[What is established in the management of celiac disease?] / Was ist gesichert in der Therapie der Zöliakie?

Nowadays, celiac disease is well-established in internal medicine as an autoimmune disease induced by gluten as a trigger. Undoubtedly similarly well-established is the gluten-free diet. It is the only recognized therapy for celiac disease to date. However, this presents some pitfalls in its implementation, which will be discussed in the following review. In addition, current developments that have the potential to significantly change both diagnosis and treatment of celiac disease are discussed. On the one hand, such an outlook was chosen since colleagues want to be "ready" when such developments are integrated into daily clinical routine. On the other hand, the realization that the field of mucosal immunology is moving forward has the potential to lift the spirits of the reader.

[Frequent Gastro-Intestinal Disorders: Management of Functional Dyspepsia and Irritable Bowel Syndrome in Clinical Practice]. / Häufige Magen-Darm-Beschwerden: Management der funktionellen Dyspepsie und des Reizdarm-Syndroms in der Praxis.

Frequent Gastro-Intestinal Disorders: Management of Functional Dyspepsia and Irritable Bowel Syndrome in Clinical Practice Abstract: Functional dyspepsia (FD) and irritable bowel syndrome (IBS), two common gastrointestinal entities with overlapping symptoms, should be diagnosed according to Rome IV criteria. This includes one or more of the following symptoms: in FD, postprandial fullness, early satiation, epigastric pain or burning; in IBS, recurrent abdominal pain associated with defecation, change in frequency of stool or form of stool. To exclude structural diseases, attention should be paid to alarm symptoms. As far as treatment is concerned, a stepwise scheme proves to be effective for both diseases. Step 1: doctor-patient discussion with explanation of diagnosis and prognosis as well as clarification of therapy goals; lifestyle adaptations; use of phytotherapeutics; step 2: symptom-oriented medication: for FD, PPIs or prokinetics; for IBS, antispasmodics, secretagogues, laxatives, bile acid sequestrants, antidiarrheals, antibiotics, probiotics; step 3: visceral analgesics (antidepressants).

Nutrition in Inflammatory Bowel Disease.

BACKGROUND: Westernization, above all associated changes in diet, has been postulated to be one of the most important factors contributing to the increasing incidence in inflammatory bowel disease (IBD), consisting mainly of Crohn's disease and ulcerative colitis. SUMMARY: Diet represents a crucially important and intuitively relevant topic for IBD patients. Although a substantial number of patients are prone to follow dietary advice from a variety of sources, including the lay press, there is intriguingly little scientific evidence for such an incitement. This may result in physicians being insufficiently informed about various aspects of nutrition, precluding adequate guidance of their patients with IBD. Importantly, IBD patients are at risk to develop deficiencies in iron, vitamin B12, folic acid, and several micronutrients, which may even be more pronounced in patients with active disease and those following a restrictive diet. This review aims to summarize the latest data from clinical and epidemiological studies investigating diet and its effect on the course of the disease and to outline the most important nutrient deficiencies in IBD patients. Key Messages: A western diet with an imbalance between omega-6 (n-6)/omega-3 (n-3) polyunsaturated fatty acids (PUFAs), in favor of n-6 PUFAs, may increase the risk of IBD, whereas a diet high in fruits and vegetables may decrease the risk of IBD. Many approaches to influence the course of IBD with dietary intervention exist. However, to induce or maintain remission in IBD with a change of diet is still in its infancy, and more dietary research is needed before we can apply it in daily practice. Patients with IBD, even in remission, have to be screened regularly for malnutrition.

Cross-Contamination with Gluten by Using Kitchen Utensils: Fact or Fiction?

A risk of cross-contamination exists when preparing a gluten-free (GF) meal in kitchen facilities that usually handle gluten-containing (GC) foods. Cross-contamination with gluten may occur during the preparation or cooking process; however, published data are lacking on gluten cross-contamination from kitchenware. This study was conducted to determine whether cross-contamination occurs through shared domestic kitchenware and, if so, which cleaning method is most reliable for avoiding this cross-contamination. Kitchenware (wooden spoon, colander, ladle, and knife) previously used to cook and/or prepare GC foods was used for the preparation of GF foods (bread and pasta). The gluten concentration of the GF foods was then determined using an established enzyme-linked immunosorbent assay. A PCR assay was also used to detect the presence of wheat ω-gliadin DNA in the food samples. Three cleaning methods were assessed to determine the concentrations of gluten and wheat DNA in GF foods cooked with utensils cleaned directly after the preparation of GC foods. Contrary to our expectations, gluten was not detected in relevant and quantifiable amounts in our samples (<20 mg/kg). The cleaning method used did not influence gluten concentrations: all samples contained <10 mg/kg. Based on PCR analyses, the only sample with lower cycle threshold ( CT) values (i.e., higher concentration of wheat DNA) was from the contaminated ladle used to serve GF pasta. This outcome led to the hypothesis that shared ladles pose a higher risk for contamination of GF foods than do shared wooden spoons, colanders, or knives. Cross-contamination with gluten in a kitchen environment may occur, but kitchen utensils used for preparing GC pasta and for cutting GC bread should not pose a relevant problem to patients with celiac disease, at least in a domestic environment.

A Comparative Study on Carbohydrate Estimation: GoCARB vs. Dietitians.

GoCARB is a computer vision-based smartphone system designed for individuals with Type 1 Diabetes to estimate plated meals' carbohydrate (CHO) content. We aimed to compare the accuracy of GoCARB in estimating CHO with the estimations of six experienced dietitians. GoCARB was used to estimate the CHO content of 54 Central European plated meals, with each of them containing three different weighed food items. Ground truth was calculated using the USDA food composition database. Dietitians were asked to visually estimate the CHO content based on meal photographs. GoCARB and dietitians achieved comparable accuracies. The mean absolute error of the dietitians was 14.9 (SD 10.12) g of CHO versus 14.8 (SD 9.73) g of CHO for the GoCARB (p = 0.93). No differences were found between the estimations of dietitians and GoCARB, regardless the meal size. The larger the size of the meal, the greater were the estimation errors made by both. Moreover, the higher the CHO content of a food category was, the more challenging its accurate estimation. GoCARB had difficulty in estimating rice, pasta, potatoes, and mashed potatoes, while dietitians had problems with pasta, chips, rice, and polenta. GoCARB may offer diabetic patients the option of an easy, accurate, and almost real-time estimation of the CHO content of plated meals, and thus enhance diabetes self-management.

Celiac disease diagnosis still significantly delayed - Doctor's but not patients' delay responsive for the increased total delay in women.

BACKGROUND: There is insufficient data on diagnostic delay and associated factors in celiac disease (CeD) as well as on its potential impact on the course of disease. METHODS: Specifically taking its two components - patients' and doctors' delay - into account, we performed a large systematic patient survey study among unselected CeD patients in Switzerland. RESULTS: We found a mean/median total diagnostic delay of 87/24 months (IQR 5-96), with a range from 0 up to 780 months and roughly equal fractions of patients' and doctors' delay. Both mean/median total (93.1/24 vs. 60.2/12, p<0.001) and doctors' (41.8/3 vs. 23.9/2, p<0.001) diagnostic delay were significantly higher in female vs. male patients, whereas patients' delay was similar, regardless of preceding irritable bowel syndrome diagnosis. Patients with a diagnostic delay shorter than 2 years were significantly less often in need of steroids and/or immunosuppressants, substitution for any nutritional deficiency but more often free of symptoms 6 and 12 months after diagnosis. CONCLUSIONS: There is a substantial diagnostic delay in CeD, which is associated with a worse clinical outcome and significantly longer in female patients. This increased diagnostic delay in women is due to doctors' but not patients' delay and cannot be explained by antecedent IBS prior to establishing the CeD diagnosis.