A SMALL DOSE OF ETHANOL INCREASES THE EXHALATION OF MERCURY IN LOW-LEVEL-EXPOSED HUMANS

Inorganic mercury is mainly eliminated by urinary and fecal excretion, but it is also eliminated by exhalation and sweat. There are only a few reports on exhalation of mercury in humans. In volunteers with short-term mercury exposure, an increased exhalation of mercury was found after alcohol intake. The aim of this study was to determine mercury in end-exhaled air and the influence of ethanol on mercury exhalation in subjects with longterm mercury exposure from diet, amalgam fillings, or the work environment. Fourteen subjects, with different grades of mercury exposure, were given 0.2 g ethanol/kg body weight. Measurements of mercury in end-exhaled air were performed before and after alcohol intake. Mercury in end-exhaled air could be detected in all subjects. In 10 individuals without amalgam fillings the mercury concentration was 3 to 12 pg/L. A marked increase, in general about fivefold, in mercury concentrations in end-exhaled air was seen in all subjects 30 min after intake of alcohol, regardless of the level of mercury exposure. Higher ethanol doses resulted in higher mercury levels in end-exhaled air and longer time periods before a return to background levels. An increase was seen even after an ethanol dose of only 0.1 g ethanol/kg body weight (about 0.08 L wine). The decrease in exhaled mercury at higher alcohol doses followed approximately zero-order kinetics and probably reflects the elimination of ethanol in tissues. In conclusion, low levels of mercury can be detected in end-exhaled air also in individuals without amalgam fillings. About a fivefold increase was seen 30 min after alcohol intake, and the relative increase seemed to be independent of the body burden of mercury. Exhalation of mercury represents only a small percentage of the total elimination of mercury.     

Video capsule endoscopy for previous overt obscure gastrointestinal bleeding in patients using anti‐thrombotic drugs

Background and Aim: Little is known about the causes of overt obscure gastrointestinal bleeding (OGIB) in patients using anti‐thrombotic therapy. We aimed to describe video capsule endoscopy (VCE) findings and to identify factors associated with positive findings in these patients. Methods: We carried out a retrospective study of 56 patients who underwent VCE for evaluation of previous overt OGIB during anti‐thrombotic therapy. VCE studies were re‐evaluated by a gastroenterologist blinded to clinical details. Clinical data included in the multivariate analysis were sex, age, indication for and type of anti‐thrombotic therapy, hemodynamic instability on admission, type of blood loss, hemoglobin on admission, use of a proton pump inhibitor, NSAID use, time between bleeding episodes and VCE, and whether or not anti‐thrombotic therapy was resumed before the VCE study. Results: A probable cause for gastrointestinal bleeding was identified in 28 (50%) of the 56 studies. Angiodysplasia was found in 19 patients. Twenty‐two studies showed a possible cause in the small bowel. Multivariate logistic regression analysis showed that reinstitution of anti‐thrombotic therapy before VCE was carried out was the only independent predictor of positive VCE findings (OR: 8.61, 95% CI: 1.20–60.42, P = 0.032). Conclusions: Small intestinal angiodysplasia was the most common cause for overt OGIB. Reinstitution of withdrawn anti‐thrombotic drugs before the VCE examination was carried out was associated with positive VCE findings in multivariate analysis.     

Bleeding from gastrointestinal angioectasias is not related to bleeding disorders - a case control study

Background  

Angioectasias in the gastrointestinal tract can be found in up to 3% of the population. They are typically asymptomatic but may sometimes result in severe bleeding. The reasons for why some patients bleed from their angioectasias are not fully understood but it has been reported that it may be explained by an acquired von Willebrand syndrome (AVWS). This condition has similar laboratory findings to congenital von Willebrand disease with selective loss of large von Willebrand multimers. The aim of this study was to find out if AVWS or any other bleeding disorder was more common in patients with bleeding from angioectasias than in a control group.     

Evidence-based use of methotrexate in children with rheumatic diseases: a consensus statement of the Working Groups Pediatric Rheumatology Germany (AGKJR) and Pediatric Rheumatology Austria

Juvenile idiopathic arthritis (JIA) is the most common diagnosis in children and adolescents with rheumatic disorders. In many children and adolescents, JIA is successfully treated with non-steroidal anti-inflammatory drugs (NSAID) and physiotherapy. However, in a significant number of cases the disease is resistant to this therapy, and treatment with second line disease-modifying antirheumatic drugs (DMARDs) is required. Methotrexate (MTX) is frequently referred to as first-choice second-line agent for the treatment of JIA. To increase drug safety, the Working Groups for Children and Adolescents with Rheumatic Diseases in Germany (AGKJR) and Pediatric Rheumatology Austria have initiated the formulation of evidence-based recommendations. Evidence is based on consensus expert meetings, a MEDLINE search with the key words Methotrexate and juvenile arthritis limited to age 0–18 years, standard textbooks and review articles, data from the central registry of the German Research Center for Rheumatic Diseases (Deutsches Rheumaforschungszentrum Berlin DRFZ), experience with MTX in adults with rheumatoid arthritis (RA), and recommendations of the German Society of Rheumatology (DGRh). Based on these data, evidence and recommendations are graded, and evidence-based recommendations for the use of MTX in children and adolescents with rheumatic disease are presented.Section Pharmacotherapy of the Working Group Pediatric Rheumatology Germany and Austria: I. Foeldvari; J.P. Haas, A. Haeffner, D. Hobusch,G. Horneff, A. Hospach, R. Keitzer, G. Klaus, M. Metzler, H. Michels, T. Niehues, I. Pilz, M. Sailer Höck, M. Schöntube, L. Schuchmann, K. Schumacher, H.W. Seyberth, E. Siemers, A. Urban, E. Weißbarth-Riedl. Working Group Pediatric Rheumatology North-Rhine-Westfalia: S. Benseler, G. Bürk, S. Fahl, I. Foeldvari, D. Föll, M. Frosch, G. Ganser, S. Kastner, I. Kleine, E. Lainka, K. Mönkemöller, J. Neubert, U. Neudorf, T. Niehues, J. Roth, S. Seeliger, N. Wagner, R. Wieland, H. Winowski.     

Plasma Cholecystokinin and Gallbladder Responses to Increasing Doses of Bombesin in Celiac Disease

Impaired postprandial gallbladder emptying inceliac disease has been attributed to an absence ofappropriate cholecystokinin release. To determine if aflat jejunal mucosa in celiac patients is related to a reduced cholecystokinin-secretingcapacity, increasing doses of bombesin were infused intosix patients with celiac disease and a flat jejunalmucosa (group A), in seven celiac patients with a normal jejunal mucosa while on a gluten-free diet(group B), and in seven healthy controls (group C).Bombesin induced significant (P < 0.05) increments ofplasma CCK to a maximum value of 1.0 ± 0.3 pM in group A, to 1.5 ± 0.3 pM in group B, andto 1.2 ± 0.3 pM in group C (NS between groups),that were accompanied by significant (P < 0.05)gallbladder emptying responses of 70 ± 4% ingroup A, 47 ± 10% in group B and 65 5% in group C.Dose-response relationships were not different betweengroups. We conclude that there is no major impairment ofgallbladder responsiveness to bombesin or ofcholecystokinin-secreting capacity in patients with a flat jejunal mucosadue to celiac disease.