The Dutch evidence-based guideline 'Coeliac disease and dermatitis herpetiformis' contains instructions for detection and treatment of coeliac disease. Coeliac disease has a high prevalence: 0.5 - 1.3%. The disease has a broad spectrum of symptoms, frequently also outside the gastrointestinal tract. Relatives of patients and persons with autoimmune diseases, microscopic colitis, IgA deficiency and syndromes of Down, Turner and Williams have an increased risk of coeliac disease. Detection is carried out by determination of IgA antibodies to tissue transglutaminase and endomysium. Testing for IgA antibodies to gliadin is only recommended in children younger than 2 years. Absence of HLA-DQ2 and DQ8 indicates that coeliac disease is most unlikely. The diagnosis should be confirmed by small bowel biopsy. Single biopsy following gluten ingestion is sufficient for diagnosis at all ages. After the diagnosis, patients should be referred to a dietician. Additionally, a yearly follow-up by a paediatrician or internal medical specialist with appropriate gastroenterology specialisation is recommended.
Download full-text PDF |
Source |
---|
Arch Dermatol Res
January 2025
Division of Gastroenterology and Hepatology, 200 1st Street SW, Rochester, MN, 55905, USA.
Background: Celiac disease (CeD) has shown an association with autoimmune disorders including vitiligo and alopecia areata (AA). Ritlecitinib, a JAK3 and TEC kinase family inhibitor, has been approved for treatment of patients with AA and is in late-stage development for vitiligo. Ritlecitinib inhibits cytotoxic T cells, NK cells, and B cells which play a role in the pathogenesis of CeD.
View Article and Find Full Text PDFInt J Surg Case Rep
January 2025
Karnali Academy of Health Science, Jumla, Nepal.
Introduction And Importance: Splenic artery aneurysm is extremely rare but potentially life threatening disease which poses great challenge in diagnosing due to non-specific nature of clinical presentation. Rarely, it presents with upper gastrointestinal bleeding i.e.
View Article and Find Full Text PDFDiabetes
January 2025
Barbara Davis Center for Diabetes, University of Colorado, Aurora, CO, USA.
Increasing evidence shows that pathogenic T cells in type 1 diabetes (T1D) that may have evaded negative selection recognize post-translational modified (PTM) epitopes of self-antigens. We have investigated the profiles of autoantibodies specifically targeting the deamidated epitopes of insulinoma antigen-2 extracellular domain (IA-2ec) to explore their relationship with T1D development. We compared the characteristics of autoantibodies targeting the IA-2ec Q>E epitopes (PTM IA-2ecA) as well as those targeting the IA-2ec unmodified epitopes (IA-2ecA) in participants across different stages of T1D development and in individuals with other types of diabetes and other kinds of autoimmunity.
View Article and Find Full Text PDFJ Clin Endocrinol Metab
January 2025
Division of Diabetes, Endocrinology and Metabolism, Baylor College of Medicine, Houston, TX.
Context: When clinically stable, patients with A-β+ Ketosis-Prone Diabetes (KPD) manifest unique markers of amino acid metabolism. Biomarkers differentiating KPD from type 1 (T1D) and type 2 diabetes (T2D) during hyperglycemic crises would accelerate diagnosis and management.
Objective: Compare serum metabolomics of KPD, T1D and T2D patients during hyperglycemic crises, and utilize Classification and Regression Tree (CART) modeling to distinguish these forms of diabetes.
Ann Endocrinol (Paris)
January 2025
Service d'Endocrinologie, Diabétologie, Métabolisme, Nutrition; Hôpital Huriez, CHU Lille; Inserm U1190, Institut Génomique Européen pour le Diabète, Université de Lille, F-59000 Lille, France. Electronic address:
The differential diagnosis of primary hyperparathyroidism can be considered clinically, biologically and radiologically. Clinically, primary hyperparathyroidism should be suspected in case of diffuse pain, renal lithiasis, osteoporosis, repeated fracture, cognitive or psychiatric disorder, or disturbance of consciousness. Nevertheless, the differential diagnosis of primary hyperparathyroidism is mainly biological, particularly in atypical forms, which must be differentiated from hypercalcemia with hypocalciuria or non- elevated PTH on the one hand, and from normo-calcemia with elevated PTH, hypophosphatemia or hypercalciuria on the other.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!