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Celiac.com 06/06/2024 - Microscopic colitis is a type of chronic inflammatory bowel disease characterized by persistent watery diarrhea, abdominal pain, cramps, bloating, weight loss, nausea, fecal incontinence, and dehydration. It comprises two distinct sub-types: collagenous colitis and lymphocytic colitis, both leading to non-bloody watery diarrhea. In contrast, celiac disease is an autoimmune disorder triggered by gluten consumption, resulting in damage to the small intestine. Despite their differences, recent studies have hinted at a potential association between microscopic colitis and celiac disease, necessitating further investigation. Utilizing National Inpatient Data for Analysis This study utilized the National Inpatient Sample (NIS) database spanning four years (2016–2019) to conduct a comprehensive analysis of the relationship between microscopic colitis and celiac disease. Through specified International Classification of Diseases, 10th Edition (ICD-10) codes, patients with and without microscopic colitis, along with the presence or absence of coexisting celiac disease, were identified. Statistical analyses, including univariate and multi-variate methods, were employed to assess the association while adjusting for various confounding factors. The study encompassed a vast dataset of over 26 million patients, providing robust insights into this intriguing link. Key Findings and Clinical Implications The analysis revealed a significant association between microscopic colitis and celiac disease, supported by both univariate and multi-variate analyses. Interestingly, celiac disease emerged as an independent risk factor for increased mortality among microscopic colitis patients, although it did not significantly impact the mean hospital stay. These findings underscore the need for heightened awareness and clinical vigilance in managing patients with coexisting microscopic colitis and celiac disease. Moreover, the study's large-scale approach and comprehensive analysis contribute valuable insights into the complex interplay between these gastrointestinal disorders, paving the way for more targeted treatments and improved patient outcomes. This study delved into the intriguing association between microscopic colitis and celiac disease using extensive population-based data from the National Inpatient Sample (NIS) database spanning four years (2016–2019). The investigation aimed to elucidate this relationship with robust statistical analyses while controlling for various confounding factors. Here's a detailed summary of the study's key aspects and findings: Exploring the Link Between Microscopic Colitis and Celiac Disease The study analyzed data from over 26 million patients, identifying those with and without microscopic colitis and assessing the presence or absence of coexisting celiac disease. Statistical analyses, including univariate and multi-variate methods, were employed to evaluate the association while adjusting for confounding factors such as age, race, hospital characteristics, and comorbidities. Association and Impact The analysis revealed a significant association between microscopic colitis and celiac disease, supported by both univariate and multi-variate analyses. Interestingly, celiac disease emerged as an independent risk factor for increased mortality among microscopic colitis patients. However, there was no significant impact on the mean hospital stay. Clinical Implications These findings highlight the clinical relevance of understanding the link between microscopic colitis and celiac disease, emphasizing the need for vigilant monitoring and appropriate management for patients with coexisting conditions. The study's population-based approach and comprehensive analysis contribute valuable insights for informed decision-making in healthcare. Future Directions The study sets the stage for further research focusing on mechanistic aspects, prospective studies to establish causality, and exploring therapeutic interventions. Addressing limitations related to data accuracy and histologic subtypes is crucial for refining our understanding and improving clinical management. This study establishes a probable association between microscopic colitis and celiac disease, backed by rigorous statistical analyses. It also identifies celiac disease as an independent risk factor for increased mortality among microscopic colitis patients. These findings provide a foundation for future research and clinical considerations, aiming to optimize patient care and outcomes in the realm of gastrointestinal health. Source: journals.lww.com
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Exploring Other Causes of Villous Atrophy Beyond Celiac Disease
Scott Adams posted an article in Spring 2024 Issue
Celiac.com 02/10/2024 - Villous atrophy, a condition marked by the blunting or flattening of the microscopic structures called villi in the small intestine, is most commonly associated with celiac disease. However, emerging research and clinical observations have unveiled a spectrum of diverse conditions beyond celiac disease that can lead to villous atrophy. This article explores the lesser-known contributors to villous atrophy, shedding light on various health conditions that may present with similar histological changes in the small intestine. While celiac disease remains a prominent cause, understanding these alternative pathways to villous atrophy is crucial for accurate diagnosis, appropriate management, and a comprehensive approach to gastrointestinal health. From autoimmune disorders to infections and drug-induced reactions, exploring the multifaceted nature of villous atrophy enhances our grasp of gastrointestinal pathology and guides clinicians toward more nuanced and personalized patient care. Other Conditions Associated with Villous Atrophy In the following sections, we delve into a comprehensive exploration of diverse health conditions intricately linked to villous atrophy, shedding light on their unique associations and implications for gastrointestinal health. Eosinophilic Enteritis Eosinophilic enteritis is an inflammatory disorder characterized by an increased presence of eosinophils in the gastrointestinal tract. Eosinophils are a type of white blood cell involved in the immune response. In eosinophilic enteritis, these cells infiltrate the walls of the intestines, causing inflammation and damage. This inflammatory process can lead to various symptoms, including abdominal pain, diarrhea, and malabsorption. In some cases, the inflammation may result in villous atrophy, affecting the absorptive capacity of the small intestine. Diagnosis often involves endoscopic procedures with tissue biopsy to evaluate the extent of inflammation and associated damage. Crohn's Disease Crohn's disease is a chronic inflammatory bowel disease that can affect any part of the gastrointestinal tract, from the mouth to the anus. In the small intestine, Crohn's disease can cause inflammation and damage to the intestinal lining, leading to complications such as strictures and fistulas. In some cases, individuals with Crohn's disease may experience villous atrophy, particularly in areas of the small intestine affected by inflammation. The severity of villous atrophy can vary among patients with Crohn's disease, and its presence may contribute to malabsorption issues and nutritional deficiencies. Management often involves anti-inflammatory medications, immunosuppressants, and, in severe cases, surgical intervention to address complications. Giardiasis Giardiasis is an intestinal infection caused by the parasite Giardia lamblia. This parasitic infection can lead to symptoms such as diarrhea, abdominal cramps, and bloating. In addition to the acute phase of the infection, chronic giardiasis has been associated with villous atrophy in some cases. The mechanisms by which Giardia lamblia causes villous atrophy are not fully understood, but it is believed to involve both direct damage to the intestinal lining and an immune response triggered by the presence of the parasite. Diagnosis typically involves stool tests to detect the parasite, and treatment includes antiparasitic medications. Common Variable Immunodeficiency (CVID) Common Variable Immunodeficiency (CVID) is a primary immunodeficiency disorder characterized by impaired antibody production, leading to increased susceptibility to infections. Some individuals with CVID may experience gastrointestinal symptoms, including chronic diarrhea and malabsorption. In severe cases, villous atrophy can occur, impacting the absorption of nutrients in the small intestine. The association between CVID and villous atrophy underscores the complex interplay between the immune system and the intestinal mucosa. Management involves immunoglobulin replacement therapy to address the immune deficiency and supportive measures for gastrointestinal symptoms. Autoimmune Enteropathy Autoimmune enteropathy is a rare autoimmune disorder that primarily affects the small intestine. In this condition, the immune system mistakenly attacks the cells of the intestinal lining, leading to severe inflammation and damage. Villous atrophy is a characteristic feature of autoimmune enteropathy, affecting the absorptive surface area of the small intestine. Individuals with autoimmune enteropathy often present with persistent diarrhea, malabsorption, and failure to thrive. Diagnosis requires extensive evaluation, including endoscopic procedures and tissue biopsy. Treatment involves immunosuppressive medications to modulate the autoimmune response and manage symptoms. Human Immunodeficiency Virus (HIV) Advanced Human Immunodeficiency Virus (HIV) infection can result in various gastrointestinal complications, affecting both the upper and lower parts of the digestive tract. HIV-associated enteropathy may involve villous atrophy, contributing to malabsorption and nutritional deficiencies. The mechanisms leading to villous atrophy in HIV infection are multifactorial, involving both direct viral effects and immune-mediated processes. Additionally, opportunistic infections and other HIV-related complications can further impact the gastrointestinal mucosa. Management includes antiretroviral therapy to control HIV replication and supportive measures to address nutritional deficiencies and associated symptoms. Regular monitoring and a multidisciplinary approach are crucial in the care of individuals with HIV-associated gastrointestinal conditions. Dermatitis Herpetiformis (DH) Dermatitis herpetiformis is a chronic skin condition characterized by intensely itchy, blistering skin lesions. While DH primarily manifests as a skin disorder, its connection to celiac disease is well-established. Both conditions share a common trigger: gluten ingestion. DH is considered the skin manifestation of celiac disease, and individuals with DH often have underlying gluten sensitivity. The immune response triggered by gluten in susceptible individuals leads to the formation of IgA antibodies, which deposit in the skin, causing the characteristic skin lesions. While DH predominantly affects the skin, it is crucial to recognize its association with celiac disease, as individuals with DH may also experience villous atrophy in the small intestine. Therefore, a gluten-free diet is not only essential for managing skin symptoms but also for addressing the underlying celiac disease and preventing intestinal damage. Diagnosis involves skin biopsy for characteristic IgA deposits and, in some cases, intestinal biopsy to assess the extent of villous atrophy. Treatment primarily revolves around strict adherence to a gluten-free diet, often complemented by medications to control skin symptoms. Managing DH effectively requires a multidisciplinary approach, involving dermatologists, gastroenterologists, and dietitians to address both the skin manifestations and the underlying celiac disease. Idiopathic Sprue Idiopathic sprue is a term used for cases of sprue (malabsorption syndrome) where the cause is unknown. It may include cases that do not fit the criteria for celiac disease or other known causes of malabsorption. It shares some features with celiac disease, such as malabsorption and damage to the small intestine, but it lacks specific diagnostic markers for celiac disease. Diagnosis may involve excluding other causes of malabsorption, and it may be considered when typical celiac disease markers are absent. Tropical Sprue Tropical sprue is a malabsorption syndrome that occurs in tropical regions, and its exact cause is not fully understood. It is thought to be associated with infections or environmental factors. It presents with symptoms of malabsorption, such as diarrhea, weight loss, and nutritional deficiencies. It is more commonly observed in tropical regions but can occur in non-tropical areas as well. Collagenous Sprue Collagenous sprue is a rare disorder characterized by collagen deposition in the small intestine. The cause is not well-established. It leads to malabsorption and features similar to celiac disease but is distinguished by the characteristic collagen band in the intestinal lining. Diagnosis involves histological examination of small intestinal biopsies. The management of collagenous sprue may involve a combination of treatments, including a gluten-free diet and immunosuppressive medications. Corticosteroids or other immunosuppressants may be prescribed. Peptic Duodenitis Peptic duodenitis, a condition characterized by inflammation of the duodenal lining due to exposure to stomach acid, shares a commonality with celiac disease in its potential to induce villous atrophy. In peptic duodenitis, the inflammatory response triggered by gastric acid can extend into the duodenum, disrupting the delicate balance of the intestinal mucosa. This sustained inflammation may lead to changes in the architecture of the small intestine, including the villi, finger-like projections crucial for nutrient absorption. The damage incurred can result in villous atrophy, akin to the characteristic intestinal changes observed in celiac disease. Helicobacter Pylori Helicobacter pylori, a bacterium known for its association with gastric ulcers and gastritis, has been implicated in gastrointestinal conditions that extend beyond the stomach, including potential involvement in villous atrophy akin to celiac disease. The presence of H. pylori in the duodenum and small intestine has been linked to chronic inflammation and alterations in mucosal architecture. The bacterium's ability to induce immune responses may contribute to the damage of the intestinal villi, compromising their structure and functionality. This shared consequence of villous atrophy highlights the interconnectedness of various gastrointestinal disorders and underscores the need for comprehensive investigations to discern the specific triggers and mechanisms at play. While celiac disease and H. pylori-related duodenal changes differ in their etiology, understanding the potential overlap in their impact on intestinal health is crucial for accurate diagnosis and tailored therapeutic interventions. Small Intestinal Bacterial Overgrowth (SIBO) Small intestinal bacterial overgrowth (SIBO) is recognized for its capacity to disrupt the normal balance of microorganisms in the small intestine, leading to various gastrointestinal manifestations. In some cases, SIBO has been associated with mucosal damage, mirroring the villous atrophy observed in conditions like celiac disease. The overgrowth of bacteria in the small intestine can interfere with nutrient absorption and trigger an inflammatory response, potentially contributing to the erosion of the intestinal villi. While the mechanisms differ from those in celiac disease, the shared outcome of villous atrophy underscores the intricate relationship between dysbiosis and intestinal health. Lymphoma Lymphoma, a form of cancer that originates in the lymphatic system, can exhibit parallels with celiac disease in terms of inducing villous atrophy. In some cases, individuals with longstanding untreated celiac disease may face an elevated risk of developing enteropathy-associated T-cell lymphoma (EATL), a rare but serious complication. EATL is characterized by the infiltration of malignant T lymphocytes into the intestinal mucosa, leading to structural changes reminiscent of villous atrophy. While lymphoma and celiac disease differ fundamentally, the shared manifestation of villous atrophy underscores the intricate interplay between chronic inflammation and the potential oncogenic transformations within the gastrointestinal milieu. Thiamine (Vitamin B1) Deficiency There is some old research that indicates that prolonged low thiamine (vitamin B1) may cause thinning of the microvillus membrane. While these conditions may share some clinical features with celiac disease, the differences in their etiology, histopathology, and diagnostic criteria make them distinct entities. Accurate diagnosis and differentiation often require a thorough clinical evaluation, including serological tests, histopathological examination, and consideration of geographic or idiopathic factors. Consulting with a gastroenterologist or healthcare professional is essential for proper diagnosis and management. Drug-Associated Enteropathy: Medications Associated with Villous Atrophy Understanding the intricate interplay between medications and intestinal well-being is paramount for individuals managing chronic health conditions. While medications play a pivotal role in alleviating symptoms and improving overall health, certain drugs may harbor the potential to influence the delicate environment of the small intestine. This section delves into the impact of various medications on the intestinal villi, focusing on conditions that may lead to villous atrophy. From common pain relievers to immunosuppressive drugs, the discussion aims to shed light on the nuanced relationship between medications and gastrointestinal health. It underscores the importance of informed healthcare decisions, proactive monitoring, and open communication between patients and healthcare providers to mitigate potential complications and ensure optimal intestinal function during the course of medical treatments. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) are commonly used to alleviate pain and inflammation, but prolonged and excessive use has been associated with adverse effects on the gastrointestinal (GI) tract. NSAIDs can cause irritation and inflammation in the small intestine, potentially leading to villous atrophy. The mechanism involves the inhibition of cyclooxygenase enzymes, which play a role in maintaining the integrity of the GI mucosa. Individuals relying on NSAIDs for chronic pain management should be cautious and work closely with healthcare providers to monitor and mitigate potential GI complications. Immunosuppressive Drugs Immunosuppressive drugs, such as methotrexate and mycophenolate mofetil, are crucial in managing autoimmune conditions and preventing organ rejection after transplantation. While these medications target the immune system to curb excessive responses, they may also impact the gastrointestinal lining. Long-term use could lead to intestinal complications, including villous atrophy. Healthcare providers prescribing immunosuppressive drugs carefully assess the risk-benefit profile for each patient and monitor closely for potential adverse effects on the GI tract. Chemotherapy Drugs Chemotherapy, a cornerstone in cancer treatment, aims to eradicate rapidly dividing cells, including cancerous ones. However, the impact isn't limited to tumors, and normal, healthy cells may also be affected. The rapidly renewing cells in the small intestine are particularly susceptible, potentially resulting in damage to the villi and compromising the absorptive capacity of the intestines. Individuals undergoing chemotherapy should discuss potential gastrointestinal side effects with their oncologist to address and manage any complications that may arise. Some Antibiotics Certain antibiotics, such as tetracycline and ampicillin, may disrupt the balance of the gut microbiota, leading to gastrointestinal disturbances. While these antibiotics target harmful bacteria, they can also affect beneficial microbes, influencing the overall health of the intestinal lining. The intricate relationship between antibiotics and the gut underscores the importance of judicious antibiotic use and, when necessary, the simultaneous administration of probiotics to support a healthy gut environment. Proton Pump Inhibitors (PPIs) Proton Pump Inhibitors (PPIs), commonly prescribed for acid reflux and gastroesophageal reflux disease (GERD), reduce stomach acid production. Prolonged use of PPIs has been linked to changes in the small intestine, potentially impacting the structure and function of the villi. Individuals relying on PPIs for an extended period should collaborate with healthcare providers to assess the necessity of continued use and explore alternative approaches to manage acid-related conditions. Opioid Pain Medications Opioid pain medications, including morphine and oxycodone, are known for their analgesic properties but are also associated with side effects such as constipation. Chronic use of opioids may lead to intestinal issues, affecting the normal functioning of the small intestine. It is crucial for healthcare providers to carefully manage opioid prescriptions, considering the potential impact on the gastrointestinal tract, and to explore alternative pain management strategies whenever possible. Patients should communicate openly with their healthcare team about any digestive issues experienced during opioid therapy to ensure timely intervention and support. Conclusion In conclusion, the journey through conditions associated with villous atrophy extends far beyond the realms of celiac disease. This exploration has highlighted the intricate interplay of various factors that can impact the health of the small intestine, leading to structural changes in the form of villous atrophy. Recognizing these diverse contributors is pivotal for healthcare professionals navigating the complexities of gastrointestinal disorders. As we deepen our understanding of the nuanced manifestations of villous atrophy, we pave the way for improved diagnostic accuracy and tailored treatment strategies. The heterogeneity of conditions linked to villous atrophy underscores the need for a holistic and individualized approach to patient care, ensuring that the intricacies of each case are addressed with precision and empathy. Through continued research and clinical vigilance, we strive to unravel the mysteries of these conditions and enhance the well-being of individuals facing the challenges of villous atrophy. Further reading on the topic of other causes of villous atrophy: Not All That Flattens Villi Is Celiac Disease: A Review of Enteropathies -
Celiac.com 07/27/2011 - Based on associations made between microscopic colitis and celiac disease in scientific literature, but limited population-based data, a team of researchers set out to assess rates of microscopic colitis in celiac disease. The research team included M. Stewart, C. N. Andrews, S. Urbanski, P. L. Beck, and M. Storr. They were looking to better understand how these two diseases might be connected, and to identify any factors that might cause them to occur together. This led them to conduct a population-based review of all people diagnosed with celiac disease and microscopic colitis in a large Canadian medical center over a 5-year period. To do that, they searched endoscopy and pathology databases to find all diagnosis made for celiac disease and microscopic colitis within the Calgary Health Region between 2004 and 2008. To get accurate results, they made sure to standardize age and gender data from their study with 2006 Canadian Census data. They then used standardized incidence ratios (SIR) to figure out how often the two disease occur together. In the study population, they found, over a five-year period, 763 patients diagnosed with celiac disease, and 1106 diagnosed with microscopic colitis. In the general population, the standard rates of celiac disease ran from 10.4 to 15.7 per 100,000 people, while the standard rates of microscopic colitis ran from 16.9 to 26.2 per 100,000 people. The study team found 40 patients with both celiac disease and microscopic colitis, 21 of whom were females aged 40–60 years. In the celiac disease group, microscopic colitis occurred at an annual rate of 11.4 per 1000 cases of celiac disease with an overall SIR of 52.7. These findings showed a strong association between microscopic colitis and celiac disease. In fact, the diseases occurred together in the study population at rates of about 50-times those expected in the general population. One prominent finding was that middle-aged women suffered especially high rates of celiac disease together with microscopic colitis. Therefore, the team recommends that middle-aged women with celiac disease and persistent diarrhea undergo lower endoscopy with biopsies to check for microscopic colitis. Source: Alimentary Pharmacology & Therapeutics. 2011;33(12):1340-1349.
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Moving Toward Clinical Consensus on Microscopic Enteritis
Jefferson Adams posted an article in Latest Research
Celiac.com 04/20/2015 - Microscopic enteritis is an inflammatory condition of the small bowel that leads to gastrointestinal symptoms, nutrient and micronutrient deficiency. The idea of microscopic enteritis arose from mucosal changes associated with celiac disease and was originally described in detail by Marsh in 1992. Microscopic enteritis is marked by microscopic or sub-microscopic abnormalities such as microvillus changes and enterocytic alterations in the absence of definite macroscopic changes using standard modern endoscopy. A recent study addresses the need to characterize disorders with microscopic and submicroscopic features, currently regarded as functional or non-specific entities, to obtain further understanding of their clinical relevance. Following the 5th International Course in Digestive Pathology in Bucharest in November 2012, an international group of 21 interested pathologists and gastroenterologists formed a working party with a view to formulating a consensus statement on Microscopic enteritis. The research team included Kamran Rostami, David Aldulaimi, Geoffrey Holmes, Matt W. Johnson, Marie Robert, Amitabh Srivastava, Jean-François Fléjou, David S. Sanders, Umberto Volta, Mohammad H. Derakhshan, James J Going, Gabriel Becheanu, Carlo Catassi, Mihai Danciu, Luke Materacki, Kamran Ghafarzadegan, Sauid Ishaq, Mohammad Rostami-Nejad, A. Salvador Peña, Gabrio Bassotti, Michael N. Marsh, and Vincenzo Villanacci. The team reviewed statements about the etiology, diagnosis and symptoms associated with microscopic enteritis and proposes an algorithm for its investigation and treatment. They employed a five-step agreement scale (ranging from strong agreement to strong disagreement) to score 21 statements, independently. They found strong agreement on all statements about Microscopic enteritis histology (95%-100%). They found 85% to 100% agreement regarding statements concerning diagnosis, while agreement on a statement about the management of microscopic enteritis ranged from the 60% to 100%. They also found general agreement between experts on clinical presentation (75%-95%) and pathogenesis (80%-90%) of Microscopic enteritis. Lastly, they found strong agreement on the histological definition of Microscopic enteritis. The weaker agreement on management invites further studies, better definitions and clinical trials to produce quality guidelines for management. This microscopic enteritis consensus is a step toward greater recognition of a significant issue for symptomatic patients previously labelled as non-specific or functional enteropathy. Source: World J Gastroenterol. 2015 Mar 7; 21(9): 2593–2604. doi: 10.3748/wjg.v21.i9.2593. PMCID: PMC4351208 -
Celiac.com 04/27/2011 - People with microscopic enteritis have microscopic and sub-microscopic changes that are associated with symptoms of gluten sensitive enteropathy, and which lead to micronutrient deficiencies. A team of researchers recently set out to examine microscopic enteritis and the pathomechanism of malabsorption. The research team included Kamran Rostami, David Al Dulaimi, Mohammad Rostami Nejad, Vincenzo Villanacci, and Mihai Danciu. They are affiliated variously with the School of Medicine, University of Birmingham, UK, the Department of Gastroenterology, Alexander Hospital in Redditch, UK, the Nejad Research Center of Gastroenterology and Liver disease, Shaheed Beheshti University, M.C., in Tehran, Iran, the 2nd Department of Pathology, Spedali Civili, University of Brescia Italy, and the “Gr. T. Popa” University of Medicine and Pharmacy in Iasi, Romania. Signs of microscopic enteritis include subtle mucosal abnormalities with no pronounced inflammation, villous effacement, erosions or ulcerations when observed with conventional light microscopy. In cases of microscopic enteritis intraepithelial lymphocytes usually fall within the normal range <25/100 enterocytes (microenteropathy), or increased (lymphocytic enteritis). Microscopic enteritis is the driving force behind atypical forms of celiac disease, previously known as 'potential' and 'latent' celiac disease. Even when there are no major mucosal changes, systemic, microscopic inflammation is a key player in pathophysiology of micro-nutrient deficiency. Microscopic enteritis or celiac disease with milder, Marsh 0–II, enteropathy is the most common feature of atypical gluten sensitivity, while celiac disease with macroscopic enteritis, and Marsh IIa–c is less common. Importantly, and in contrast to much prevailing belief, symptom severity in celiac disease seems to be unrelated to the degrees or length of affected bowel. The microenteropathy may eventually develop into pronounced villous atrophy, but one interesting finding was that severe mucosal damage does not necessarily mean worse symptoms. People with mild symptoms can have more severe damage, while those with little or no visible damage can have more severe symptoms. The finding that nutritional deficiency can be seen in patients presenting with even submicroscopic enteropathy casts doubt on the notion that severe mucosal changes, such as villous atrophy, are the sole driver of malabsorption. In fact, more and more, systemic inflammation seems to be the main driver of nutritional deficiency in such cases. Pro-inflammatory cytokines, such as TNF, appear to act at the enterocyte level, inhibiting the uptake of micronutrients like iron and phosphate. From this, it appears that malabsorption in celiac disease is secondary to inflammation and cytokine stimulation. This might explain why some patients experience milder, 'atypical' enteropathy that acts just like full-blown celiac disease. In fact, inflammation triggered by gluten-sensitized lymphocytes and cytokine stimulation seems to drive the micronutrient deficiencies in celiac disease patients, with or without villous atrophy. This finding is supported by several studies that show malabsorption syndrome to be no worse in patients with villous atrophy than in those with microenteropathy (Marsh 0–II). This theory is further bolstered by the fact that many people suffer from non-symptomatic, silent celiac disease with villous atrophy, and mucosal lesions that persist after years of successful gluten-free treatment. Over the last few years, the only type of gluten sensitivity doctors have identified is atypical presentation with microenteropathy resulting in micronutrient deficiencies. However, the team points to recent studies by Kurppa et al., and Ludvigsson et al., that suggest simple changes can improve life quality for celiac disease patients with milder enteropathy. The researchers feel strongly that patients with milder enteropathy and positive serology may benefit from a gluten-free diet, and that autoantibodies might have a more reliable positive predictive value than histology, especially in early enteropathy. Diagnosing celiac disease in its early stages, especially with little or no mucosal damage, can be very challenging. However, new studies are paving the way toward a better understanding of gluten sensitivity with microenteropathy. As a result, more patients with microenteropathy, symptoms of micronutrient deficiency and positive serology are being presented with the possible benefits of a gluten-free diet. Source: Autoimmun Highlights (2010) 1:37–38. DOI 10.1007/s13317-010-0006-4
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