noted in clinical practice—patients with these chronic inflammatory bowel conditions often experience anal complications. For celiac disease, the study identified a significant association with an increased risk of malignant neoplasm of the anus, a rare but serious form of anal cancer. This suggests that people with celiac disease may need to be more vigilant about monitoring for anal cancers. Other interesting findings include a potential link between irritable bowel syndrome and hemorrhoidal disease, and between colorectal cancer and benign neoplasm of the anus. While these associations need further exploration, they provide new avenues for research and clinical attention. Implications for Celiac Disease The link between celiac disease and anal cancer is particularly noteworthy. Celiac disease is characterized by an autoimmune response to gluten, which can lead to chronic inflammation in the gut. This chronic inflammation could contribute to the development of cancerous conditions, including in areas beyond the intestines, such as the anal canal. While more research is needed to fully understand the connection, this study highlights the importance of regular monitoring and early detection efforts for patients with celiac disease, especially concerning malignancies. Conclusion This study is significant in that it provides robust evidence supporting the causal relationship between certain intestinal and anal diseases. The use of Mendelian randomization strengthens the findings by reducing potential biases that have complicated earlier studies. For patients with celiac disease, Crohn's disease, ulcerative colitis, or other intestinal conditions, these findings emphasize the need for regular screening for anal diseases. The ability to understand these risks better may lead to improved prevention strategies and tailored medical advice for individuals with these chronic conditions. Read more at: nature.com Watch the video version of this article:

Celiac.com 01/11/2022 - Researchers still don't have a good idea about rates of celiac disease in people with irritable bowel disease. Some studies indicate that it's possible for both diseases to occur together in the same patient. A team of researchers recently set out to investigate the prevalence of celiac disease in Saudi Arabian children with irritable bowel disease. The research team included Mamdouh Qadi, Medical Student, Mohammed Hasosah, MD, Anas Alamoudi, Medical Student, Abdullah AlMansour, Medical Student, Mohammed Alghamdi, Medical Student, Faisal Alzahrani, Medical Student, Sultan Alzahrani, Medical Student, and Bader Khawaji, PhD. They are variously affiliated with the College of Medicine, King Saud bin Abdulaziz University for Health Sciences, Jeddah, Saudi Arabia; the King Abdullah International Medical Research Center, Jeddah, Saudi Arabia; and the Ministry of the National Guard—Health Affairs, Jeddah, Saudi Arabia. For their retrospective study the research team enrolled Saudi patients between 1 and 18 years of age, who were diagnosed with irritable bowel disease and celiac disease based on positive antibody screening and biopsy, from January 2011 to January 2020, at the Pediatric Gastroenterology Department at National Guard Hospital, Jeddah, Saudi Arabia. They excluded any patient with an immunodeficiency disorder. Of the nearly fifty enrolled patients with irritable bowel disease, they found four with celiac disease. The researchers found that the patients' height and weight when diagnosed with irritable bowel disease improved significantly by the time this study was conducted, but they found no significant connections between Ulcerative Colitis and celiac disease, or Crohn's disease and celiac disease. Most importantly in this case, the team found no significant connections between the rates of celiac disease and irritable bowel disease in children. The team members called for additional prospective multi-center studies to further clarify rates of celiac disease in children with irritable bowel disease. Read more in Global Pediatric Health

Celiac.com 06/17/2020 - Researchers have found no connection between dietary gluten consumption, and the rates of Crohn’s disease or ulcerative colitis in women without celiac disease, according to data from Digestive Disease Week. The researchers found that for women without celiac disease, "eating gluten does not increase a person's chance of being diagnosed with IBD. We found that dietary gluten intake was not associated with increased risk for ulcerative colitis or Crohn's disease,” says Emily W. Lopes, MD, from Massachusetts General Hospital in Boston. A team of researchers including Lopez and her colleagues carried out a prospective study of more than 208,000 women without prior diagnosis of celiac disease or IBD at baseline, selected from the Nurses' Health Study, Nurses' Health Study II, and Health Professionals Follow-up Study for over a 20 year period. The team used semiquantitative food frequency questionnaires given at baseline and every 4 years to calculate the total average dietary intake over the follow-up. They also reviewed patient records to confirm self-reported cases of Crohn’s and UC. The team used quintile categories of gluten intake with Cox proportional hazard modeling to calculate multivariable-adjusted hazard ratio and 95% confidence intervals for risk for celiac disease and UC. All models were adjusted for age, BMI, smoking, total caloric intake, dietary pattern, physical activity, appendectomy and medications correlated with risk for IBD. The team found 272 cases of celiac disease, and 359 cases of ulcerative colitis, over 2,026,573 person-years. Investigators found no link between dietary gluten consumption and patient risk for celiac disease or ulcerative colitis incidence. There was no difference between refined grains and whole grains as the main source of gluten intake, once data was adjusted. Also, neither baseline age, BMI or smoking status changed the findings. The findings do not cover patients with IBD, since, as Dr. Lopez notes, "...we did not study the impact of gluten intake on those already diagnosed with IBD, thus we cannot expand our results to this population.” This data was to be presented as part of Digestive Disease Week 2020: Lopes EW, et al. Abstract 847. Presented at: Digestive Disease Week; May 2-5, 2020; Chicago (meeting canceled). Read more at Healio.com

Celiac.com 05/15/2020 - The opinions of researchers are currently divided over the connection between celiac disease and inflammatory bowel diseases (IBD). A team of researchers recently set out to to assess evidence for an association between celiac disease and IBD, using a systematic review and meta-analysis. The research team included Maria Ines Pinto-Sanchez, Caroline L. Seiler, Nancy Santesso, Armin Alaedini, Carol Semrad, Anne R. Lee, Premysl Bercik, Benjamin Lebwohl, Daniel A. Leffler, Ciaran P. Kelly, Paul Moayyedi, Peter H. Green, and Elena F. Verdu. They are variously affiliated with the Department of Medicine, Farncombe Family Digestive Research Institute, McMaster University, Hamilton, Ontario, Canada; the Department of Clinical Epidemiology & Biostatistics, McMaster University, Hamilton, Canada; the Celiac Disease Center at Columbia University, New York, New York; the Celiac Disease Center at University of Chicago Medicine, Chicago, Illinois; and the Department of Gastroenterology, Beth Israel Deaconess Medical Center, Boston, Massachusetts. The team scoured medical databases including MEDLINE, EMBASE, CENTRAL, Web of Science, CINAHL, DARE, and SIGLE through June 25, 2019. They looked specifically for studies that determined celiac disease risk in patients with IBD, and IBD in patients with celiac disease, compared with controls of any type. To assess bias risk, they used the Newcastle-Ottawa Scale, and GRADE to calculate the certainty level of the evidence. They found nearly 10,000 studies, and included 65 studies in their assessment. Compared with control subjects, moderate certainty evidence revealed that patients with IBD had an increased risk of celiac disease, while celiac disease patients also had an increased risk for IBD. Compared with control subjects, low-certainty evidence showed that celiac disease patients have a higher risk of anti-Saccharomyces antibodies, a serologic marker of IBD, There was also low certainty evidence for no difference in risk of HLA-DQ2 or DQ8 in patients with IBD, compared with control subjects, and very low certainty evidence for an increased risk of anti-tissue transglutaminase in patients with IBD, compared with control subjects. The results showed that IBD patients had a slightly lower risk of anti-endomysial antibodies, compared with control subjects, but these results are not certain. The team's systematic review and meta-analysis showed that celiac patients have an increased risk of IBD, and IBD patients have an increased risk of celiac disease, compared with controls subjects. The team is calling for high-quality prospective cohort studies to calculate levels of celiac disease-specific and IBD-specific biomarkers in patients with IBD and celiac disease. Certainly, the idea that IBD and celiac disease may be connected in some way does not seem far fetched. Stay tuned for more on this and other issues. Read more at gastrojournal.org

Celiac.com 12/02/2019 - Parkinson’s development can take many paths, with factors like genetics, aging, and environmental conditions all playing roles. Most people with Parkinson’s disease experience non-motor-symptoms, such as chronic constipation and/or impairment of gastrointestinal (GI) transit, long before the disease manifests clearly. Researcher Tomasza Brudek recently reviewed available medical literature for a possible link between Inflammatory Bowel Disease (IBD) and Parkinson's Disease. Brudek is affiliated with both the Research Laboratory for Stereology and Neuroscience, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital in Copenhagen, Denmark; and the Copenhagen Center for Translational Research, Copenhagen University Hospital, Bispebjerg and Frederiksberg Hospital in Copenhagen, Denmark. Build-up of α-synuclein protein in the form of Lewy bodies and Lewy neurites, and degeneration of substantia nigra dopamine neurons are classic clinical markers of Parkinson's Disease. Major features of Parkinson's Disease include inflammatory responses manifested by glial reactions, T cell infiltration, and increased expression of inflammatory cytokines, along with other toxic mediators derived from activated glial cells. Experimental, clinical and epidemiological data suggest that intestinal inflammation influences the development of Parkinson's Disease, while more and more studies suggest that Parkinson's disease may begin in the gut long before any motor symptoms show up. Patients with inflammatory bowel disease (IBD) have a higher risk of developing Parkinson's Disease compared with non-IBD individuals. Gene association study has found a genetic link between IBD and Parkinson's Disease, and an evidence from animal studies suggests that gut inflammation, similar to that observed in IBD, may induce loss of dopaminergic neurons. Based on preclinical models of Parkinson's Disease, some clinicians hypothesize that the early stages of early in Parkinson's Disease are marked by enteric microbiome changes, and gut infections triggering α-synuclein release and aggregation. Because gastrointestinal pathology can play such an important role in Parkinson's Disease development, there's good reason to believe that IBD and IBD treatments can influence Parkinson's Disease risk. This review underscores how important it is for physicians to be aware of Parkinson's Disease symptoms in IBD patients. Read more in the Journal of Parkinson's Disease, vol. 9, no. s2, pp. S331-S344, 2019

Celiac.com 05/16/2018 - Galectins are a family of animal lectins marked by their affinity for N-acetyllactosamine-enriched glycoconjugates. Galectins control several immune cell processes and influence both innate and adaptive immune responses. A team of researchers recently set out to assess the role of galectins, particularly galectin-1 (Gal-1), in the treatment of celiac disease. The research team included Victoria Sundblad, Amado A. Quintar, Luciano G. Morosi, Sonia I. Niveloni, Ana Cabanne, Edgardo Smecuol, Eduardo Mauriño, Karina V. Mariño, Julio C. Bai, Cristina A. Maldonado, and Gabriel A. Rabinovich. The researchers examined the role of galectins in intestinal inflammation, particularly in Crohn’s disease, ulcerative colitis, and celiac disease patients, as well as in murine models resembling these inflammatory conditions. Maintaining the fine balance between host immunity and tolerance promotes gut homeostasis, and helps to prevent inflammation. To gain insight into the role of Gal-1 in celiac patients, the team demonstrated an increase in Gal-1 expression following a gluten-free diet along with an increase in the frequency of Foxp3+ cells. The resolution of the inflammatory response may promote the recovery process, leading to a reversal of gut damage and a regeneration of villi. Among other things, the team’s findings support the use of Gal-1 agonists to treat severe mucosal inflammation. In addition, Gal-1 may serve as a potential biomarker to follow the progression of celiac disease treatment. Gut inflammation may be governed by a coordinated network of galectins and their glycosylated ligands, triggering either anti-inflammatory or pro-inflammatory responses. That network may influence the interplay between intestinal epithelial cells and the highly specialized gut immune system in physiologic and pathologic settings. The team’s results demonstrate that the anti-inflammatory and tolerogenic response associated with gluten-free diet in celiac patients is matched by a substantial up-regulation of Gal-1. This suggests a major role of this lectin in favoring resolution of inflammation and restoration of mucosal homeostasis. This data highlights the regulated expression of galectin-1 (Gal-1), a proto-type member of the galectin family, during intestinal inflammation in untreated and treated celiac patients. Further study of this area could lead to better understanding of the mechanisms behind celiac disease, and potentially to a treatment of the disease. Source: Front. Immunol., 01 March 2018. The researchers in this study are variously affiliated with the Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IBYME), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Centro de Microscopía Electrónica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina; the Instituto de Investigaciones en Ciencias de la Salud (INICSA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Córdoba, Argentina; the Laboratorio de Glicómica Funcional y Molecular, Instituto de Biología y Medicina Experimental (IBYME), Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires, Argentina; the Sección Intestino Delgado, Departamento de Medicina, Hospital de Gastroenterología Dr. C. Bonorino Udaondo, Buenos Aires, Argentina; the Unidad de Patología, Hospital de Gastroenterología, Bonorino Udaondo, Buenos Aires, Argentina; the Instituto de Investigaciones, Universidad del Salvador, Buenos Aires, Argentina; and the Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.