Celiac disease (CeD) is a chronic small intestinal autoimmune disease initiated by dietary gluten in genetically predisposed individuals. Till date, the only effective treatment for CeD is the gluten-free diet (GFD). However, not all patients achieve full histological recovery despite GFD. Thus, it is crucial to assess the treatment response and improvement in the villous architecture following GFD. Therefore, present study investigated the potential of NMR-based metabolomics for identifying non-invasive biomarkers for assessing treatment response. Comprehensive metabolic profiling of 120 biological samples comprising of small intestinal mucosal biopsies, blood plasmas and urines collected at two time points (before and after 6-8 months of GFD) from CeD patients (n = 20) was carried out using proton NMR spectroscopy. The levels of arginine glutamate, and glutamine were significantly reduced in both intestinal mucosa and blood plasma of CeD patients after GFD compared to their baseline values. These amino acids play an important role in intestinal energy metabolism, and alleviating inflammation, thereby contributing to healing mechanisms of small intestinal mucosa, following GFD. A logistic regression statistical model based on the combination of the above three blood plasma metabolites demonstrated AUC of 0.980, Youden index 0.900 with a sensitivity and a specificity of 90 % and 100 % for monitoring treatment response in CeD patients after GFD. The study revealed a panel of non-invasive plasma biomarkers (arginine, glutamate and glutamine) which may serve as surrogates of mucosal healing and treatment response in CeD patients, however, the findings need to be validated in a large cohort of patients.

Celiac disease (CeD), triggered by gliadin exposure, necessitates therapeutic strategies that establish an antigen-specific immune tolerance. This study explores the therapeutic efficacy and mechanism of rapamycin-gliadin composite nanoparticles (PLN-GR) for CeD treatment. In vivo analyses demonstrated the efficient uptake of PLN-GR by antigen-presenting cells (APCs), particularly Kupffer cells and splenic dendritic cells (DCs), driving their tolerogenic phenotypic transformation. In a murine CeD model, PLN-GR administration significantly enhanced gluten tolerance and mitigated intestinal inflammation, as indicated by reduced paw edema and improved histopathological parameters. Mechanistically, PLN-GR induced macrophage metabolic reprogramming from glycolysis to oxidative phosphorylation, concomitant with elevated serum itaconate levels. This metabolic shift potentiated interorgan immunoregulatory crosstalk, expanding PD-L1+ tolerogenic splenic DCs while suppressing pathogenic Th1 cell populations. Bone marrow-derived macrophages (BMDMs) from Acod1-/- mice (deficient in itaconate synthesis) failed to induce DC tolerance upon PLN-GR treatment. However, supplementation with the itaconate derivative 4-octyl itaconate (4-OI) restored PD-L1 expression in DC2.4 cells in vitro, revealing that itaconate induces and stabilizes the tolerant DC phenotype. These findings underscore PLN-GR as a novel nanotherapeutic platform for CeD, achieving gliadin-specific tolerance through hepatic-splenic immunometabolic reprogramming and itaconate-dependent PD-L1 regulation, thereby offering a translatable strategy for autoimmune disease management.

The etiology of bone loss in celiac disease (CeD) remains a clinical challenge, with uncertainties present such as the extent of involvement of malabsorption and inflammation-induced osteoresorption processes in development of osteopenia/osteoporosis (OPN/OP), or reasons for failure to achieve healthy bone mass (BMD) even after long-term gluten-free diet (GFD) treatment. This observational prospective study explores the in vitro osteoclastogenic potential of peripheral blood precursors originating from adult active (newly diagnosed and untreated) celiac disease patients (aCeD) and describes the longitudinal changes in osteoclastogenesis after long-term adherence to GFD. To find connections between in vitro observations and in vivo bone metabolism changes, serum levels of 25(OH)D3, PTH, bCTX, PINP, CRP, IL-6, RANKL and OPG were measured before and after GFD and levels of these markers were correlated with the rate of osteoclastogenesis in vitro. OPG and IL-6 showed associations with BMD and/or presence of OPN/OP. Patients after GFD (CeD-GFD) exhibited improved BMD and increased serum 25(OH)D3 levels, alongside reduced bCTX and PINP levels. Compared to healthy donors, aCeD osteoclast genesis in vitro was higher and, surprisingly, remained elevated even in CeD-GFD patients. Negative correlation was found between osteoclastogenesis rate and serum OPG in aCeD, while osteoclastogenesis rate positively correlated with PTH in CeD-GFD. These results highlight OPG as marker for risk of OPN/OP in CeD and suggest that improvement of BMD after GFD is a result of uncoupling between bone metabolism and osteoresorptive action of osteoclasts after GFD.

Optimal detection of eosinophilic esophagitis (EoE) and celiac disease (CeD) requires appropriate sampling of the upper gastrointestinal tract during endoscopy. However, endoscopic biopsy guidelines are poorly followed in clinical practice. A quality improvement (QI) initiative was undertaken to improve adherence to published EoE and CeD biopsy guidelines by creating standardized biopsy protocols.

A biopsy form with disease-specific biopsy protocols was created and implemented. Endoscopists were initially asked to complete the form pre-procedure to indicate anticipated biopsies. After integration into the electronic health records (EHR), the form was completed by the primary treating clinician at the time endoscopy was requested. Data were collected through chart review of endoscopy and pathology reports. Statistical process control charts were used to analyze these metrics: adherence to biopsy guidelines (outcome measure), biopsy form utilization (process measure), and immediate and delayed procedural complications (balancing measures). Baseline adherence to biopsy guidelines was determined by retrospective chart review of upper endoscopies performed pre-intervention.

Overall adherence to biopsy guidelines improved from an average of 45% to 78.9% with our interventions. Improvement was sustained during the 2-year study period. Adherence to biopsy guidelines improved from an average of 55% to 84% for EoE and from 13.3% to 69.5% for CeD. Decreased variability in biopsy practice was noted over time. The EHR-integrated form led to consistently high utilization (>90%). Both immediate and delayed complications remained zero.

Standardization of endoscopic biopsies using an EHR-integrated pre-procedure checklist leads to improved and sustained adherence to recommended EoE and CeD biopsy guidelines.

Celiac disease and food-allergy are both food-related chronic immune disorders with a common pathogenic link being breakdown in the gut tolerance to otherwise innocuous food antigens. Notwithstanding the similarities, there are significant differences in the pathogenesis of both disorders, which translates to variations in clinical presentations, diagnostic tools and disease epidemiology. The past few decades have witnessed a global increase in prevalence and incidence of both disorders, driven both by true rise due to epidemiological factors and unmasking of previously undiagnosed disease due to better diagnostics and health seeking behavior, related to economic factors. Worldwide as more cases are diagnosed, disparities in healthcare and resources available for disease management are increasingly becoming more relevant but are infrequently discussed. In this review we will discuss the global epidemiology of celiac disease and food allergy, their epidemiological risk factors and future directions for their improved diagnosis and management.

Celiac crisis (CC) is a rare but potentially life-threatening complication of celiac disease (CD), characterized by severe diarrhea, electrolyte imbalances, and metabolic disturbances. We report the case of a 32-year-old pregnant woman presented significant dehydration, weight loss, and steatorrheic stools. Diagnosis was confirmed by duodenal biopsy, with rapid improvement following a gluten-free diet (GFD) and corticosteroids. The diagnosis of CC was established based on the acute clinical presentation and rapid improvement following a GFD and corticosteroid therapy. This case highlights the importance of early recognition and prompt management of CC, particularly in undiagnosed or untreated CD, to prevent severe maternal and fetal complications.

BACKGROUND Multiple autoimmune syndromes are caused by immune dysregulation pathways and shared genetic polymorphisms, resulting in the coexistence of multiple autoimmune disorders. Systemic sclerosis (SSc) and systemic lupus erythematosus (SLE) are connective tissue diseases with distinct pathogenesis. Celiac disease (CD) is an immune-mediated small intestine pathology. Previous case reports have documented the coexistence of SLE and CD, SSc and CD, and SSc and SLE (overlap syndrome). CASE REPORT A 21-year-old woman with juvenile SSc and interstitial lung disease was admitted with fever, cough, and ongoing lower abdominal pain, diarrhea, and weight loss for the previous 3 months. Laboratory investigations revealed leukopenia, normocytic normochromic anemia, and thrombocytopenia, with positive antinuclear antibody and anti-double-stranded DNA. SLE was diagnosed, and the patient was started on a steroid and hydroxychloroquine. Celiac serology was ordered, followed by an upper gastrointestinal endoscopy, with biopsy. The results of both tests indicated CD. The patient was advised to follow a gluten-free diet and was started on hydroxychloroquine, mycophenolate mofetil, and prednisolone. CONCLUSIONS Our patient's presentation of CD and SLE occurring 9 years after SSc onset is unique. Individuals with one autoimmune disease have approximately a 25% chance of developing another. Limited case reports discuss CD in patients with SSc and the association between CD and SLE. To the best of our knowledge, no prior reports documented the coexistence of SSc, SLE, and CD. This case report underscores the importance of investigating autoimmune syndromes based on clinical presentation, as rare associations can occur.

Duodenal involvement in celiac disease (CD) can be patchy, with a subset of patients demonstrating histopathological involvement limited to the bulb. This study evaluates whether bulb-restricted CD represents a distinct subgroup associated with lower titers of immunoglobulin A anti-tissue transglutaminase antibody (TTG-IgA) compared to distal duodenal CD in pediatric patients. Additionally, we assess the impact of a no-biopsy approach for pediatric CD with TTG-IgA ≥10 times the upper limit of normal (TTG-IgA ≥10× ULN) on the relative frequency of bulb-restricted CD among biopsied patients.

Incident pediatric CD cases were identified retrospectively between 2017 and 2022. A no-biopsy approach for TTG-IgA ≥10× ULN was locally implemented in 2020. Serum TTG-IgA was categorized as negative, equivocal, positive TTG-IgA <10× ULN, and positive TTG-IgA≥ 10× ULN. Biopsies were classified by Marsh score and site of involvement.

Of the 405 cases included (mean age = 9.6 years, female-to-male ratio = 2.1:1), bulb-restricted CD was present in 7.4%. TTG-IgA was negative or equivocal in 60.0% of bulb-restricted CD, compared to 5.3% of distal duodenal CD (odds ratio [OR] = 26.6; 95% confidence interval [CI] = [11.1-63.3], p < 0.001). Notably, no bulb-restricted CD cases attained TTG-IgA ≥10× ULN, compared to 48.5% of distal duodenal CD. Following local implementation of the no-biopsy approach for TTG-IgA ≥10× ULN, the relative percentage of bulb-restricted CD significantly increased from 4.6% to 12.4% (OR = 2.9, 95% CI = [1.4-6.4], p = 0.004).

Pediatric CD with isolated bulb pathology presents with lower serum TTG-IgA titers than cases with distal duodenal involvement. Implementation of the no-biopsy approach increased the relative proportion of bulb-limited CD, as these cases were not associated with TTG-IgA ≥10× ULN.

Coeliac disease (CD) is an autoimmune disorder treated with a gluten-free diet (GFD), requiring substantial changes in food choices and eating habits. This study explores the challenges faced by adults living with CD focusing on the theme of food literacy (FL), namely functional, relational, and system FL competencies.

A secondary analysis of data obtained through an online questionnaire was conducted. Adults living with CD in Québec, Canada and subscribed to Coeliaque Québec's newsletter were invited to complete a questionnaire. Using the critical incident method, respondents described a negative experience in their journey living with CD. Content analysis was done in a deductive and inductive manner, based on the 2022 Slater Food Literacy framework adapted to CD.

A total of 743 patients were included in the analysis. The qualitative analysis resulted in 11 codes under the three themes of FL. Patients reported challenges in finding reliable nutrition and medical information, managing a GFD in social settings, explaining CD and preventing gluten contamination, preparing balanced gluten-free (GF) meals, and making informed food choices. Patients reported on the negative impact of the GFD on their relationship with food, and how CD inhibits conviviality. Finally, patients addressed the need to advocate for GF food access in grocery stores and restaurants.

This study highlights the broad impacts of effectively managing CD and the GFD on patients' functional, relational and system FL competencies. Future research should explore how social and economic factors further interact with FL competencies of adults living with CD.

Autoimmune thyroid diseases (ATD) are the most prevalent autoimmune disorders associated with celiac disease (CD). Both conditions can often be detected through serological screening in asymptomatic patients over several years. Various guidelines for screening thyroid disease (TD) are available in children with CD and vice versa.

We conducted a systematic review to identify the most recent and relevant guidelines, comparing their recommendations to analyze key differences and suggesting a practical clinical approach.

Out of 1,294 articles reviewed, we identified 20 guidelines published between January 2013 and January 2024. These guidelines, primarily from gastroenterological organizations in Europe and North America, recommend different timings and methods for screening the co-occurrence of these diseases, both at diagnosis and during follow up. Some guidelines recommend only clinical follow-up without routine serological screening. There is limited consensus on screening for TD [using thyroid-stimulating hormone test (TSH)] in asymptomatic children newly diagnosed with CD, and even less agreement on screening for CD [using anti-transglutaminase antibodies (tTG) immunoglobulin A (IgA) test and total IgA] in children newly diagnosed with TD. No standardized procedures exist for managing patients with isolated low tTG and human leukocyte antigen (HLA) genotyping is rarely recommended as a first- line screening method.

Over the past decade, there has been a growing recognition of the importance of identifying children with co-occurrence of CD and TD who could benefit from early treatment, even in the absence of symptoms. However, international guidelines still show a lack of consensus regarding screening for these frequently associated autoimmune diseases, with notable differences in the use of HLA testing and follow-up protocols.

Coeliac crisis (CC) is a rare, potentially life-threatening manifestation of coeliac disease (CD).

To comprehensively explore the clinical aspects, management strategies, and outcomes related to CC in both adult and paediatric populations.

We conducted a comprehensive literature search to identify studies eligible for inclusion up to 28 December 2024. The study protocol was registered in PROSPERO (CRD42024510682).

A total of 46 included articles and 195 patients were analyzed. The median age of presentation was 18 years (range: 8 months to 83 years), predominantly affecting the paediatric population. An overwhelming majority (180 patients, 92.8 %) had CC as their first presentation, whereas the others were previously diagnosed CD cases with poor adherence to gluten-free diet (GFD). Clinically, patients presented with diarrhoea (88.2 %), abdominal pain (72.8 %), vomiting (56.4 %), confusion and lethargy (11.3 %). Electrolyte derangements in the form of hypokalemia (89.7 %) and hyponatremia (64.1 %), along with metabolic acidosis (79.5 %) and hypoalbuminemia (76.9 %), reflected the severity of malabsorption. Treatment with GFD caused clinical improvement in 186 (95.4 %) patients and mostly favourable long-term outcomes.

CC is a poorly understood, life-threatening complication of CD. Given its similarity with infectious conditions, clinicians require a high index of suspicion for recognizing CC to diagnose early and provide proper management.

Celiac disease is defined as a systemic immunological disorder caused by gluten (gliadin and other prolamin) in genetically predisposed individuals, who present with a variety of gluten-dependent symptoms, specific antibodies, the presence of the HLA DQ2 and DQ8 histocompatibility antigen, and enteropathy. Its prevalence, depending on the studied population and methodology, is estimated at 0.75-1.6% of the general population. During the complex immune reaction it induces, most cells involved in inflammatory processes are activated, which leads to the gradual atrophy of intestinal villi and the proliferation of enterocytes within intestinal crypts. The pathogenesis of celiac disease is extremely complicated and is still the subject of research. According to the current diagnostic guidelines, the following criteria should be taken into account: clinical symptoms (intestinal and extraintestinal), the presence of antibodies against tissue transglutaminase in the IgA class, the level of total IgA, and the presence of typical histological changes in duodenal biopsies. Diet-resistant celiac disease is one of the most important clinical challenges, causing serious complications. Currently, the basic method for treating celiac disease is an elimination diet (i.e., the exclusion of products that may contain gluten from the diet), however, new therapeutic strategies are still being sought, mainly based on supplementation with exogenous endopeptidases, modification of the immune response, and the use of zonulin inhibitors and transglutaminase 2 inhibitors. Clinical trials of new drugs are ongoing. The gradually expanding knowledge about the pathogenesis of celiac disease may allow for the development of new therapeutic strategies for both patients with a mild disease course, as well as those that are diet-resistant.

A large proportion of individuals with coeliac disease (CeD) remain undiagnosed.

The aim of this study was to assess serological screening for CeD in the adult general population.

The study was based on the fourth Trøndelag Health Study, a population-based study performed 2017-2019 in Nord-Trøndelag County, Norway, including 56 042 participants >20 years of age (54% participation rate). Serum samples were analysed with a dual antitransglutaminase 2 (TG2) IgA and IgG assay and seropositive participants were invited to endoscopy with duodenal biopsies. A CeD diagnosis was given if mucosal damage (Marsh grade 3) was found.

Histological evaluation of 657 seropositive participants confirmed CeD in 423. The positive predictive value (PPV) of a positive TG2 IgA was 73.3% (95% CI 69.7% to 77.0%) for biopsy-confirmed CeD. TG2 IgA ≥10 times the upper limit of normal (ULN), as used in the no-biopsy approach in children, increased the PPV to 88.1% (95% CI 84.8% to 91.4%). Primary TG2 IgG response was found in 87 participants, five of whom had biopsy-confirmed CeD. One of the participants with CeD primarily responding with TG2 IgG was IgA deficient. The PPV of a positive TG2 IgG was 5.8% (95% CI 1.9% to 12.9%) and of TG2 IgG ≥10× ULN was 9.5% (95% CI 1.2% to 30.4%) for biopsy-confirmed CeD in TG2 IgA-negative individuals.

The TG2 IgA assay showed excellent abilities as a screening tool for CeD in the adult general population. However, the diagnostic accuracy of TG2 IgG was too poor for selectively identifying individuals with CeD.

Diagnosis of coeliac disease (CD) with mild mucosal changes is difficult for all parties involved. We aimed to determine the power of T cell receptor (TCR)γδ+ intra-epithelial lymphocytes (IELs) in discriminating CD from other causes of intra-epithelial lymphocytosis using a new monoclonal antibody.

A total of 167 cases categorised as coeliac (117 untreated CD, classified according to Marsh, updated by Ensari, including 29 type 1, 29 type 2, 39 type 3 and 20 treated CD), and non-coeliac groups (24 controls and 26 non-coeliac IELosis) based on clinical, serological and histological data were studied for IEL counts enumerated per 100 enterocytes using haematoxylin and eosin, CD3, TCR δ-stains.

TCRγδ+ IELs were significantly higher in CD (24.83 ± 16.13) compared to non-CD (6.72 ± 6.32) and were correlated with the degree of mucosal damage. Both γδ+ IEL count and ratio showed higher performance in differentiating untreated coeliacs from controls, with a sensitivity of 83.76; 85.57 and specificity of 95.83; 79.17, respectively. TCRγδ+ IEL counts distinguished type 1 CD (20.41 ± 13.57) from non-coeliac IELosis (9.42 ± 7.28) (p = 0.025). Discriminant analysis revealed that villus/crypt ratio, γδ+ and CD3+ IEL counts, γδ+/CD3+IEL ratio, IEL distribution pattern were potent discriminants and correctly classified 82.3% of cases while the algorithm accurately diagnosed 93.4% of cases.

The new antibody detecting γδ+ IELs in FFPE sections revealed thresholds of 10.5 for γδ+ IELs and 14% for γδ+/CD3+IEL ratio which distinguished coeliacs from non-coeliacs with high sensitivity and specificity, particularly in cases with normal villus/crypt axis including type 1 CD, non-CD IELosis and controls. A 'coeliac algorithm' based on γδ+ IELs is proposed with the hope that it will be used in the histopathological diagnostic approach by the pathology community.

To characterize the frequency and predictors of follow-up endoscopic biopsy in patients with celiac disease.

The utility of routine follow-up biopsy in patients after a diagnosis of celiac disease is uncertain, especially in patients whose symptoms resolve on the gluten-free diet.

Using the Merative MarketScan U.S. commercial insurance and Medicare databases, we identified 30,737 patients with biopsy-diagnosed celiac disease. We followed them until they had a second duodenal biopsy (our primary outcome) or insurance coverage ended.

Among the patients with celiac disease we identified, 5976 (19.4%) underwent a follow-up biopsy. The median time between initial and follow-up biopsies was 16.8 months. Compared with younger patients, those aged 20 years or older had an increased likelihood of undergoing a follow-up biopsy (cumulative incidence rate at 5 y for patients age ≥20 y was 36.0%, 95% CI: 35.0%-37.1% vs 21.9%, 95% CI: 20.5%-23.4% in patients age ≤19 y). Follow-up biopsies occurred less frequently in more recent calendar years. Follow-up biopsy was more common among patients with an Elixhauser Comorbidity Index of 1 (hazard ratio: 1.09; 95% CI: 1.01-1.17) or ≥2 (hazard ratio: 1.28; 95% CI: 1.20-1.37) compared with patients with an index of zero. Among patients who had a follow-up biopsy, 57% had a celiac disease-related symptom recorded in the 30 days before the procedure.

Follow-up duodenal biopsy is performed in a substantial minority of U.S. patients with celiac disease. Adult age and increased comorbidity burden were associated with a greater likelihood of follow-up biopsy. Just under half of follow-up biopsies are performed for routine surveillance, in the absence of persistent symptoms.

Celiac disease is a chronic inflammatory condition of the small bowel caused, in genetically predisposed subjects, by the ingestion of gluten and characterised by a broad clinical polymorphism, ranging from patients with an asymptomatic or paucisymptomatic disease. The clinical presentation ranges from the presence of minor, apparently unrelated symptoms or first-degree kinship with known patients to severe intestinal malabsorption and all its clinical consequences and complications. Even if a large body of research improved our understanding of the molecular basis of celiac disease pathophysiology, enhancing the identification of new targets for future new treatments, an accurate gluten-free diet remains the mainstay of the therapy for this condition, restoring a normal absorptive mucosa. It is very rare, nowadays, to deal with patients with severe malabsorption syndrome secondary to celiac disease. Consequently, physicians are currently less prone to search for nutritional deficiencies in celiac disease. To pinpoint the possibility of both a disease-related and a diet-induced vitamin deficiency, we reviewed the literature on vitamin deficiency in this condition and reported the impact both in untreated and treated patients with celiac disease. A gluten-free diet must be tailored for each patient to meet nutritional targets: the pre-existence or diet-induced intake inadequacies should be carefully considered for an effective management of celiac disease.

Celiac disease is attributable to a combination of genetic predisposition and exposure to dietary gluten, with immune system involvement. The incidence is increasing globally, and the societal economic burden of celiac disease stretches beyond the cost of gluten-free food. This enteropathy that affects the small intestine has been related to different disorders and comorbidities. Thus, the implications of suffering from this disease are multidimensional and need further consideration. Celiac disease is a serious condition that remains under-recognized, resulting in an increased need for programs for better management. This review aims to summarize the current evidence regarding celiac diseases, with special emphasis on clinical implications, diagnosis, dietary management, socioeconomical aspects, and future perspectives.

The interplay between fatty acids (FAs) and celiac disease (CD) is a burgeoning field of research with significant implications for understanding the pathophysiology and potential therapeutic avenues for this autoimmune disorder. CD, triggered by gluten consumption in susceptible individuals, presents with a range of intestinal and extra-intestinal symptoms impacting various bodily functions. The disruption of intestinal tight junctions (TJs) by gluten proteins leads to increased gut permeability and subsequent inflammatory responses mediated by T-cells. FAs, crucial components of cell membranes, play diverse roles in inflammation and immune regulation. In fact, FAs have been shown to modulate inflammatory processes through various mechanisms. Studies have highlighted alterations in FA profiles in individuals with CD, indicating potential implications for disease pathogenesis and micronutrient deficiencies. Moreover, the exploration of FAs as biomarkers for CD diagnosis offers promising avenues for future research and therapeutic interventions. Understanding the intricate relationship between FAs and CD could lead to novel approaches in managing this complex autoimmune disorder. Therefore, this review article aims to provide an overview of the connection between FAs and inflammation in CD.

This study aimed to characterize micronutrient deficiencies, including iron, ferritin, folic acid, vitamin D, zinc (Zn), vitamin B12, and copper, in patients with celiac disease, and evaluated the effects of these deficiencies on selected hematological parameters, including hemoglobin and mean corpuscular volume (MCV). Celiac disease (CeD), an immune-mediated disorder affecting the small bowel, is associated with genetic factors and micronutrient deficiencies. This meta-analysis was performed in accordance with the PRISMA guidelines. Literature searches of multiple databases retrieved 4140 studies, of which 45 were selected. Risk of Bias was performed in accordance with the STROBE checklist. Meta-analysis revealed a significant difference in hemoglobin levels between patients with CeD and controls (standardized mean difference (SMD) -0.59 (95% confidence interval (CI) -0.8459 to -0.3382); P = 0.0003). Iron levels were lower in patients with CeD (SMD ≈ -0.4 (95% CI -0.7385 to -0.0407); P = 0.0334), as were ferritin (SMD -0.6358 (95% CI -0.8962 to -0.3755); P = 0.0002), folic acid (SMD -0.5446 (95% CI -0.9749 to -0.1142); P = 0.0187), and vitamin D (SMD -0.4011 (95% CI -0.8020 to -0.0001); P = 0.0499) levels, while Zn levels were significantly reduced (SMD -1.1398 (95% CI -2.0712 to -0.2084); P = 0.0242). No significant differences were found in MCV, or copper or vitamin B12 levels between patients with CeD and controls. This study highlighted significantly higher micronutrient deficiencies in patients diagnosed with CeD than in controls, underscoring the importance of systematic nutritional assessment and multidisciplinary management to address micronutrient deficiencies and minimize negative health impact(s).

The American Diabetes Association (ADA) "Standards of Care in Diabetes" includes the ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, an interprofessional expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations and a full list of Professional Practice Committee members, please refer to Introduction and Methodology. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

Celiac disease is a chronic, immune-mediated enteropathy with symptoms triggered by exposure to dietary gluten in genetically predisposed individuals. The only available management option is lifelong adherence to a gluten-free diet. This randomized, double-blind, placebo-controlled, parallel-group, single-center study tested the effects of the cathepsin S inhibitor RO5459072 on the immune response to a 13-day gluten challenge in 19 participants with celiac disease (ClinicalTrials.gov: NCT02679014). Nine participants in the RO5459072 arm received 100 mg study drug b.i.d. (200 mg daily); 10 received a placebo. The primary end point was the number of responders to the gluten challenge (defined as individuals with an increase in the number of gliadin-specific, IFNγ-secreting T cells detected using an ELISPOT assay). However, there was a weak response to the gluten challenge across both arms. Few participants had an increase in gliadin-specific, IFNγ-secreting T cells, and the antigen-specific responses (anti-tTG and anti-DGP antibodies) were weaker than expected in both arms. Therefore, the primary end point was not met, although the study was underpowered to detect a treatment effect under these circumstances. Pharmacodynamic findings suggested that RO5459072 had some beneficial effects. Fewer participants in the RO5459072 arm exhibited gliadin-specific IFNγ-secreting T cells after 6 days' gluten intake. Participants in the RO5459072 arm also showed decreased intestinal permeability, and a decrease in the number of circulating B cells, CD4+ and CD8+ T cells compared to baseline. Nevertheless, the absence of clear effects on the response to a gluten challenge indicates that inhibition of cathepsin S may not be an effective treatment strategy for celiac disease.

Currently, the main treatment for celiac disease (CD) is the gluten-free diet (GFD). This observational cohort study investigated the impact of CD and 1 year of GFD on gut function and microbiome.

A total of 36 newly diagnosed patients and 36 healthy volunteers (HVs) were studied at baseline and at 12-month follow-up. Small bowel water content (SBWC), whole gut transit time (WGTT), and colon volumes were measured by magnetic resonance imaging. Stool sample DNA was subjected to shotgun metagenomic sequencing. Species-level abundances and gene functions, including CAZymes (carbohydrate active enzymes) were determined.

SBWC was significantly higher in people with CD (157 ± 15 mL) vs (HVs 100 ± 12 mL) (P = .003). WGTT was delayed in people with CD (68 ± 8 hours) vs HVs (41 ± 5 hours) (P = .002). The differences reduced after 12 months of GFD but not significantly. Well-being in the CD group significantly improved after GFD but did not recover to control values. CD fecal microbiota showed a high abundance of proteolytic gene functions, associated with Escherichia coli, Enterobacter, and Peptostreptococcus. GFD significantly reduced Bifidobacteria and increased Blautia wexlerae. Microbiome composition correlated positively with WGTT, colonic volume, and Akkermansia municphilia but negatively with B wexerelae. Following GFD, the reduction in WGTT and colonic volume was significantly associated with increased abundance of B wexlerae. There were also significant alterations in CAZyme profiles, specifically starch- and arabinoxylan-degrading families.

CD impacted gut function and microbiota. GFD ameliorated but did not reverse these effects, significantly reducing Bifidobacteria associated with reduced intake of resistant starch and arabinoxylan from wheat.

gov, number: NCT02551289.

Histological assessment is essential for the diagnosis and management of celiac disease. Current scoring systems, including modified Marsh (Marsh-Oberhuber) score, lack inter-pathologist agreement. To address this unmet need, we aimed to develop a fully automated, quantitative approach for histology characterisation of celiac disease. Convolutional neural network models were trained using pathologist annotations of hematoxylin and eosin-stained biopsies of celiac disease mucosa and normal duodenum to identify cells, tissue and artifact regions. Biopsies of duodenal mucosa of varying celiac disease severity, and normal duodenum were collected from a large central laboratory. Celiac disease slides (N = 318) were split into training (n = 230; 72.3%), validation (n = 60; 18.9%) and test (n = 28; 8.8%) datasets. Normal duodenum slides (N = 58) were similarly divided into training (n = 40; 69.0%), validation (n = 12; 20.7%) and test (n = 6; 10.3%) datasets. Human interpretable features were extracted and the strength of their correlation with Marsh scores were calculated using Spearman rank correlations. Our model identified cells, tissue regions and artifacts, including distinguishing intraepithelial lymphocytes and differentiating villous epithelium from crypt epithelium. Proportional area measurements representing villous atrophy negatively correlated with Marsh scores (r =  - 0.79), while measurements indicative of crypt hyperplasia positively correlated (r = 0.71). Furthermore, features distinguishing celiac disease from normal duodenum were identified. Our novel model provides an explainable and fully automated approach for histology characterisation of celiac disease that correlates with modified Marsh scores, potentially facilitating diagnosis, prognosis, clinical trials and treatment response monitoring.

For patients with celiac disease (CeD), the only current management option is adherence to a strict gluten-free diet (GFD); however, many patients on a GFD continue to experience symptoms with a significant impact on quality of life. Potential new treatments for CeD are under development and a validated patient-reported outcome measure is required to evaluate their utility in clinical trials. The purpose of this article is to provide a history of the development of the Celiac Disease Symptom Diary (CDSD) 2.1© for use in clinical trials.

Qualitative and quantitative studies were conducted from 2010 to 2021, including concept elicitation and cognitive debriefing interviews with adult and adolescent participants with CeD (N = 93) diagnosed via biopsy and/or serology and input from eight interviews with CeD clinical experts. During these studies, different iterations of the CDSD were presented to the US Food and Drug Administration and the European Medicines Agency, and modifications were made in line with their feedback.

These studies ultimately led to the development of CDSD 2.1©, a daily diary which focuses on key symptoms of CeD (abdominal pain, bloating, diarrhea, nausea and tiredness). This patient-reported outcome measure was readily understood by adult and adolescent participants with CeD and content validity was demonstrated in both populations.

CDSD 2.1© is a content-valid patient-reported outcome measure developed in accordance with best practices and regulatory guidance. A thorough exploration of the psychometric properties of CDSD 2.1© for both adult and adolescent participants with CeD is ongoing to support utilization in clinical trials.

This paper aims to provide a comprehensive overview of the pathophysiology of atrial fibrillation (AF) and celiac disease (CD) individually while also exploring the emerging evidence of a potential association between the two conditions.

The pathophysiology of AF, the most prevalent arrhythmia globally, and CD, an autoimmune condition triggered by gluten consumption, is examined. Genetic, structural, electrophysiological, and inflammatory factors contributing to their development are explored.

AF involves irregular atrial activity leading to electrical and structural remodeling of the atrium. CD is characterized by an immune response to gluten, primarily associated with HLA-DQ2 and HLA-DQ8 genetic mutations, resulting in damage to intestinal tissue. Emerging research suggests a link between AF and CD, possibly mediated through inflammation, fibrosis, and electromechanical delays in the atrium.

Understanding the association between AF and CD carries significant clinical implications. Recognition of this relationship can assist in identifying individuals at higher risk for AF and inform proactive management strategies. Additionally, it underscores the importance of comprehensive care for CD patients, considering potential cardiac implications. Further research is warranted to elucidate precise mechanisms and explore potential therapeutic interventions targeting common pathways, opening avenues for enhanced patient care and future investigations.

Gastroesophageal reflux disease (GERD) is a commonly recognized cause of dysphagia. Conversely, eosinophilic esophagitis (EoE) and celiac disease are rarer and often overlooked as dysphagia culprits. Overlap between these conditions complicates diagnosis and delays appropriate treatment. This review aims to clarify the distinctive dysphagia characteristics in each condition, explore potential overlaps, and offer guidance on differentiation.

Recent studies have advanced our understanding of dysphagia mechanisms in GERD, EoE, and celiac disease, particularly in characterizing disordered motility and dysphagia's natural history. While upper endoscopy, biopsies, and manometry remain crucial in dysphagia assessment, novel diagnostic tools are emerging. New insights highlight the significance of cytokine-induced mucosal injury in all three conditions, revealing potential connections where mucosal damage in one disorder may contribute to the development of others.

GERD, EoE, and celiac disease can coexist and present with similar symptoms. Distinguishing between them often entails upper endoscopy, esophageal biopsies, pH testing, and celiac serologies. EoE should be considered when GERD patients fail proton pump inhibitor therapy or when celiac patients have persistent esophageal symptoms despite a gluten-free diet. Consider celiac disease if dysphagia accompanies iron deficiency anemia, malabsorptive diarrhea, or osteoporosis. Recognizing the potential overlap between these conditions is crucial for guiding clinical evaluation and therapy.

Introduction: Performing a tandem endoscopy and colonoscopy in selected individuals has advantages, such as the early detection of benign and/or precancerous foregut diseases; it is efficient, and it may allow added therapies. It may also have disadvantages, such as generating anxiety from false-positive screening, possible harm from further testing, and unproven cost-effectiveness. Aims: We aimed to examine the prevalence of foregut endoscopic and histologic abnormalities in subjects referred for screening/surveillance colonoscopy who also underwent a tandem endoscopy. We wanted to (1) assess implications for cancer detection, intervention, and surveillance of precancerous foregut abnormalities, (2) identify benign foregut lesions, and (3) generate data on the utilities of this tandem approach. Patients and Methods: A retrospective cohort study of consecutive subjects referred for screening or surveillance colonoscopy who also underwent an endoscopy. Based on national screening guidelines, responses to prompting questions, personal or family history, or other risk factors, subjects were assigned to tandem endoscopy with biopsies (modified Seattle and Sydney protocols), under one anesthesia. Results: Of the 1004 patients referred for colonoscopy, 317 (32%) underwent tandem endoscopy. There were 214 women and 103 men. There were 237 Whites, 16 Asians, 40 Blacks, and 24 Hispanics. Median age was 59 (range 19-85). At endoscopy, we identified actionable benign (45%) peptic, inflammatory, and H. pylori-related abnormalities, and premalignant findings (i.e., intestinal metaplasia, 27%, dysplasia, 2%, and cancer 0.9%), comparable to the premalignant (40.3%) and malignant (0.6%) colonoscopy yield. Conclusions: When implemented based on national screening guidelines, tandem EGD and colonoscopy combines Barrett's esophagus and gastric cancer screening in one examination, and it has a high yield in a diverse US population.

Liver involvement is common in celiac disease (CeD), and up to 4.6% of patients with cryptogenic cirrhosis have CeD. We investigated the prevalence of CeD in patients with cryptogenic cirrhosis and assessed liver-related outcomes in them on GFD when compared with a propensity score-matched cohort of patients with cryptogenic cirrhosis without CeD.

Consecutive patients with cryptogenic cirrhosis were screened for CeD using IgA anti-tissue transglutaminase antibody (anti-tTG) followed by antiendomysial antibody and duodenal and liver biopsies, on which IgA/anti-tTG colocalization studies were performed. These patients and a cohort of patients with cryptogenic cirrhosis without CeD (1:4 CeD: no CeD matched using propensity score matched for age, sex, Child-Turcotte-Pugh [CTP] and model for end-stage liver disease [MELD]) were initiated on GFD plus standard of care and standard of care, respectively, and followed up for liver-related outcomes for 1 year.

Of 232 patients with cryptogenic cirrhosis, 14 had high anti-tTG Ab (16.9 ± 10.5 fold rise), with 9 antiendomysial antibody-positive and 11 (4.7%) biopsy-proven CeD. IgA/anti-tTG Ab colocalization was demonstrated in 7/8 liver and 10/11 duodenal biopsies. Patients with cryptogenic cirrhosis with definite CeD (n = 11) and matched cohort without CeD (n = 44) were similar at baseline (age: 31.3 ± 7.7 vs 31.8 ± 9.3 years; 5 [45.5%] vs 15 [34.1%] females; MELDNa 9 [interquartile-range: 8-15.5] vs 12 [9-15]; CTP 7 [6-7.5] vs 6 [5.75-7]). Patients with CeD on GFD improved significantly on follow-up compared with those without CeD (follow-up MELDNa: 9 [7.5-10.5] vs 18.5 [12-20]; P = 0.001 and follow-up CTP: 5 [5-5] vs 8 [7-9]; P < 0.001) with less frequent further decompensations and similar mortality (9.1% vs 18.2%; P = 0.67).

Approximately 4.7% of patients with cryptogenic cirrhosis have biopsy-proven CeD, and their liver-related outcomes improve with GFD.

Celiac disease (CeD) has an estimated prevalence of 1%-3%. The classical clinical presentation is malabsorption, but now patients may present with more subtle symptoms such as constipation, osteoporosis, or iron deficiency anemia. Children may also present with poor growth.CeD has a strong genetic component, and high-risk groups include first-degree relatives with CeD, patients with co-existing autoimmune diseases, and patients with chromosomal aberrations.

Diagnostic tests for CeD include duodenal histology, serology, and genetic testing. Duodenal histology has traditionally been the gold standard of diagnosis. However, serological tests, especially IgA tissue transglutaminase antibodies (TTG-IgA), are widely used and diagnostic algorithms are based primarily on TTG-IgA as a starting point. Human leukocyte antigen typing may also be incorporated to determine genetic risk for CeD. Guidelines for children endorse biopsy avoidance provided high levels of TTG-IgA, with diagnostic accuracy being comparable to duodenal biopsy. Confirmation may be achieved by identifying IgA endomysial antibodies in a separate blood sample. Subjects with low positive TTG-IgA levels and subjects with IgA deficiency need a biopsy to establish a diagnosis of CeD. The clinical follow-up of CeD usually includes a repeat TTG-IgA examination. In adults, healing may be delayed or incomplete, and a rare consequence of refractory celiac disease is transformation to enteric T-cell lymphoma.

Laboratory testing, in particular TTG-IgA, plays a central role in the diagnosis and has an accuracy comparable to histology. Diagnostic algorithms utilizing laboratory testing are critical for the development of novel strategies to improve diagnosis.

Celiac disease (CD) may be frequently undiagnosed due to the absence of characteristic gastroenterologic symptoms in many CD patients. Our objective was to diagnose CD by utilizing documented oral manifestations such as Recurrent Aphthous Stomatitis (RAS) and Molar-Incisor Hypomineralization (MIH).

The study comprised sixty children who presented with complaints of RAS lesions. The MIH group consisted of 40 children, while the control group comprised 20 children without MIH lesions, ranging in age from 7 to 13 years. After the dental examination, all children were given a questionnaire to assess whether they had any previous history of general symptoms related to CD. Following that, diagnostic testing for celiac disease were conducted, including serological tests such as Tissue transglutaminase IgA (tTG-IgA), Endomysium Antibody (EMA), and Total IgA, as well as genetic tests for HLA-DQ2 and HLA-DQ8.

The statistical analysis, conducted using Fisher's Exact, Yates' Continuity Correction, Fisher Freeman Halton, and Student's t tests, revealed no significant differences between the groups (p < 0.05). Within the MIH group, 3 children exhibited border tTG-IgA values, while another 3 had positive tTG-IgA results. Two of these 6 children had also positive EMA and HLA results. Following a biopsy procedure, these two children were ultimately diagnosed with celiac disease (CD).

In this study, while children initially presented to the clinic with complaints of recurrent aphthous stomatitis (RAS), 2 children (5% of the MIH group) were diagnosed with CD shortly after the onset of MIH lesions. CD enhanced the likelihood of observing some oral manifestations particularly recurrent aphtous stomatitis and developmental enamel defects. We recommend that dentists be cautious about diagnosing CD when RAS lesions and DEDs and/or MIH lesions are present, whether or not other indications of this systemic disease exist.

Background: Celiac disease is a chronic small intestinal immune-mediated enteropathy precipitated by exposure to dietary gluten, affecting approximately 1% of the global population and two million Americans. An increasing number of studies have identified a link between celiac disease and adverse maternal and fetal outcomes during pregnancy and after birth. Additionally, both celiac disease and pregnancy are associated with an increased risk for nutrient deficiencies, specifically vitamin B12 and folate. Methods: This review examines the current literature related to the folate trap and vitamin B12 deficiency in patients with celiac disease and pregnant women independently and provides rationale for future research to explore the relationship between the folate-to-12 ratio in pregnant women with celiac disease. Results: Deficiencies in vitamin B12 are linked with several negative maternal and fetal health outcomes including pre-eclampsia, gestational diabetes, spontaneous abortion/miscarriage, preterm birth, neural tube defects, intrauterine growth restriction, and low gestational age and birthweight. Conclusions: Folic acid supplementation is widely recommended during pregnancy, but complementary vitamin B12 supplementation is not standard. Physicians should consider celiac disease screening during pregnancy as well as vitamin B12 supplementation.

In this editorial, we comment on an article published in the recent issue of the World Journal of Gastroenterology. Celiac disease (CeD) is a disease occurring in genetically susceptible individuals, which is mainly characterized by gluten intolerance in the small intestine and clinical symptoms such as abdominal pain, diarrhea, and malnutrition. Therefore, patients often need a lifelong gluten-free diet, which greatly affects the quality of life and expenses of patients. The gold standard for diagnosis is intestinal mucosal biopsy, combined with serological and genetic tests. At present, the lack of safe, effective, and satisfactory drugs for CeD is mainly due to the complexity of its pathogenesis, and it is difficult to find a perfect target to solve the multi-level needs of patients. In this editorial, we mainly review the pathological mechanism of CeD and describe the current experimental and improved drugs for various pathological aspects.

Celiac disease (CeD) is a common autoimmune condition, with a prevalence of ~1%. Currently, a gluten-free diet (GFD) is the only treatment option. Due to fortification rules excluding gluten-free products in the United States of America (U.S.A.), understanding the nutritional adequacy of a GFD is important for promoting optimal health among those with CeD. Cross-sectional examination of multiple 24 h dietary recalls from a study sample of 50 adults and 30 teens with CeD was used to determine nutritional adequacy and excesses according to U.S.A. recommendations. The results were compared with those of 15,777 adults and 2296 teens from a nationally representative sample not reporting CeD, the National Health and Nutrition Examination Survey (NHANES) 2009-2014. Compared with NHANES, our study population was more at risk of low folate and carbohydrate (adults) consumption, and of excessive niacin and vitamin A (teens), as well as saturated and total fat consumption (adults). Overall, though, compared with NHANES, our study participants had similar nutrient concerns but fewer nutritional imbalances, with some notable exceptions. In addition to maintaining a GFD, individuals with CeD should be counseled to maintain a balanced diet and to pay attention to nutrient-dense foods. Special attention should be given to teens in providing dietary counseling to potentially mitigate the risk of future morbidity.

Celiac disease, a prevalent autoimmune disorder, can present atypically with fat malabsorption and coagulopathy due to vitamin K malabsorption. A 64-year-old male presented with haemoptysis and severe anaemia (Hb 6 g/dl). Despite normal previous coagulation tests, admission laboratory tests revealed an international normalised ratio (INR) of 7.0 and iron deficiency anaemia. Initial blood products and vitamin K treatment corrected the INR temporarily, but the patient's haemoptysis returned, and his INR values continued to rise. Further investigation revealed celiac disease with fat malabsorption, leading to vitamin K malabsorption and along with a previously prescribed antiplatelet aggregation therapy, this led to diffuse alveolar haemorrhage. A gluten-free diet and vitamin supplementation normalised the patient's INR and stopped the bleeding. This case highlights the importance of considering celiac disease in unexplained coagulopathies and the effectiveness of dietary management.

Celiac disease can cause severe coagulopathy due to fat malabsorption and vitamin K deficiency.High suspicion is required for atypical presentations of celiac disease.A gluten-free diet is essential for managing celiac disease and normalising coagulation profiles.

To examine whether patients with non-infectious uveitis (NIU) are at increased risk for celiac disease (CeD).

Celiac antibody testing was completed in 112 patients. The control group included patients who had undergone upper endoscopy for suspicion of CeD.

2/112 (1.79%) of patients with NIU had positive anti-tTG serology and CeD was confirmed in both patients. When compared to the expected risk of CeD in the general Israeli population of 0.31%, this corresponded to an odds ratio of 5.77 (95% CI 1.4118 to 23.4737, P = 0.049). Three additional patients had positive serology for CeD but the diagnosis was not confirmed.

An increased risk of CeD was detected in patients with NIU. We therefore recommend screening for CeD in NIU patients. Larger prospective studies are required to further validate these results.

We aimed to evaluate symptom outcomes in those on a gluten-free diet during the 5 years after diagnosis.

Celiac disease is common; however, little is known about long-term symptom outcomes.

We performed a retrospective chart review on individuals with celiac disease followed at a tertiary referral center between 2012 and 2018. To minimize bias, strict inclusion/exclusion criteria were utilized. Only those with definitive biopsy-proven celiac disease, on a gluten-free diet, and with systematic follow-up were included. The standardized care at this center reduced the risk that decisions on testing and follow-up visits were determined by symptom status. Summary statistics were computed and generalized linear models with a logit link were used to associate the proportion of symptomatic visits with various covariates using R statistical programming.

Of the 1023 records reviewed, 212 met inclusion/exclusion criteria; 146 (69%) were female and the mean age at diagnosis was 43 (range: 11 to 84 y old). During follow-up, over 50% remained symptomatic, with many having the same symptoms that prompted the diagnosis. The only predictors for remaining symptomatic were female sex and younger age at diagnosis. Abnormal serology during follow-up and small bowel normalization were not predictive.

In individuals with definitive celiac disease with systematic long-term follow-up in a Celiac Clinic, roughly half remained symptomatic despite a gluten-free diet. Many suffer from the same symptoms that prompted the diagnosis of celiac disease. Small bowel healing and abnormal serology in follow-up were not predictive of remaining symptomatic. These findings stress the importance of long-term care in celiac disease.

Fibromyalgia (FMS) is a common musculoskeletal disorder with many causes. People with fibromyalgia often have the same symptoms as people with celiac disease (CD). Demonstration of the coordination and frequency of FMS and CD is important for effective treatment.

This is a single center cross-sectional clinical study. The study included 60 patients who were diagnosed with CD by the Gastroenterology Clinic based on American College of Gastroenterology (ACG) criteria. Patients were also asked to complete the Widespread Pain Index (WPI), Symptom Severity Scale (SSS), and Fibromyalgia Impact Questionnaire (FIQ) to diagnose fibromyalgia and assess its severity. The results were used to analyze the frequency of concomitance and relationship between the two diseases.

The relationship between the clinical types of CD and the presence of fibromyalgia was insignificant. Analysis of the relationship between the pathologic typing of biopsy and fibromyalgia frequency was insignificant. Those with antibodies more frequently met criteria for fibromyalgia (P = 0.04, P = 0.04, respectively).

Presence of clinical extraintestinal manifestations in patients with CD should lead clinicians to consider FMS as a possible diagnosis. This points to the importance for clinicians in all subspecialties to be aware of the various symptoms and diseases associated with FMS.

Gluten comprises an intricate network of hundreds of related but distinct proteins, mainly "gliadins" and "glutenins," which play a vital role in determining the rheological properties of wheat dough. However, ingesting gluten can trigger severe conditions in susceptible individuals, including celiac disease, wheat allergy, or non-celiac gluten sensitivity, collectively known as gluten-related disorders. This review provides a panoramic view, delving into the various aspects of gluten-triggered disorders, including symptoms, diagnosis, mechanism, and management. Though a gluten-free diet remains the primary option to manage gluten-related disorders, the emerging microbial and plant biotechnology tools are playing a transformative role in reducing the immunotoxicity of gluten. The enzymatic hydrolysis of gluten and the development of gluten-reduced/free wheat lines using RNAi and CRISPR/Cas technology are laying the foundation for creating safer wheat products. In addition to biotechnological interventions, the emerging artificial intelligence technologies are also bringing about a paradigm shift in the diagnosis and management of gluten-related disorders. Here, we provide a comprehensive overview of the latest developments and the potential these technologies hold for tackling gluten sensitivity.

This study aimed to investigate the changes in serum Anti-Müllerian Hormone (AMH) levels, sex hormone levels, follicle-stimulating hormone (FSH)/luteinizing hormone (LH) ratio in patients with celiac disease (CeD), and their correlation with clinical characteristics and nutrient levels.

This cross-sectional study collected clinical and biochemical data from a total of 67 females diagnosed with CeD and 67 healthy females within the reproductive age range of 18-44 years. The study was conducted at a tertiary hospital between September 2016 and January 2024. Both groups underwent comprehensive clinical and laboratory assessments. Serum levels of AMH and sex hormones were quantified using chemiluminescence immunoassay, and their associations with CeD clinical features and nutrient levels were thoroughly analyzed.

The study included 67 patients and 67 controls with a mean age of 36.7±7.6 years. No statistically significant differences were found between the two groups in mean age, BMI, FSH, LH, E2, P levels, FSH/LH, menstrual irregularities, abortions history, parity, and gravidity (all P>0.05). However, AMH, T, FER, FA, Zn, and Se levels were significantly lower, and PRL levels were higher in the CeD group (all P<0.05). Spearman's correlation analysis showed that AMH levels were negatively correlated with age, tTG level, disease duration, and Marsh grading (P<0.05).

This study highlights the association between impaired ovarian function in CeD patients and disease severity and nutrient levels. Early detection and intervention for ovarian function abnormalities are imperative to enhance fertility potential in CeD patients.

The past 50 years of interdisciplinary research in humans and model organisms has delivered unprecedented insights into the mechanisms through which diet affects energy balance. However, translating these results to prevent and treat obesity and its associated diseases remains challenging. Given the vast scope of this literature, we focus this Review on recent conceptual advances in molecular nutrition targeting the management of energy balance, including emerging dietary and pharmaceutical interventions and their interactions with the human gut microbiome. Notably, multiple current dietary patterns of interest embrace moderate-to-high fat intake or prioritize the timing of eating over macronutrient intake. Furthermore, the rapid expansion of microbiome research findings has complicated multiple longstanding tenets of nutrition while also providing new opportunities for intervention. Continued progress promises more precise and reliable dietary recommendations that leverage our growing knowledge of the microbiome, the changing landscape of clinical interventions, and our molecular understanding of human biology.