No abstract

Increased gastrointestinal permeability was found in celiac disease already 20 years ago. Originally a genetical defect was supposed leading to elevated permeability and later to celiac disease. However, patients under long-term gluten-free diet normalized their permeability tests. On the other side, unaffected relatives of patients with celiac disease showed high permeability but not different from patients with irritable bowel syndrome and with a tendency for normalization during follow-up. In active symptomatic celiac disease, permeability is elevated in the gastroduodenum – measured by sucrose test – as well as in the small intestine – measured by lactulose/mannitol ratio. The sensitivity in active celiac disease is high (near 100%), the specificity is low due to high permeability in many intestinal diseases as in acute infectious gastroenteritis, Crohn’s disease, nonsteroidal anti-inflammatory drug treatment, etc. In contrast, lactulose/mannitol test permeability is much less sensitive in silent celiac disease without diarrhea (74%). The real importance of permeability disease is established by its use for follow-up of celiac patients under gluten-free diet whereas it is correlated to the degree of mucosal atrophy. In vitro tests also show increased lactulose mucosal to serosal flux in celiac disease, but not correlated to oral permeability test. In conclusion, lactulose/mannitol test is the only noninvasive functional test in celiac disease which has essential importance in active celiac disease and in follow-up under diet.

Objective: Systematic investigations on the status of fat-soluble vitamins in patients with acute renal failure (ARF) are lacking and hence no recommendations for vitamin supply can be defined for these subjects. Thus we compared the status of fat-soluble vitamins, of transport molecules and some vitamin-dependent proteins in patients with ARF and healthy controls. Setting: Nephrology unit of a university hospital. Patients and Methods: Eight patients with ARF requiring hemodialysis therapy were investigated and 28 healthy volunteers served as controls. Plasma concentrations of retinol (vitamin A) and retinol-binding protein (RBP), 25-OH and 1,25-(OH)₂ vitamin D₃, of parathyroid hormone (PTH), of α-tocopherol (vitamin E) and of phylloquinone (vitamin K), osteocalcin and noncarboxylated osteocalcin, respectively, were measured and plasma lipoprotein fractions (as vitamin transport vehicle) were evaluated. Results: Vitamin A levels were decreased (p < 0.001), but RBP levels were normal in ARF patients. Vitamin D₃ metabolites 25-OH and 1,25-(OH)₂ vitamin D₃ plasma levels were profoundly depressed, and PTH was elevated (p < 0.001). Vitamin E plasma concentration was reduced (p < 0.001) but this cannot be accounted for by decreased LDL cholesterol or triglyceride levels. In contrast, vitamin K plasma level was rather elevated in ARF patients with a broad range of individual values. Blood coagulation was normal but total and carboxylated osteocalcin were decreased. No correlation of vitamin K concentrations and any of the plasma lipoprotein fractions could be identified. Conclusion: With the exception of vitamin K, profound deficiencies of fat-soluble vitamins develop in patients with ARF. Current recommendations for vitamin supplementation are inadequate and should be re-evaluated for these patients.

EMAs seem to be produced in the small bowel mucosa of celiac patients, but not in other tissues such as gastric mucosa. The production of EMAs could not be initiated under standard in vitro conditions and therefore, such as in vitro challenge cannot be used for diagnostic purposes.

Background: An increased permeability to sugars is found in the intestine of untreated patients with coeliac disease after oral ingestion. Aim: To test whether in vitro permeability resembles in vivo permeability tests and whether an in vitro gliadin gluten challenge could be performed by an in vitro permeability test. Methods: We measured in vivo (urinary excretion after sucrose–lactulose–mannitol ingestion) and in vitro permeability (by mini‐Ussing chambers) in 25 healthy controls, 12 relatives of coeliac disease patients, 19 treated, eight partly treated and 16 untreated patients with coeliac disease. Results: In vivo sugar permeability was increased in nearly all coeliac patients. Additionally, in vitro permeability to lactulose (P=0.0007), mannitol (P=0.004) and sucrose (P=0.042) was higher in untreated patients with coeliac disease. It correlated with in vivo permeability (sucrose τ=0.61, P=0.006; lactulose τ=0.41, P < 0.0001; mannitol τ=– 0.56, P=0.62) and was dependent on mucosal damage. An in vitro gliadin challenge over 24 h could not significantly change in vitro permeability in treated patients with coeliac disease. Conclusions: An in vitro permeability test capable of measuring elevated permeability in coeliac mucosa was described, but this test cannot replace oral gluten challenge by in vitro gliadin incubation.