Non-Celiac Gluten Sensitivity (NCGS) is a syndrome characterized by intestinal and extra-intestinal symptoms related to the ingestion of gluten-containing food, in subjects that are not affected by either celiac disease or wheat allergy. Given the lack of a NCGS biomarker, there is the need for standardizing the procedure leading to the diagnosis confirmation. In this paper we report experts’ recommendations on how the diagnostic protocol should be performed for the confirmation of NCGS. A full diagnostic procedure should assess the clinical response to the gluten-free diet (GFD) and measure the effect of a gluten challenge after a period of treatment with the GFD. The clinical evaluation is performed using a self-administered instrument incorporating a modified version of the Gastrointestinal Symptom Rating Scale. The patient identifies one to three main symptoms that are quantitatively assessed using a Numerical Rating Scale with a score ranging from 1 to 10. The double-blind placebo-controlled gluten challenge (8 g/day) includes a one-week challenge followed by a one-week washout of strict GFD and by the crossover to the second one-week challenge. The vehicle should contain cooked, homogeneously distributed gluten. At least a variation of 30% of one to three main symptoms between the gluten and the placebo challenge should be detected to discriminate a positive from a negative result. The guidelines provided in this paper will help the clinician to reach a firm and positive diagnosis of NCGS and facilitate the comparisons of different studies, if adopted internationally.

Gut microbiota are permanent residents of humans with the highest concentrations being found in human colon. Humans get the first contact with bacteria at delivery, and microbiota are subject of permanent change during the life. The individual microbiota pattern is highly variable and varying environmental conditions, e.g., diets, antigen exposure, infections, or medication, as well as genetics, age, or hygiene factors, strongly influence the bacterial community. A fine interaction between the host and microbiota determines the outcome of health or disease. The gut immune system is constantly challenged to distinguish between commensal non-invasive bacteria and potential pathogens. Goblet cells produce mucins that prevent most gut bacteria from penetrating through intestinal epithelial barrier, and Paneth cells are the main supplier of anti-microbial defensins. Gut epithelial and immune cells recognize bacteria via surface markers and they initiate an adequate immune answer. A dysbiosis is noticed in several diseases, but the crucial role in pathogenesis has to be proven. Prebiotics or probiotics are discussed as valuable tools to preserve or restore a healthy gut community.

Gluten-related disorders have recently been reclassified with an emerging scientific literature supporting the concept of non-celiac gluten sensitivity (NCGS). New research has specifically addressed prevalence, immune mechanisms, the recognition of non-immunoglobulin E (non-IgE) wheat allergy and overlap of NCGS with irritable bowel syndrome (IBS)-type symptoms. This review article will provide clinicians with an update that directly impacts on the management of a subgroup of their IBS patients whose symptoms are triggered by wheat ingestion.

Sarcopenia, frailty, cachexia and malnutrition are widespread syndromes in older people, characterized by loss of body tissue and related to poor outcome. The aim of the present cross-sectional study was to assess the prevalence of these syndromes and their overlap in older medical inpatients. Patients aged 70 years or older who had been admitted to the internal medical department of a German university hospital were recruited. Sarcopenia, frailty, cachexia and malnutrition were assessed in a standardized manner according to current consensus definitions. Prevalence rates of these syndromes and their constituents and the concurrent occurrence of the syndromes (overlap) were calculated. One hundred patients (48 female) aged 76.5 ± 4.7 years with a BMI of 27.6 ± 5.5 kg/m2 were included. The main diagnoses were gastroenterological (33%) and oncological diseases (31%). Sarcopenia was present in 42%, frailty in 33%, cachexia in 32% and malnutrition in 15% of the patients. 63% had at least one syndrome: 32% one, 11% two, 12% three and 8% all four. All four syndromes are characterized by significant weight loss during the last 12 months, which was most pronounced in malnourished patients and least pronounced in frail patients, and by significantly reduced physical performance. All syndromes were significantly pairwise related, except malnutrition and frailty. In 19% of patients sarcopenia and frailty occurred concurrently, in 20% frailty and cachexia and in 22% sarcopenia and cachexia with or without additional other syndromes. All malnourished patients except one were also cachectic (93%) and 80% of malnourished patients were also sarcopenic. 53% of malnourished patients were in addition frail, and these patients were affected by all four syndromes. Nearly two thirds of older medical inpatients had at least one of the tissue loss syndromes sarcopenia, frailty, cachexia and malnutrition. The syndromes overlapped partly and were interrelated. Future studies with larger patient groups and longitudinal design are required to clarify the significance of single and concurrent occurrence of these syndromes for clinical outcome and successful therapy.

Chronic liver diseases are a major cause of morbidity and mortality worldwide. Recently, gut dysbiosis was identified as an important factor in the pathogenesis of liver diseases. The relationship between gut microbiota and the liver is still not well understood; however, dysfunction of the gut mucosal barrier (“leaky gut”) and increased bacterial translocation into the liver via the gut–liver axis probably play crucial roles in liver disease development and progression. The liver is an important immunological organ, and, after exposure to gut-derived bacteria via portal circulation, it responds with activation of the innate and adaptive immune system, leading to hepatic injury. A better understanding of the pathophysiological links among gut dysbiosis, the integrity of the gut barrier, and the hepatic immune response to gut-derived factors is essential for the development of new therapies to treat chronic liver diseases.