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Celiac Disease

Editor: Muhammad Haseeb Updated: 2/4/2025 3:25:03 PM

Introduction

Celiac disease is an autoimmune disorder triggered by an immune-mediated response of the small intestine to dietary gluten, which is a protein found in wheat, barley, and rye. Although traditionally viewed as a gastrointestinal condition primarily associated with malabsorption, it is now more accurately classified as an autoimmune disorder with systemic manifestations.[1] Celiac disease occurs in genetically predisposed individuals and results in a lifelong condition characterized by immune-mediated damage to the lining of the small intestine due to the immune response to gluten. This damage is evidenced by villous atrophy, crypt hyperplasia, and infiltration of the lamina propria by immune cells, which in turn leads to malabsorption of essential nutrients, including micronutrients, fat-soluble vitamins, iron, vitamin B12, and folate. Typical gastrointestinal symptoms include diarrhea, abdominal discomfort, bloating, and constipation. However, celiac disease can also present with extraintestinal manifestations such as fatigue, weight loss, skin rashes, anemia, and osteoporosis.[2] Growth failure is a frequent additional symptom in children with celiac disease (see Image. Intestinal Changes in Celiac Disease).

Detection of disease-specific antibodies, such as anti-tissue transglutaminase (tTG)–immunoglobulin A (IgA) or "tTG-IgA" and anti-endomysial antibodies (EMAs), is a key initial step in diagnosing suspected celiac disease. Most patients require a small intestinal biopsy to confirm the diagnosis and assess the extent of mucosal damage. The only effective treatment for celiac disease is the strict and complete exclusion of gluten from the diet, which involves lifelong adherence to a strict gluten-free diet (GFD). Maintaining a GFD is essential for symptom resolution and the prevention of long-term complications, with most patients responding well to this dietary modification.[3][4][5] Regular medical follow-up is necessary to monitor adherence and promptly identify and manage any disease-related complications.

Etiology

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Etiology

The etiology of celiac disease is multifactorial, involving a combination of genetic, environmental, and immunological factors. The primary genetic predisposition is associated with specific human leukocyte antigen (HLA) class II genes, particularly HLA-DQ2 and HLA-DQ8, which are found in nearly all individuals with celiac disease. However, genetics alone does not cause the condition, as many people with these genes never develop celiac disease.[6] 

The essential environmental trigger for celiac disease is dietary gluten, which is a protein found in wheat, barley, and rye, which induces a dysregulated immune response in susceptible individuals. Gluten is broken down into smaller peptides, such as gliadin, which are deamidated by the enzyme transglutaminase-2 (tTG2). This modification enhances their binding affinity to HLA-DQ2 and HLA-DQ8 molecules, triggering T-cell activation and an inflammatory response that leads to small intestinal enteropathy.[7] 

Epidemiology

Celiac disease affects approximately 1% of the global population. Serologic testing estimates its prevalence at 1.4%, while small intestinal biopsy, performed less frequently, indicates a prevalence of 0.7%. The occurrence varies by geographic region, with higher rates observed in populations of European descent, as well as in individuals from Saudi Arabia and the Saharawi, an ethnic group indigenous to the Western Sahara.[8] Women are diagnosed more frequently than men, possibly due to hormonal influences, genetic susceptibility, and a greater tendency to seek medical care for symptoms.[9]

Celiac disease is more prevalent among individuals with other autoimmune disorders, such as type-1 diabetes, with rates ranging from 1.6% to 16.4%, significantly higher than in the general population. This association is likely due to shared genetic susceptibility, particularly the HLA-DQ2 and HLA-DQ8 haplotypes, which are common in both celiac disease and various autoimmune conditions.[10] First-degree relatives of individuals with celiac disease have an increased prevalence of approximately 7.5%, with the highest risk seen in monozygotic twins (>70%), followed by siblings (8.9%), offspring (7.9%), and parents (3.0%).[11][12]

Pediatric patients are more likely to receive an earlier diagnosis than adults due to differences in clinical presentation. Children often exhibit classic signs of malabsorption, such as chronic diarrhea and growth failure, which prompt earlier evaluation. In contrast, adults frequently present with nonspecific symptoms, including abdominal pain, anemia, and chronic fatigue, leading to delayed diagnosis. Additionally, increased awareness and routine screening in pediatric populations facilitate earlier detection, whereas many adult cases go undiagnosed for extended periods.[13]

Adolescents transitioning from pediatric to adult care, no longer under parental supervision, may be less likely to adhere to treatment and miss follow-up appointments, leading to underreporting of the true prevalence of celiac disease in adults. Additionally, some patients diagnosed at a young age strictly follow dietary recommendations, become asymptomatic and seronegative, and no longer report having celiac disease. As celiac disease is a lifelong condition with no known cure, its true prevalence should be similar in children and adults. Reported differences likely reflect diagnostic disparities, underreporting, and suboptimal long-term medical follow-up.[14]

Pathophysiology

Celiac disease results from a combination of genetic, environmental, and immune factors that trigger an inappropriate immune response to dietary gluten found in wheat, barley, and rye. A key trigger is gliadin, a protein component of gluten, which has a central role in initiating the pathological process. During digestion, gluten is broken down into smaller peptides, including gliadin. In individuals with celiac disease, these peptides resist complete digestion and exhibit strong immunogenicity. They cross the intestinal epithelial barrier and enter the lamina propria, where tTG modifies them through deamidation. This modification enhances their ability to bind to HLA-DQ2 and HLA-DQ8 molecules on antigen-presenting cells (APCs).

The peptide-HLA complexes formed on APCs are then presented to circulating CD4+ T cells, which recognize them as harmful. This recognition triggers 3 key immune responses:

  • CD4+ T cells release pro-inflammatory cytokines, driving inflammation, crypt hyperplasia, and the destruction of intestinal villi, collectively resulting in enteropathy.
  • Stimulated B cells produce autoantibodies, such as tTG-IgA.
  • Cytotoxic CD8+ T cells are recruited to attack intestinal epithelial cells, exacerbating villous atrophy and disrupting the intestinal lining.[15][7]

Gliadin also increases intestinal permeability, allowing more peptides to pass through the intestinal barrier and interact with the immune system. This increased permeability, often referred to as "leaky gut," further exacerbates the abnormal inflammatory response in patients with celiac disease.[16] This inflammation not only impairs nutrient absorption but also contributes to the clinical manifestations of celiac disease, which extend beyond digestive symptoms to systemic health effects.

In healthy individuals, tTG remains harmless because it does not trigger an autoimmune response, and no tTG-IgA is produced. In contrast, in those with celiac disease, tTG activity is upregulated, generating deamidated gliadin peptides that APCs present to CD4+ T cells. However, only individuals with the genetic markers HLA-DQ2 or HLA-DQ8 can form these peptide-HLA complexes, a crucial step in initiating the autoimmune cascade.

Interestingly, many people carry HLA-DQ2 or HLA-DQ8 without ever developing celiac disease. Factors that might trigger gluten intolerance in genetically predisposed individuals include infections that alter immune responses, disruptions in the gut microbiome following antibiotic use, and physiological changes during pregnancy. Evidence suggests that certain infections, such as rotavirus and adenovirus, may predispose individuals to develop celiac disease, while others, like those caused by Helicobacter pylori, may offer protective effects.[1][17]

Most individuals with the HLA-DQ2 and HLA-DQ8 genes tolerate gluten like other food proteins despite their genetic susceptibility. The reason why only a minority develop celiac disease remains unclear, although non-HLA genetic factors and additional environmental triggers likely contribute. Further research is needed to understand these mechanisms better. In conclusion, celiac disease develops when genetically predisposed individuals consume dietary gluten, which triggers a pathological inflammatory response leading to characteristic intestinal damage and associated systemic signs and symptoms.[1]

Histopathology

The histopathology of celiac disease reflects an immune-mediated enteropathy of the small intestine (see Image. High Magnification Micrograph of Celiac Disease). A hallmark feature is villous atrophy, or the flattening of the intestinal villi, which reduces the surface area available for nutrient absorption. Crypt hyperplasia occurs as a compensatory response to villous atrophy; the depth and number of crypts at the base of the villi increase, indicating heightened cell turnover.

The villous-to-crypt (V:C) ratio in patients with celiac disease is reduced when villous atrophy and crypt hyperplasia are present. In untreated individuals, the V:C ratio is often less than 2:1, and can be as low as 1:1 or even lower in severe cases. In healthy individuals without celiac disease, the typical V:C ratio is approximately 3:1, with well-formed villi and appropriately sized crypts that facilitate optimal nutrient absorption.[18]

In addition, intraepithelial lymphocytosis reflects the inflammatory response to gliadin peptides, as intraepithelial lymphocytes, particularly CD8+ T cells, infiltrate the epithelial layer. Beneath the epithelium, the lamina propria also shows increased infiltration of immune cells, including T and B cells, as well as plasma cells.[19][20] Several studies have demonstrated that adherence to a GFD leads to significant histological improvement, with normalization of the V:C ratio in most children and substantial improvement in adults.[18]

History and Physical

Patients with celiac disease exhibit a broad spectrum of gastrointestinal and extraintestinal symptoms influenced by age and individual factors. Gastrointestinal symptoms arise from malabsorption due to villous atrophy in the small intestine, reducing the absorptive surface and digestive enzyme production. Extraintestinal manifestations result from the systemic effects of chronic inflammation and malabsorption.[11] Clinicians must consider both classical and atypical presentations to accurately diagnose celiac disease.

Gastrointestinal Symptoms

  • Adults: Hallmark symptoms include diarrhea and unexplained weight loss. Other common complaints include abdominal distension, bloating, discomfort, nausea, vomiting, steatorrhea, and constipation. 
  • Children: Key presenting symptoms include poor weight gain, which is often associated with decreased appetite, irritability, and diarrhea. Parents may also report a history of abdominal distension, vomiting, or constipation.

Extraintestinal Symptoms

  • Hematologic: Fatigue, pallor, and dyspnea in both adults and children may indicate anemia resulting from the malabsorption of iron, folate, and vitamin B12.
  • Neurologic: Adults may present with muscle weakness, paresthesias, ataxia, and chronic headaches. In children, some studies suggest an association between celiac disease and attention-deficit/hyperactivity disorder (ADHD) or developmental disorders, although evidence of causality remains inconclusive.[21]
  • Musculoskeletal: Both children and adults may experience arthralgias, myalgias, and bone pain. Adults may also have a history of fractures associated with osteopenia or osteoporosis.[22]
  • Growth and reproduction: Infertility and recurrent pregnancy loss have been linked to celiac disease, likely due to nutritional deficiencies and chronic inflammation. In children, short stature, dental enamel defects, and delayed puberty may result from malabsorption and subsequent malnutrition.[23]

Physical Examination Findings

Physical examination, in both children and adults, may reveal low weight with reduced muscle mass, abdominal distension or tenderness, muscle weakness, joint or bone tenderness, pallor from anemia, cheilosis or glossitis due to vitamin deficiencies, and skin rashes.[24] Dermatitis herpetiformis, an intensely pruritic vesicular rash, is pathognomonic for celiac disease and may indicate the diagnosis even in the absence of gastrointestinal symptoms.[25]

Clinicians must carefully identify both gastrointestinal and extraintestinal symptoms, along with key physical examination findings, to accurately diagnose and manage celiac disease in children and adults.

Evaluation

When the history and physical examination suggest celiac disease, the 2023 American College of Gastroenterology (ACG) guidelines recommend initial serologic testing with tTG-IgA in patients who are not IgA-deficient.[20] Testing should be conducted while the patient follows a gluten-containing diet for at least 6 to 8 weeks. If IgA deficiency has not been previously assessed, a total IgA measurement should be obtained simultaneously. In cases of confirmed IgA deficiency, IgG-based testing is recommended.

A negative tTG-IgA value has a high negative predictive value, particularly in patients without IgA deficiency and with a low-to-moderate pretest probability of celiac disease. In many cases, a negative tTG-IgA effectively rules out celiac disease. However, in patients with a high pretest probability, such as children with growth failure or adults with reproductive issues, the possibility of seronegative celiac disease or a false-negative result should be considered. Further evaluation with additional serologic tests or biopsies is warranted in such cases.[11]

EMA is an alternative serologic test that helps confirm celiac disease when tTG-IgA results are borderline or equivocal. A positive EMA may be considered diagnostic in children with high-level tTG-IgA (>10 times the upper limit of normal) if the family opts for a non-biopsy approach. However, EMA is not routinely used as an initial test due to its higher cost and labor-intensive process compared to tTG-IgA. EMA testing relies on indirect immunofluorescence, a technically demanding method with results that may vary based on observer interpretation.

The HLA-DQ2/HLA-DQ8 genetic test is another useful alternative, which is useful for individuals already following a GFD and unable or unwilling to consume gluten for several weeks before testing. A negative HLA testing rules out celiac disease with a high degree of certainty. However, as HLA-DQ2 and HLA-DQ8 are present in approximately 30% to 40% of the general population, their presence only indicates genetic susceptibility, not a definitive diagnosis. Additionally, this test is typically more expensive than tTG-IgA and EMA tests, and it may not be covered by medical insurance.[11]

If tTG-IgA level is elevated, the next step is esophagogastroduodenoscopy (EGD) with multiple duodenal biopsies in both children and adults to confirm the diagnosis of celiac disease. Guidelines recommend 1 or 2 biopsies from the duodenal bulb and 4 from the distal duodenum to reduce the risk of false-negative results. Characteristic histologic findings, such as villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis, confirm the diagnosis of celiac disease, particularly in seronegative or borderline cases. Additionally, small bowel biopsies can help identify non-celiac enteropathies or malabsorptive disorders, aiding in the exclusion of celiac disease.[26][27][28] For accurate biopsy results, the patient must consume a gluten-containing diet to ensure the histopathological features of celiac disease are detectable. The 2023 ACG guidelines strongly recommend EGD with biopsies for diagnostic confirmation but recognize that some children and adults may be unwilling or unable to undergo the procedure, offering alternative diagnostic approaches.[11]

Celiac disease screening is generally not recommended for asymptomatic individuals. However, testing should be considered for certain groups with increased risk factors, including a first-degree relative with celiac disease. Individuals with an affected parent, sibling, or child have a 10 to 15% higher risk of developing celiac disease. The condition is also strongly associated with autoimmune disorders, including type-1 diabetes, autoimmune thyroid disease, and autoimmune liver disease. Additionally, genetic conditions such as Down syndrome and Turner syndrome are also associated with an increased risk, and patients may benefit from screening for celiac disease.

Treatment / Management

The cornerstone of managing celiac disease is strict adherence to a GFD, which alleviates symptoms, promotes intestinal healing, and prevents long-term complications. Lifelong medical follow-up is essential to achieve treatment goals, including intestinal healing and, in children, normal growth and development. Most patients respond well to a GFD, with symptoms typically improving within days to weeks. A study involving 80% of patients experienced a reduction in diarrhea episodes within 60 days.[11][29]

Foods containing wheat, barley, and rye, which all contain gluten, are staples in many diets worldwide. Gluten-free grains include corn, rice, buckwheat, amaranth, quinoa, millet, and sorghum.[20] Patients must be educated on avoiding cross-contamination and identifying gluten in processed foods, medications, and supplements. In addition, it is crucial to check nutrition labels for "gluten-free" certification to ensure food safety. Specialists, particularly registered dietitians, play a vital role in helping patients understand how to effectively implement a GFD. Unresponsive individuals require an assessment of compliance, which may include repeat serology testing. Noncompliance can be either intentional or unintentional, as some people may unknowingly consume "hidden" gluten.[30][31] Conflicting reports exist regarding the safety of oat consumption for those with celiac disease.

Oats are generally considered non-immunogenic for people with celiac disease and are usually well tolerated. However, some studies have reported gastrointestinal symptoms in patients after consuming oats, possibly due to gluten contamination or an immunologic reaction to avenin, a protein found in oats. When uncontaminated, oats can add variety to a GFD and enhance dietary quality by increasing fiber and protein intake. The Academy of Nutrition and Dietetics supports the inclusion of oats, and long-term studies have confirmed their safety for people with celiac disease over extended periods.[32](A1)

Following a GFD imposes a significant burden on individuals with celiac disease and their families. GFD alternatives for staples such as bread, pasta, and wheat flour are often more expensive and may be perceived as less palatable.[33] Families must decide whether to adopt the GFD for everyone or only for the affected individual. The former can be cost-prohibitive, whereas the latter complicates meal preparation and may create a sense of isolation for the family member with celiac disease. Dining out adds another challenge, often requiring careful scrutiny of menus or inquiries about potential gluten in the food. Beer made from gluten-free grains such as sorghum, millet, rice, or buckwheat offers a safe alternative.[34] Nutritional support involves assessing patients for deficiencies in iron, calcium, folate, zinc, and vitamins D and B12. A gluten-free multivitamin can be beneficial for overall health. Lifelong follow-up includes regular bloodwork as clinically indicated, such as a complete blood count and testing for iron stores, ferritin, folate, and vitamin D and B12 levels. 

Additional monitoring should include assessing patients with risk factors for osteopenia or osteoporosis and ensuring sufficient calcium and vitamin D intake. Clinicians should consider screening for patients with celiac disease and other associated disorders, such as dermatitis herpetiformis and neuropathy. Patients with celiac disease may face psychosocial and mental health challenges, including anxiety and depression, which should be routinely addressed. Individualized care is essential, particularly for children and pregnant patients, with a focus on growth, development, and maternal-fetal health.

The ACG recommends regular monitoring of serologic markers to assess antibody levels, as declining values generally indicate adherence to a GFD and mucosal healing.[35] Routine re-biopsy is not advised due to a lack of evidence that it improves clinical outcomes. However, patients with persistent symptoms despite adherence to a GFD should undergo further evaluation, including follow-up small intestinal biopsies, to identify other inflammatory conditions or refractory celiac disease (RCD).[20]

Managing celiac disease requires lifelong adherence to a GFD, supported by ongoing medical follow-up to ensure nutritional adequacy, intestinal healing, and symptom resolution. Comprehensive care, including dietary education, psychosocial support, and monitoring for complications, is essential for improving quality of life and preventing long-term complications.

Differential Diagnosis

The differential diagnoses for celiac disease include various conditions that present with similar gastrointestinal or systemic symptoms, such as other enteropathies and malabsorptive disorders. A thorough history, physical examination, negative celiac-specific serologic markers, and small bowel biopsy results without villous atrophy or crypt hyperplasia help differentiate celiac disease from other disorders.

The differential diagnoses of celiac disease include:

  • Non-celiac gluten sensitivity presents with symptoms similar to celiac disease, and affected patients may respond to a GFD.
  • Irritable bowel syndrome is characterized by abdominal pain and cramping, diarrhea, constipation, and bloating. 
  • Inflammatory bowel disease, including Crohn disease and ulcerative colitis, can resemble celiac disease with symptoms such as abdominal discomfort, diarrhea, and weight loss.
  • Lactose intolerance, which may cause abdominal cramping, bloating, gas, and diarrhea, can occur in celiac disease due to villous atrophy but may also develop independently of celiac disease.
  • Small intestinal bacterial overgrowth, presenting with bloating, diarrhea, gas, nausea, fatigue, malabsorption, and unintended weight loss, may mimic celiac disease.
  • Food allergies or sensitivities, such as fructose intolerance, can cause symptoms such as bloating and diarrhea.
  • Autoimmune enteropathy is a rare and severe condition, which often presents with diarrhea and histopathologic findings similar to celiac disease.[36]
  • Tropical sprue, endemic to certain tropical regions, leads to malabsorption with villous atrophy on biopsy and responds to antibiotic treatment.
  • Giardiasis can cause diarrhea and malabsorption, with biopsy findings showing villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis. The presence of Giardia trophozoites on the surface of the villi helps distinguish it from celiac disease, ruling out celiac as the cause of the histologic findings.[37] 
  • Pancreatic insufficiency causes malabsorption and steatorrhea, which can mimic celiac disease.
  • Nonsteroidal anti-inflammatory drugs, olmesartan, chemotherapeutic agents, immunosuppressants, and antibiotics can induce enteropathy with villous atrophy. Symptoms include diarrhea, weight loss, and abdominal pain, with intestinal biopsy revealing various histologic findings consistent with enteropathy but not specifically celiac disease.[38]

The differential diagnoses in pediatric patients include cow milk protein allergy, gastroesophageal reflux disease, cystic fibrosis, and wheat allergy. These conditions also present with abdominal discomfort, signs of malabsorption, and poor growth.

Prognosis

With early diagnosis and strict adherence to a GFD, the prognosis for celiac disease is generally excellent. Most patients experience significant symptom relief within weeks to months, with mucosal healing typically occurring within 6 to 24 months, depending on the severity of intestinal damage at diagnosis. Long-term adherence to a GFD lowers the risk of complications, including malnutrition, osteoporosis, anemia, autoimmune disorders, and malignancies such as enteropathy-associated T-cell lymphoma.[35][39] However, the prognosis is less favorable for patients with RCD, which is characterized by persistent or recurrent symptoms and villous atrophy, despite adhering to a GFD for at least 6 to 12 months.

RCD is relatively rare, affecting approximately 1% of patients with celiac disease. Most cases are type-1, which typically has a better prognosis and may respond to treatments such as nutritional support, corticosteroids, and immunosuppressive therapies. However, individuals with RCD type-2 have a less favorable prognosis. Their intestinal biopsies show aberrant intraepithelial lymphocytes, which indicate a heightened risk of progression to enteropathy-associated T-cell lymphoma. Researchers are exploring therapies such as purine analogs, monoclonal antibodies, Janus kinase (JAK1/JAK3) inhibitors, and autologous stem cell transplantation. The 5-year survival rate for RCD type-2 is approximately 50%.[40] Regular follow-up is crucial to monitor dietary adherence, nutritional status, and related conditions, optimizing outcomes and enhancing quality of life. Early diagnosis and ongoing patient education are crucial in preventing complications and improving long-term prognosis.

Complications

Celiac disease can lead to various complications, as mentioned below, many of which can be prevented by adhering to a GFD.

  • Malabsorption and nutritional deficiencies may cause anemia, skeletal abnormalities, and an increased fracture risk due to osteoporosis in adults, as well as poor growth in children.
  • Celiac disease is also associated with a higher prevalence of gastrointestinal malignancies, including enteropathy-associated T-cell lymphoma and small intestinal adenocarcinoma.[41] 
  • Dermatitis herpetiformis is strongly linked to celiac disease and usually improves with a GFD.
  • Celiac disease is also associated with peripheral neuropathy, ataxia, and psychiatric conditions such as depression and anxiety.
  • Celiac disease can cause reproductive problems, including infertility and adverse pregnancy outcomes.[6][41][32]
  • Celiac disease increases the risk of pneumococcal infections, including sepsis and pneumonia, even with adherence to a GFD. The ACG guidelines recommend considering pneumococcal vaccination for all patients with celiac disease, particularly those who did not receive the complete pneumococcal vaccination series during childhood.[11]

Deterrence and Patient Education

Patient education is crucial for managing celiac disease and ensuring long-term adherence to a GFD. Clinicians should instruct patients and caregivers on identifying gluten-containing foods, reading food labels, and preventing cross-contamination during food preparation. They should also educate families about hidden sources of gluten in medications, supplements, and processed foods. Additionally, clinicians can direct patients to reputable GFD lists to help them make informed dietary choices and minimize the risk of unintentional gluten consumption. These lists, often provided by celiac disease advocacy organizations or food safety authorities, offer a comprehensive range of certified gluten-free or safe products for individuals with celiac disease.

Encouraging patients to rely on trusted sources ensures they have up-to-date and accurate information, promotes better dietary compliance, and reduces stress when making food choices. These resources can be invaluable for shopping or dining out, providing patients with the confidence to manage their condition. Collaboration with a registered dietitian offers personalized dietary guidance and helps patients navigate social and cultural challenges, such as dining out and traveling.

Clinicians should also address potential psychosocial impacts, such as feelings of isolation or anxiety, and provide resources for support groups and reliable information. Emphasizing the importance of strict adherence to the GFD is crucial to prevent complications and improve quality of life. Regular follow-up appointments should include reassessing dietary adherence, symptom management, and reinforcing education to ensure optimal outcomes.

Pearls and Other Issues

The ACG 2023 guidelines provide comprehensive recommendations for healthcare providers. Key facts to keep in mind regarding celiac disease include:

  • Initial screening should include testing for tTG-IgA. Healthcare providers should use IgG-based serologic testing for patients with IgA deficiency.
  • Small intestinal biopsy remains the gold standard for diagnosis, with multiple biopsies recommended, except in selected pediatric cases with elevated tTG-IgA levels and positive EMA.
  • The goal of GFD therapy is intestinal healing, and healthcare providers should set individualized goals for each patient.
  • Gluten-detection devices in food or biospecimens should be avoided due to their lack of standardization and clinical validation.
  • The use of probiotics lacks sufficient evidence to support routine use.
  • Incorporating gluten-free oats is considered safe and recommended to improve overall diet quality and diversity.
  • Patients should receive pneumococcal vaccination due to the increased risk of infections.
  • Case findings can enhance celiac disease detection in clinical practice. By implementing case finding, healthcare providers can identify at-risk patients who might otherwise remain undiagnosed, leading to earlier intervention and improved outcomes. However, mass screening for celiac disease in the community is not recommended.[11]

Enhancing Healthcare Team Outcomes

The interprofessional healthcare team plays a vital role in diagnosing, treating, and educating patients with celiac disease. Clinicians, including primary care providers and gastroenterologists, diagnose the condition through thorough clinical evaluation, serologic testing, and biopsy. Nurses contribute by providing patient education, offering support throughout the diagnostic process, and assisting with symptom management and follow-up care. School nurses ensure that gluten-free foods are available to students and educate teachers and cafeteria staff about the importance of preventing food sharing among children with celiac disease. Specialists, particularly registered dietitians, play a key role in helping patients understand how to implement a GFD. They provide personalized dietary guidance, addressing challenges such as food selection, label reading, and preventing cross-contamination to ensure strict adherence to the GFD.

Additionally, psychologists or counselors may assist in addressing the psychosocial aspects of living with a chronic condition, such as stress management, anxiety, and feelings of isolation. Social workers can help families reduce the financial burden of purchasing gluten-free foods by connecting them with resources, support programs, and financial assistance options as needed. Collaboration among healthcare professionals ensures comprehensive care, from accurate diagnosis to effective disease management and ongoing patient support, ultimately enhancing outcomes and quality of life for individuals with celiac disease.

Media


(Click Image to Enlarge)
<p>Intestinal Changes in Celiac Disease

Intestinal Changes in Celiac Disease. Histopathological features of celiac disease, highlighting mucosal damage and villous atrophy.

GeneFood


(Click Image to Enlarge)
<p>High Magnification Micrograph of Celiac Disease

High Magnification Micrograph of Celiac Disease. A very high magnification micrograph showing histopathological changes in celiac disease, stained with hematoxylin and eosin (H&E).

Nephron, Public Domain, via Wikimedia Commons 

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