Research LettersOsteopenia in patients with clinically silent coeliac disease warrants screening
Summary
Bone-mineral density was measured in 19 clinically silent coeliac patients. The density was low, comparable with that in coeliac cases, and improved by gluten-free diet.
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Cited by (172)
Treatment of gluten-related disorders
2021, Gluten-Related Disorders: Diagnostic Approaches, Treatment Pathways, and Future PerspectivesA gluten-free diet (GFD) is the current standard of care for all patients with celiac disease (CeD) including its classic, nonclassic, and silent forms, as well as for dermatitis herpetiformis, gluten ataxia, and nonceliac gluten sensitivity. Following a GFD involves restricting certain food items, thus care must be taken to ensure a balanced diet that provides both macronutrients and micronutrients. Further, a GFD requires major lifestyle changes for the patients and their families. Moreover, despite attempts to maintain a strict GFD, gluten exposure is common given the extensive use of gluten in the food industry. Hence, repeated and accurate counseling of patients and their families by skilled/specialized dieticians forms an essential part of the treatment. Other best practices to be considered by physicians include monitoring and correction of nutritional deficiencies related to CeD, prevention of bone loss, vaccinations for certain infections, voluntary screening of family members, and keeping a high index of suspicion for CeD-associated autoimmune disorders and extraintestinal manifestations affecting the liver, bone, etc. All patients with CeD should be assessed at regular intervals for improvement and adherence on a GFD, since almost a third of patients fail to show a satisfactory response. Monitoring and appropriate treatment of issues uniquely associated with a GFD, including a higher risk of metabolic syndrome, fatty liver, dietary deficiencies, and constipation, are also important.
Interestingly, insights gleaned into the pathogenesis of CeD over the past two decades have provided options for targeted therapies that may be useful as alternatives/adjunctive to a GFD. Based on their mechanisms of action, these therapies may be classified as belonging to one of the following approaches. The first approach involves decreasing the immunogenicity of gluten, using glutenases like latiglutenase or kuma, genetic modification of wheat that is the most common source of gluten, microwave thermal treatment of hydrated wheat kernels, and gluten pretreatment prior to ingestion, with either bacterial/fungal-derived endopeptidases or microbial transglutaminase. The second approach involves intraluminal gluten-binding drugs like polymer p(HEMA-co-SS), single-chain fragment variable, and antigluten antibody AGY. The third approach antagonizes zonulin, a molecule regulating intestinal epithelial tight junctions that mediate gliadin transport. The fourth approach involves intestinal tissue transglutaminase enzyme inhibition to decrease deamidation of gliadin peptides taken-up by the mucosa, into epitopes with enhanced immunogenicity, using agents like ZED1227, si-RNA therapy, etc. The fifth approach seeks to prevent downstream immune activation after exposure to gliadin peptides, using Human Leukocyte Antigen blockers that prevent presentation of gluten-derived antigens by dendritic cells to T cells, immune-tolerizing therapies like the vaccine Nexvax2 and the nanoparticle-based Tolerogenic Immune Modifying Particles-Glia, cathepsin inhibitors, corticosteroids, elafin, etc., and anticytokine agents targeting interleukin-15/interleukin-21, CCR9–CCL25 interaction, γc receptor, etc. Overall, among the novel therapies on the anvil, glutenases, and strategies that modulate immune activation appear to be some of the promising therapies based on preliminary results.
Is osteoporosis an autoimmune mediated disorder?
2017, Bone ReportsThe last two decades have marked a growing understanding of the interaction occurring between bone and immune cells. The chronic inflammation and immune system dysfunction commonly observed to occur during the ageing process and as part of a range of other pathological conditions, commonly associated with osteoporosis has led to the recognition of these processes as important determinants of bone disease. This is further supported by the recognition that the immune and bone systems in fact share regulatory mechanisms and progenitor molecules. Research into this complex synergy has provided a better understanding of the immunopathogenesis underlying bone diseases such as osteoporosis. However, existing research has largely focussed on delineating the role played by inflammation in pathogenic bone destruction, despite increasing evidence implicating autoantibodies as important drivers of osteoporosis. This review shall attempt to provide a comprehensive overview of existing research examining the role played by autoantibodies in osteoporosis in order to determine the potential for further research in this area. Autoantibodies represent promising targets for the improved treatment and diagnosis of inflammatory bone loss.
Bone and bowel diseases: Management of osteoporosis in bowel diseases
2016, Revue du Rhumatisme MonographiesDes complications osseuses sont attendues au cours des maladies inflammatoires chroniques de l’intestin (MICI) et de la maladie cœliaque en raison de la présence de plusieurs facteurs de risque. L’ostéodensitométrie doit être réalisée chez tous les patients atteints de MICI ayant des facteurs de risque et en cas de maladie cœliaque. Chez les patients atteints de MICI, les traitements anti-ostéoporotiques (bisphosphonates) sont recommandés quand il existe un antécédent personnel de fracture, une ostéoporose densitométrique et chez les patients de plus de 50 ans recevant une corticothérapie prolongée. Au cours de la maladie cœliaque, l’observance au régime sans gluten est le traitement le plus important pour prévenir la perte osseuse.
Bone complications can be observed in inflammatory bowel diseases (Crohn disease and ulcerative colitis) and in celiac disease, due to the presence of several risk factors (inflammation, low weight, corticosteroids…). Bone densitometry should be performed in patients with IBD and risk factors and in those with celiac disease. In patients with IBD, antiosteoporotic treatments as bisphosphonates are recommended in patients with previous low trauma fracture, osteoporosis and in patients over 50 years who received long term corticosteroids. In celiac disease, the gluten-free diet is the most important treatment for bone loss.
Screening of coeliac disease in undetected adults and patients diagnosed with irritable bowel syndrome in Riyadh, Saudi Arabia
2016, Saudi Journal of Biological SciencesThe present study is to determine the prevalence and implication of coeliac disease (CD) among adult Saudis and compared to those with diagnosed irritable bowel syndrome. This prospective study was conducted among 980 adults. Out of that, 482 subjects (staff and students of Riyadh Health Science College) were designated as control cohorts for undetected coeliac disease. Furthermore, another contingent of 498 subjects diagnosed with irritable bowel syndrome (IBS) at Prince Salman Hospital and Al-Iman General Hospital also constituted a segment of the overall initial 1020 subjects. Both cases and control were tested for serological markers of coeliac disease (tissues transglutaminase (tTGAs) and endomysial autoantibody (EMAs) and were confirmed by histopathology test. All the positive for cases of coeliac disease were screened for iron deficiency anaemia, Vitamin D deficiency, and osteoporosis and weight assessment. The percentage of coeliac disease in control subjects and patients diagnosed with irritable bowel syndrome (IBS) were found to be 1.9% and 9.6% respectively, about 38% of the total coeliac disease patients are among females of middle age (20–39-years) and 16% of the males in the same age range. Whereas, 20% and 25% of all coeliac disease cases with ages of 40–59 were remarked as females and males respectively. The identical nature and overlap of symptoms of the two conditions could possibly result in misdiagnosis of coeliac diseases or over-diagnosis of irritable bowel syndrome. The findings of the study might also give considerable implications of the disease in the nutritional level which is noticeable.
Acquired causes of intestinal malabsorption
2016, Best Practice and Research: Clinical GastroenterologyThis review focuses on the acquired causes, diagnosis, and treatment of intestinal malabsorption. Intestinal absorption is a complex process that depends on many variables, including the digestion of nutrients within the intestinal lumen, the absorptive surface of the small intestine, the membrane transport systems, and the epithelial absorptive enzymes.
Acquired causes of malabsorption are classified by focussing on the three phases of digestion and absorption: 1) luminal/digestive phase, 2) mucosal/absorptive phase, and 3) transport phase. Most acquired diseases affect the luminal/digestive phase. These include short bowel syndrome, extensive small bowel inflammation, motility disorders, and deficiencies of digestive enzymes or bile salts. Diagnosis depends on symptoms, physical examination, and blood and stool tests.
There is no gold standard for the diagnosis of malabsorption. Further testing should be based on the specific clinical context and the suspected underlying disease. Therapy is directed at nutritional support by enteral or parenteral feeding and screening for and supplementation of deficiencies in vitamins and minerals. Early enteral feeding is important for intestinal adaptation in short bowel syndrome. Medicinal treatment options for diarrhoea in malabsorption include loperamide, codeine, cholestyramine, or antibiotics.
Celiac disease detection in hypothyroid patients requiring elevated thyroid supplementation: A prospective cohort study
2015, European Journal of Internal MedicineCeliac disease (CD) is associated with hypothyroidism, but the disease prevalence is not thought to be great enough to warrant testing all hypothyroid patients. We hypothesized that hypothyroid patients with concomitant CD would require elevated doses of levothyroxine, and there is a threshold daily dose, above which, hypothyroid patients should be tested for CD.
Hypothyroid patients presenting to the endoscopy or endocrinology clinics at the University of Vermont Medical Center were included. Patients were categorized by whether or not they required ≥ 125 mcg/day of levothyroxine. A serum tissue transglutaminase (tTG) was performed on enrolled patients. Patients with an elevated serum tTG underwent endoscopy with duodenal biopsies. Symptoms were assessed by the Gastrointestinal Symptom Rating Scale.
Overall, 500 patients were enrolled and 29% (144 patients) required ≥ 125 mcg/day of levothyroxine. CD was detected in 9 patients. The prevalence of CD ranged from 1.8% in our entire cohort to 12.5% in patients requiring ≥ 200 mcg/day of levothyroxine. Eight patients with CD (89%) required ≥ 125 mcg/day of levothyroxine. Patients who required ≥ 125 mcg/day of levothyroxine had a significantly increased risk of CD (p < 0.001). CD was detected in 5.6% of patients requiring ≥ 125 mcg/day of levothyroxine.
Hypothyroid patients requiring elevated daily doses of levothyroxine are more likely to have CD. Hypothyroid patients requiring ≥ 125 mcg/day of levothyroxine should undergo serologic testing for CD.