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"text": "\n11566\nFunctional endoscopic sinus surgery. Concept, indications and results of the Messerklinger technique.\n\nStammberger, H\n\nPosawetz, W\n\nBeiträge in Fachzeitschriften\nISI:A1990CT88300001\n2180446.0\nNone\nNone\nThe Messerklinger technique is a primarily diagnostic endoscopic concept demonstrating that the frontal and the maxillary sinuses are subordinate cavities. Disease usually starts in the nose and spreads through the ethmoidal prechambers to the frontal and maxillary sinuses, with infections of these latter sinuses thus usually being of secondary nature. Standard rhinoscopy and sinus X-rays are frequently not sufficient to demonstrate the underlying causes for chronic or recurring acute sinusitis in the clefts of the anterior ethmoidal sinuses. The combination of diagnostic endoscopy of the lateral nasal wall with conventional or computed tomography in the coronal plane has proven to be the ideal method for the examination of inflammatory disease of the paranasal sinuses. In so doing, diseases and lesions that otherwise might have gone undiagnosed can be identified and consequently treated. Based on this diagnostic approach, an endoscopic surgical concept was developed, aiming for the underlying causes of sinus diseases instead of the secondarily involved larger sinuses. With usually very limited surgical procedures, diseased ethmoid compartments are operated on, stenotic clefts widened and prechambers to the frontal and maxillary sinuses freed from disease. In our experience, there is rarely a need for major manipulations inside the larger sinuses per se. Based on exact diagnosis, the surgical technique used allows a very individualized staging according to the prevailing pathology. In the extreme, a total sphenoethmoidectomy can be performed with this technique, although the true advantage of the technique is that even in cases of massive disease such radical procedures can be avoided. By reestablishing sinus ventilation and drainage via the natural ostia, there is also no need for fenestration of the inferior meatus. The Messerklinger technique can be applied to a wide spectrum of indications, apart from nasal polyposis. The technique has its clear limits as well as its specific problems. Adequate training and experience are required for the surgical approach, as the technique bears all the risks and hazards of all kinds of endonasal ethmoid surgery but has a minimal complication rate in the hands of an experienced surgeon. Results and complications of a series of more than 4500 patients over a period of over 10 years are presented and discussed in detail.\n\n\n"
},
{
"text": "\n19348\nCharacteristics of interferon induced tryptophan metabolism in human cells in vitro.\n\nWerner-Felmayer, G\n\nWerner, ER\n\nFuchs, D\n\nHausen, A\n\nReibnegger, G\n\nWachter, H\n\nBeiträge in Fachzeitschriften\nISI:A1989AF34500004\n2500976.0\n10.1016/0167-4889(89)90087-6\nNone\nInterferon-gamma-induced tryptophan metabolism of human macrophages was compared to ten human neoplastic cell lines of various tissue origin and to normal dermal human fibroblasts. Tryptophan and metabolites were determined in supernatants of cultures, after incubation for 48 h, by high-performance liquid chromatography with ultraviolet and fluorescence detection. With the exception of two cell lines (Hep G 2, hepatoma and CaCo 2, colon adenocarcinoma) in all of the ten other cells and cell lines tryptophan degradation was induced by interferon-gamma. Five of these ten formed only kynurenine (SK-N-SH, neuroblastoma; T 24, J 82, bladder carcinoma; A 431, epidermoid carcinoma; normal dermal fibroblasts), three formed kynurenine and anthranilic acid (U 138 MG, glioblastoma; SK-HEP-1, hepatoma; A 549, lung carcinoma). Only one line, A 498 (kidney carcinoma) showed the same pattern of metabolites as macrophages (kynurenine, anthranilic acid and 3-hydroxyanthranilic acid). Interferon-gamma regulated only the activity of indoleamine 2, -dioxygenase. All other enzyme activities detected were independent of interferon-gamma, as shown by the capacity of the cells to metabolize L-kynurenine or N-formyl-L-kynurenine. Increasing the extracellular L-tryptophan concentration resulted in a marked induction of tryptophan degradation by macrophages. Contrarily, a significant decrease of the tryptophan degrading activity was observed when the extracellular L-tryptophan concentration was increased 2-fold with SK-N-SH, T 24 and J 82, 4-fold with A 431 and A 549 and 10-fold with U 138 MG and SK-HEP-1. The activity was unaffected by extracellular L-tryptophan with dermal fibroblasts and A 498. Though interferon-gamma was the most potent inducer of tryptophan metabolism, interferon-alpha and/or -beta showed small but distinct action on some of the cells. In all cells which reacted to interferon-gamma by enhanced expression of class I and/or class II major histocompatibility complex antigens tryptophan degradation was also inducible. These results demonstrate that induction of indoleamine 2, -dioxygenase is a common feature of interferon-gamma action, that the extent of this induction is influenced by extracellular L-tryptophan concentrations and that indoleamine 2, -dioxygenase is the only enzyme in the formation of 3-hydroxyanthranilic acid from tryptophan which is regulated by interferon-gamma.\n\nReibnegger, Gilbert\n\n\n"
},
{
"text": "\n63475\nIncreased proliferation, lytic activity, and purity of human natural killer cells cocultured with mitogen-activated feeder cells.\n\nRabinowich, H\n\nSedlmayr, P\n\nHerberman, RB\n\nWhiteside, TL\n\nBeiträge in Fachzeitschriften\nISI:A1991FP10800018\n1709827.0\n10.1016/0008-8749(91)90290-R\nNone\nThe addition of mitogen-prestimulated periferal blood lymphocytes (PBL) or Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCL) cultures to enriched populations of natural killer (NK) cells obtained from PBL of normal donors in the presence of rIL-2 resulted in highly significant increases in proliferation, purity, and cytolytic activity of cultured NK cells. Two sources of enriched NK cell preparations were used: (i) Adherent-lymphokine activated killer (A-LAK) cells obtained by adherence to plastic during 24 hr activation with 10(3) Cetus U/ml rIL-2; and (ii) NK cells negatively selected from PBL by removal of high-affinity rosette-forming cells and CD3+ lymphocytes. Coculture of A-LAK cells for 14 days with autologous or allogeneic Con A-activated PBL (10(6) cells/ml) or selected EBV-transformed LCL (2 x 10(5) cells/ml) as feeder cells increased fold expansion by a mean +/- SEM of 629 fold +/- 275 (P less than 0.019) and 267 fold +/- 54 (P less than 0.0001), respectively, compared to 55 +/- 20 in A-LAK cultures without feeder cells. The addition of either activated PBL or EBV lines to A-LAK cultures also led to a significant increase in the percentage of NK cells (CD3- CD56+) (84 +/- 2.4 and 84 +/- 2.6%, respectively, P less than 0.0001 for both), compared to 53 +/- 7.2% in cultures without feeders. The presence of feeder cells in cultures of A-LAK cells also led to significantly higher anti-tumor cytolytic activity compared to control cultures, as measured against NK-sensitive (K562) and NK-resistant (Daudi) target cells. Mitogen-stimulated CD4+ PBL purified by positive selection on antibody-coated flasks were better feeders than CD8+ or unseparated PBL. In the presence of feeder cells, it was possible to generate up to 6 x 10(9) activated NK cells from 2 x 10(8) fresh PBL by Day 13 of culture. Enhanced NK cell proliferation in the presence of feeder cells was not attributable to a detectable soluble factor. The improved method for generating A-LAK or activated-NK cells should facilitate cellular adoptive immunotherapy by providing sufficient numbers of highly enriched CD3- CD56+ effector cells with high anti-tumor activity.\n\nSedlmayr, Peter\n\n\n"
},
{
"text": "\n89867\nA predictive model for respiratory syncytial virus (RSV) hospitalisation of premature infants born at 33-35 weeks of gestational age, based on data from the Spanish FLIP Study.\n\nSimões, EA\n\nCarbonell-Estrany, X\n\nFullarton, JR\n\nLiese, JG\n\nFigueras-Aloy, J\n\nDoering, G\n\nGuzman, J\n\nEuropean RSV Risk Factor Study Group\n\nBeiträge in Fachzeitschriften\nISI:000263725700001\n19063742.0\n10.1186/1465-9921-9-78\nPMC2636782\nBACKGROUND: The aim of this study, conducted in Europe, was to develop a validated risk factor based model to predict RSV-related hospitalisation in premature infants born 33-35 weeks' gestational age (GA). METHODS: The predictive model was developed using risk factors captured in the Spanish FLIP dataset, a case-control study of 183 premature infants born between 33-35 weeks' GA who were hospitalised with RSV, and 371 age-matched controls. The model was validated internally by 100-fold bootstrapping. Discriminant function analysis was used to analyse combinations of risk factors to predict RSV hospitalisation. Successive models were chosen that had the highest probability for discriminating between hospitalised and non-hospitalised infants. Receiver operating characteristic (ROC) curves were plotted. RESULTS: An initial 15 variable model was produced with a discriminant function of 72% and an area under the ROC curve of 0.795. A step-wise reduction exercise, alongside recalculations of some variables, produced a final model consisting of 7 variables: birth +/- 10 weeks of start of season, birth weight, breast feeding for < or = 2 months, siblings > or = 2 years, family members with atopy, family members with wheeze, and gender. The discrimination of this model was 71% and the area under the ROC curve was 0.791. At the 0.75 sensitivity intercept, the false positive fraction was 0.33. The 100-fold bootstrapping resulted in a mean discriminant function of 72% (standard deviation: 2.18) and a median area under the ROC curve of 0.785 (range: 0.768-0.790), indicating a good internal validation. The calculated NNT for intervention to treat all at risk patients with a 75% level of protection was 11.7 (95% confidence interval: 9.5-13.6). CONCLUSION: A robust model based on seven risk factors was developed, which is able to predict which premature infants born between 33-35 weeks' GA are at highest risk of hospitalisation from RSV. The model could be used to optimise prophylaxis with palivizumab across Europe.\n\nResch, Bernhard\n\n\n"
},
{
"text": "\n92261\nChanges in white matter as determinant of global functional decline in older independent outpatients: three year follow-up of LADIS (leukoaraiosis and disability) study cohort\n\nInzitari, D\n\nPracucci, G\n\nPoggesi, A\n\nCarlucci, G\n\nBarkhof, F\n\nChabriat, H\n\nErkinjuntti, T\n\nFazekas, F\n\nFerro, JM\n\nHennerici, M\n\nLanghorne, P\n\nO'Brien, J\n\nScheltens, P\n\nVisser, MC\n\nWahlund, LO\n\nWaldemar, G\n\nWallin, A\n\nPantoni, L\n\nBeiträge in Fachzeitschriften\nISI:000267898000002\nNone\n10.1136/bmj.b2477\nNone\nObjective To assess the impairment in daily living activities in older people with age related changes in white matter according to the severity of these changes. Design Observational data collection and follow-up of a cohort of older people undergoing brain magnetic resonance imaging after non-disabling complaints. Setting 11 European centres. Participants 639 non-disabled older patients (mean age 74.1 (SD 5.0), 45.1% men) in whom brain magnetic resonance imaging showed mild, moderate, or severe age related changes in white matter (Fazekas scale). Magnetic resonance imaging assessment also included cerebral infarcts and atrophy. Main outcome measure Transition from no disability (defined as a score of 0 or 1 on the instrumental activities of daily living scale) to disability (score >= 2) or death over three year follow-up. Secondary outcomes were incident dementia and stroke. Results Over a mean follow-up period of 2.42 years (SD 0.97, median 2.94 years), information on the main outcome was available for 633 patients. The annual rate of transition or death was 10.5%, 15.1%, and 29.5%, respectively, for patients with mild, moderate, or severe age related changes in white matter (Kaplan-Meier log rank test P<0.001). In a Cox model comparing severe with mild changes and adjusted for clinical factors of functional decline, the risk of transition to disability or death was more than twofold higher (hazard ratio 2.36, 95% confidence interval 1.65 to 3.81). The other predictors were age group, history of atrial fibrillation, and complaint of gait disturbances. The effect of severe changes remained significant independently of baseline degree of atrophy and number of infarcts. Incident stroke and dementia only slightly modified this effect. Conclusion The three year results of the LADIS study suggest that in older adults who seek medical attention for non-disabling complaints, severe age related changes in white matter independently and strongly predict rapid global functional decline.\n\nFazekas, Franz\n\n\n"
},
{
"text": "\n92611\nThe extent of lymphadenectomy seems to be associated with better survival in patients with nonmetastatic upper-tract urothelial carcinoma: how many lymph nodes should be removed?\n\nRoscigno, M\n\nShariat, SF\n\nMargulis, V\n\nKarakiewicz, P\n\nRemzi, M\n\nKikuchi, E\n\nZigeuner, R\n\nWeizer, A\n\nSagalowsky, A\n\nBensalah, K\n\nRaman, JD\n\nBolenz, C\n\nKassou, W\n\nKoppie, TM\n\nWood, CG\n\nWheat, J\n\nLangner, C\n\nNg, CK\n\nCapitanio, U\n\nBertini, R\n\nFernández, MI\n\nMikami, S\n\nIsida, M\n\nStröbel, P\n\nMontorsi, F\n\nBeiträge in Fachzeitschriften\nISI:000269280900017\n19559518.0\n10.1016/j.eururo.2009.06.004\nNone\nBackground: The role and extent of lymphadenectomy in patients with upper-tract urothelial carcinoma (UTUC) is debated. Objective: To establish whether the number of lymph nodes (LNs) removed might be associated with better cause-specific survival in patients with UTUC. Design, setting, and participants: The study included 552 consecutive patients who underwent radical nephroureterectomy (RNU) and lymphadenectomy between 1992 and 2006. Intervention: Patients were treated with RNU and lymphadenectomy. Measurements: Univariable and multivariable Cox proportional hazards regression models addressed the association between the number of LNs removed and cause-specific mortality (CSM). The number of LNs removed was coded as a cubic spline to allow for nonlinear effects. Finally, the most informative cut-off for the number of removed LNs was identified. Results and limitations: in the entire population, the number of LNs removed was not associated with CSM. in univariable (hazard ratio [HR]: 0.99; p = 0.16) or in multi-variable (HR: 0.97; p = 0.12) analyses. In contrast, in the subgroup of pNO patients (n = 412), the number of LNs removed achieved the independent predictor status of CSM (HR: 0.93; p = 0.02). Eight LNs removed was the most informative cut-off in predicting CSM (HR: 0.42; p = 0.004). The inclusion of the variable defining dichotomously the number of removed LNs (<8 vs >= 8) in the base model (age, Eastern Cooperative Oncology Group performance status, pathologic stage, grade, architecture, and lymphovascular invasion) significantly increased the accuracy in predicting CSM (+1.7%; p < 0.001). Conclusions: The extension of the lymphadenectomy in pNO UTUC patients seems to be associated with CSM. Longer survival was observed in patients in whom at least eight LNs had been removed. (C) 2009 European Association of Urology. Published by Elsevier B.V. All rights reserved.\n\nLangner, Cord\n\nZigeuner, Richard\n\n\n"
},
{
"text": "\n132779\nA global analysis of multitrial data investigating quality of life and symptoms as prognostic factors for survival in different tumor sites.\n\nQuinten, C\n\nMartinelli, F\n\nCoens, C\n\nSprangers, MA\n\nRingash, J\n\nGotay, C\n\nBjordal, K\n\nGreimel, E\n\nReeve, BB\n\nMaringwa, J\n\nEdiebah, DE\n\nZikos, E\n\nKing, MT\n\nOsoba, D\n\nTaphoorn, MJ\n\nFlechtner, H\n\nSchmucker-Von Koch, J\n\nWeis, J\n\nBottomley, A\n\nPatient Reported Outcomes and Behavioral Evidence (PROBE) and the European Organization for Research and Treatment of Cancer (EORTC) Clinical Groups\n\nBeiträge in Fachzeitschriften\nISI:000329334000022\n24127333.0\n10.1002/cncr.28382\nNone\nThe objective of this study was to examine the prognostic value of baseline health-related quality of life (HRQOL) for survival with regard to different cancer sites using 1 standardized and validated patient self-assessment tool.\n In total, 11 different cancer sites pooled from 30 European Organization for Research and Treatment of Cancer (EORTC) randomized controlled trials were selected for this study. For each cancer site, univariate and multivariate Cox proportional hazards modeling was used to assess the prognostic value (P< .05) of 15 HRQOL parameters using the EORTC Core Quality of Life Questionnaire (QLQ-C30). Models were adjusted for age, sex, and World Health Organization performance status and were stratified by distant metastasis.\n In total, 7417 patients completed the EORTC QLQ-C30 before randomization. In brain cancer, cognitive functioning was predictive for survival; in breast cancer, physical functioning, emotional functioning, global health status, and nausea and vomiting were predictive for survival; in colorectal cancer, physical functioning, nausea and vomiting, pain, and appetite loss were predictive for survival; in esophageal cancer, physical functioning and social functioning were predictive for survival; in head and neck cancer, emotional functioning, nausea and vomiting, and dyspnea were predictive for survival; in lung cancer, physical functioning and pain were predictive for survival; in melanoma, physical functioning was predictive for survival; in ovarian cancer, nausea and vomiting were predictive for survival; in pancreatic cancer, global health status was predictive for survival; in prostate cancer, role functioning and appetite loss were predictive for survival; and, in testis cancer, role functioning was predictive for survival.\n The current results demonstrated that, for each cancer site, at least 1 HRQOL domain provided prognostic information that was additive over and above clinical and sociodemographic variables.\n © 2013 American Cancer Society.\n\nGreimel, Elfriede Renate\n\n\n"
},
{
"text": "\n142777\nProton pump inhibitor intake neither predisposes to spontaneous bacterial peritonitis or other infections nor increases mortality in patients with cirrhosis and ascites.\n\nMandorfer, M\n\nBota, S\n\nSchwabl, P\n\nBucsics, T\n\nPfisterer, N\n\nSummereder, C\n\nHagmann, M\n\nBlacky, A\n\nFerlitsch, A\n\nSieghart, W\n\nTrauner, M\n\nPeck-Radosavljevic, M\n\nReiberger, T\n\nBeiträge in Fachzeitschriften\nISI:000344402000022\n25369194.0\n10.1371/journal.pone.0110503\nPMC4219684\nThe aim of this study was to assess the impact of proton pump inhibitor (PPI) intake on the development of spontaneous bacterial peritonitis (SBP) or other infections, as well as on mortality, in a thoroughly documented cohort of patients with cirrhosis and ascites.\n We performed a retrospective analysis of follow-up data from 607 consecutive patients with cirrhosis undergoing their first paracentesis at a tertiary center. A binary logistic regression model investigating the association between PPI intake and SBP at the first paracentesis was calculated. Competing risk analyses and Cox models were used to investigate the effect of PPIs on the cumulative incidence of SBP or other infections and transplant-free survival, respectively. Adjustments were made for age, hepatocellular carcinoma, history of variceal bleeding, varices and model of end-stage liver disease score.\n Eighty-six percent of patients were receiving PPIs. After adjusting for potential confounding factors, PPI intake was neither associated with increased SBP prevalence at the first paracentesis (odds ratio (OR):1.11, 5% confidence interval (95%CI):0.6-2.06; P = 0.731) nor cumulative incidence of SBP (subdistribution hazard ratio (SHR): 1.38; 95%CI:0.63-3.01; P = 0.42) and SBP or other infections (SHR:1.71; 95%CI:0.85-3.44; P = 0.13) during follow-up. Moreover, PPI intake had no impact on transplant-free survival in both the overall cohort (hazard ratio (HR):0.973, 5%CI:0.719-1.317; P = 0.859) as well as in the subgroups of patients without SBP (HR:1.01, 5%CI:0.72-1.42; P = 0.971) and without SBP or other infections at the first paracentesis (HR:0.944, 5%CI:0.668-1.334; P = 0.742).\n The proportion of cirrhotic patients with PPI intake was higher than in previous reports, suggesting that PPI indications were interpreted liberally. In our cohort with a particularly high prevalence of PPI intake, we observed no association between PPIs and SBP or other infections, as well as mortality. Thus, the severity of liver disease and other factors, rather than PPI treatment per se may predispose for infectious complications.\n\n\n"
},
{
"text": "\n145782\nLevels and function of regulatory T cells in patients with polymorphic light eruption: relation to photohardening.\n\nSchweintzger, N\n\nGruber-Wackernagel, A\n\nReginato, E\n\nBambach, I\n\nQuehenberger, F\n\nByrne, SN\n\nWolf, P\n\nBeiträge in Fachzeitschriften\nISI:000360696100035\n26032202.0\n10.1111/bjd.13930\nPMC4564948\nWe hypothesized that regulatory T cells (Tregs) are involved in the immunological abnormalities seen in patients with polymorphic light eruption (PLE).\n To investigate the number and suppressive function of peripheral Tregs in patients with PLE compared with healthy controls.\n Blood sampling was done in 30 patients with PLE [seeking or not seeking 311-nm ultraviolet (UV)B photohardening] as well as 19 healthy controls at two time points: TP1, March to June (before phototherapy); and TP2, May to August (after phototherapy). We compared the number of CD4(+) CD25(high) CD127(-) FoxP3(+) Tregs by flow cytometry and their function by assessing FoxP3 mRNA levels and effector T cell/Treg suppression assays.\n Tregs isolated from healthy controls significantly suppressed the proliferation of effector T cells at TP1 by 68% (P = 0·0156). In contrast, Tregs from patients with PLE entirely lacked the capacity to suppress effector T-cell proliferation at that time point. The medical photohardening seen in 23 patients with PLE resulted in a significant increase in the median percentage of circulating Tregs [both as a proportion of all lymphocytes; 65 6% increase (P = 0·0049), and as a proportion of CD4(+) T cells; 32.5% increase (P = 0·0049)]. This was accompanied by an increase in the expression of FoxP3 mRNA (P = 0·0083) and relative immunosuppressive function of Tregs (P = 0·083) comparing the two time points in representative subsets of patients with healthy controls tested. Seven patients with PLE not receiving 311-nm UVB also exhibited an increase in the number of Tregs but this was not statistically significant. No significant differences in Treg numbers were observed in healthy subjects between the two time points.\n An impaired Treg function is likely to play a role in PLE pathogenesis. A UV-induced increase in the number of Tregs (either naturally or therapeutically) may be a compensatory mechanism by which the immune system counteracts the susceptibility to PLE.\n © 2015 The Authors. British Journal of Dermatology published by John Wiley & Sons Ltd on behalf of British Association of Dermatologists.\n\nGruber-Wackernagel, Alexandra\n\nPerchthaler, Isabella\n\nQuehenberger, Franz\n\nSchweintzger, Nina\n\nWolf, Peter\n\n\n"
},
{
"text": "\n177610\nThe Transatlantic HbA<sub>1c</sub> gap: differences in glycaemic control across the lifespan between people included in the US T1D Exchange Registry and those included in the German/Austrian DPV registry.\n\nHermann, JM\n\nMiller, KM\n\nHofer, SE\n\nClements, MA\n\nKarges, W\n\nFoster, NC\n\nFröhlich-Reiterer, E\n\nRickels, MR\n\nRosenbauer, J\n\nDeSalvo, DJ\n\nHoll, RW\n\nMaahs, DM\n\nT1D Exchange Clinic Network and the DPV initiative\n\nBeiträge in Fachzeitschriften\nISI:000489868100001\n31557351.0\n10.1111/dme.14148\nNone\nTo compare HbA1c levels across the lifespan in people with type 1 diabetes in the USA with those in Germany/Austria, and to examine potential differences in HbA1c levels between sexes, insulin delivery methods and minority status.\n Data were extracted from the US T1D Exchange Registry (n=18 381 participants from 73 sites) and from the German/Austrian Prospective Diabetes Follow-up Registry, the DPV (n=32 643 participants from 362 sites). Mean HbA1c was calculated for each year of age for individuals aged ≤25 years, and at 2-year age intervals for individuals aged >25 years. Curves for mean HbA1c by age were estimated using locally weighted scatterplot smoothing. HbA1c differences between registries, sexes, insulin delivery methods, and minority status were assessed by age group using multiple linear regression.\n In both registries, mean HbA1c increased by ~11 mmol/mol (1.0%) between the ages of 9 and 18 years, although at quite different absolute levels: from 66 mmol/mol (8.2%) to 77 mmol/mol (9.2%) in the T1D Exchange Registry, and from 56 mmol/mol (7.3%) to 66 mmol/mol (8.2%) in the DPV. Sex differences were observed in the DPV only. In the T1D Exchange Registry, injection users had higher mean HbA1c than pump users across the lifespan, whereas in the DPV higher HbA1c levels in injection users were observed in the age groups 6 to <12 years, 12 to <18 years, and 30 to <50 years (P < 0.001). Minority status was significantly associated with higher HbA1c in most age groups in both registries.\n Significant differences in HbA1c were noted between the USA and Germany/Austria, with disparities more pronounced in early childhood through to young adulthood. Further studies should identify causes for these disparities.\n © 2019 The Authors. Diabetic Medicine published by John Wiley & Sons Ltd on behalf of Diabetes UK.\n\nFröhlich-Reiterer, Elke\n\n\n"
},
{
"text": "\n181887\nMembrane Rearrangements in the Maturation of Circulating Human Reticulocytes.\n\nMinetti, G\n\nBernecker, C\n\nDorn, I\n\nAchilli, C\n\nBernuzzi, S\n\nPerotti, C\n\nCiana, A\n\nBeiträge in Fachzeitschriften\nISI:000525532800001\n32256383.0\n10.3389/fphys.2020.00215\nPMC7092714\nRed blood cells (RBCs) begin their circulatory life as reticulocytes (Retics) after their egress from the bone marrow where, as R1 Retics, they undergo significant rearrangements in their membrane and intracellular components, via autophagic, proteolytic, and vesicle-based mechanisms. Circulating, R2 Retics must complete this maturational process, which involves additional loss of significant amounts of membrane and selected membrane proteins. Little is known about the mechanism(s) at the basis of this terminal differentiation in the circulation, which culminates with the production of a stable biconcave discocyte. The membrane of R1 Retics undergoes a selective remodeling through the release of exosomes that are enriched in transferrin receptor and membrane raft proteins and lipids, but are devoid of Band 3, glycophorin A, and membrane skeletal proteins. We wondered whether a similar selective remodeling occurred also in the maturation of R2 Retics. Peripheral blood R2 Retics, isolated by an immunomagnetic method, were compared with mature circulating RBCs from the same donor and their membrane protein and lipid content was analyzed. Results show that both Band 3 and spectrin decrease from R2 Retics to RBCs on a "per cell" basis. Looking at membrane proteins that are considered as markers of membrane rafts, flotillin-2 appears to decrease in a disproportionate manner with respect to Band 3. Stomatin also decreases but in a more proportionate manner with respect to Band 3, hinting at a heterogeneous nature of membrane rafts. High resolution lipidomics analysis, on the contrary, revealed that those lipids that are typically representative of the membrane raft phase, sphingomyelin and cholesterol, are enriched in mature RBCs with respct to Retics, relative to total cell lipids, strongly arguing in favor of the selective retention of at least certain subclasses of membrane rafts in RBCs as they mature from Retics. Our hypothesis that rafts serve as additional anchoring sites for the lipid bilayer to the underlying membrane-skeleton is corroborated by the present results. It is becoming ever more clear that a proper lipid composition of the reticulocyte is necessary for the production of a normal mature RBC.\n Copyright © 2020 Minetti, Bernecker, Dorn, Achilli, Bernuzzi, Perotti and Ciana.\n\nBernecker, Claudia\n\nDorn, Isabel\n\n\n"
},
{
"text": "\n63138\nStructure and dynamics of peptide-polynucleotide complexes.\n\nDesoye, G\n\nPorschke, D\n\nBeiträge in Fachzeitschriften\nISI:A1993LH62700008\n8343573.0\n10.1016/0301-4622(93)80021-A\nNone\nThe mode and the dynamics of LysTrpLys-binding to double helical DNA and to single stranded poly(A) has been analyzed by measurements of the chemical relaxation detected by fluorescence and of the rotational diffusion using the electric dichroism. The chemical relaxation, induced by electric field pulses, requires two exponentials for a satisfactory representation, indicating a two step reaction mechanism. The data are consistent with a bimolecular reaction step followed by a relatively slow intramolecular transition, which is expected to reflect "insertion" of the Trp-indole residues between the nucleic acid bases. The experimental data are analyzed quantitatively by global fitting with exact correction of the convolution due to the experimental device. In this procedure a complete set of relaxation curves is fitted directly to the reaction model and, thus artifacts resulting from erroneous assignments of coupled modes are avoided. According to this analysis the bimolecular reaction step is controlled by diffusion. The intramolecular transition in adenylate chains is found to be dependent on the chain length and on the ionic strength I: at I = 2.5 mM the "insertion" rate constant is 3 x 10(4) s-1 for the polymer and 2 x 10(5) s-1 for A(pA)19; the rate constant for poly(A) increases with increasing salt concentration. The corresponding "insertion" rate constant for DNA double helices with 30 kbp is 2.5 x 10(4) s-1. For DNA double helices we find again an increase of the "insertion" rate with increasing salt concentration and with decreasing chain length. The mode of LysTrpLys-binding to double helical DNA is compared with that of LysTyrLys, LysLeuLys and LysGlyLys by measurements of the rotational diffusion of complexes with restriction fragments of different chain lengths. The persistence lengths derived from these measurements do not reveal any special effects resulting from insertion of aromatic residues. Apparently "insertion" of indole rings into double helical DNA does not increase the length of the double helix, which may be attributed to a special form of insertion, e.g. partial insertion. According to these results the interaction of the indole residues of LysTrpLys with DNA double helices is not equivalent to e.g. intercalation of aromatic residues like ethidium-neither with respect to structure nor to dynamics.\n\nDesoye, Gernot\n\n\n"
},
{
"text": "\n72248\nTreatment of proximal deep-vein thrombosis with the oral direct factor Xa inhibitor rivaroxaban (BAY 59-7939): the ODIXa-DVT (Oral Direct Factor Xa Inhibitor BAY 59-7939 in Patients With Acute Symptomatic Deep-Vein Thrombosis) study.\n\nAgnelli, G\n\nGallus, A\n\nGoldhaber, SZ\n\nHaas, S\n\nHuisman, MV\n\nHull, RD\n\nKakkar, AK\n\nMisselwitz, F\n\nSchellong, S\n\nODIXa-DVT Study Investigators (with Pilger, E)\n\nBeiträge in Fachzeitschriften\nISI:000247902600009\n17576867.0\n10.1161/CIRCULATIONAHA.106.668020\nNone\nBACKGROUND: An effective and safe oral anticoagulant that needs no monitoring for dose adjustment is urgently needed for the treatment of diseases that require long-term anticoagulation. Rivaroxaban (BAY 59-7939) is an oral direct factor Xa inhibitor currently under clinical development. METHODS AND RESULTS: This randomized, parallel-group phase II trial in patients with proximal deep-vein thrombosis explored the efficacy and safety of rivaroxaban 10, 20, or 30 mg BID or 40 mg once daily compared with enoxaparin 1 mg/kg BID followed by vitamin K antagonist. Each treatment was administered for 12 weeks. The primary efficacy end point was an improvement in thrombotic burden at day 21 (assessed by quantitative compression ultrasonography; > or = 4-point improvement in thrombus score) without recurrent symptomatic venous thromboembolism or venous thromboembolism-related death. The primary safety end point was major bleeding during 12 weeks of treatment. Outcomes were adjudicated centrally without knowledge of treatment allocation. The primary efficacy end point was achieved in 53 (53.0%) of 100, 58 (59.2%) of 98, 62 (56.9%) of 109, and 49 (43.8%) of 112 patients receiving rivaroxaban 10, 20, or 30 mg BID or 40 mg once daily, respectively, compared with 50 (45.9%) of 109 patients treated with enoxaparin/vitamin K antagonist. There was no significant trend in the dose-response relationship between rivaroxaban BID and the primary efficacy end point (P=0.67). Major bleeding was observed in 1.7%, 1.7%, 3.3%, and 1.7% of patients receiving rivaroxaban 10, 20, or 30 mg BID or 40 mg once daily, respectively. There were no major bleeding events with enoxaparin/vitamin K antagonist. CONCLUSIONS: Results of this proof-of-concept and dose-finding study support phase III evaluation of the orally active direct factor Xa inhibitor rivaroxaban, because efficacy and safety were apparent in the treatment of proximal deep-vein thrombosis across a 3-fold range of fixed daily dosing.\n\nPilger, Ernst\n\n\n"
},
{
"text": "\n98302\nLack of bioequivalence between two methylphenidate extended modified release formulations in healthy volunteers.\n\nSchütz, H\n\nFischer, R\n\nGrossmann, M\n\nMazur, D\n\nLeis, HJ\n\nAmmer, R\n\nBeiträge in Fachzeitschriften\nISI:000273101800009\n19954715.0\nNone\nNone\nOBJECTIVE: To assess bioequivalence between Equasym Retard and Medikinet retard containing 20 mg methylphenidate (MPH) hydrochloride in a fed state. MATERIALS: Equasym Retard 20 mg capsules (UCB, Monheim, Germany) and Medikinet retard 20 mg capsules (Medice, Iserlohn, Germany). METHODS: This was an open, single-center, randomized, 2-period, 2-sequence, balanced cross-over study with a wash-out period of 1 week between administrations in 14 healthy male and female volunteers, aged 18 - 45 years. Blood samples were collected over 24 hours and methylphenidate plasma concentration-time data were used to calculate pharmacokinetic metrics for both formulations. The main metrics were AUC0-t and Cmax. Bioequivalence was concluded if the 90% confidence interval (CI) for the ratio between test and reference was 80 - 125% (AUC0-t, Cmax). RESULTS: All dosed subjects finished both treatment periods and were included in pharmacokinetic and safety analyses. The adverse events observed, mainly nervous system disorders (headache), were all mild or moderate in intensity and resolved without any action taken. The adverse event profile was consistent with the currently applicable SmPCs (Summaries of Product Characteristics) for Equasym Retard and Medikinet retard. Geometric means +/- SD for AUC0-t and Cmax were 35.5 +/- 10.1 ng x h/ml and 4.05 +/- 0.96 ng/ml (Equasym Retard) and 39.2 +/- 13.8 ng x h/ml and 5.26 +/- 2.11 ng/ml (Medikinet retard). The 90% geometric confidence interval for AUC0-t (extent of absorption) was within limits accepted for bioequivalence. Bioequivalence could not be demonstrated for the rate of bioavailability (Cmax); both the lower confidence limit and the point estimate were below 80% of the reference. The study has shown that both formulations lead to a similar pattern of absorption and elimination following single dose administration in the fed state, although the test formulation shows a somewhat slimmer profile, where the first peak is less pronounced. No bioequivalence could be shown within the first 4 hours. The second peak of the test was also lower than the one of the reference (both lower confidence limit and point estimate below 80%). CONCLUSIONS: The two formulations are not bioequivalent, especially if the rate and values within the first four hours after administration are taken into account.\n\nLeis, Hans-Joerg\n\n\n"
},
{
"text": "\n127816\nTCR-γ expression in primary cutaneous T-cell lymphomas.\n\nRodríguez-Pinilla, SM\n\nOrtiz-Romero, PL\n\nMonsalvez, V\n\nTomás, IE\n\nAlmagro, M\n\nSevilla, A\n\nCamacho, G\n\nLongo, MI\n\nPulpillo, Á\n\nDiaz-Pérez, JA\n\nMontes-Moreno, S\n\nCastro, Y\n\nEchevarría, B\n\nTrébol, I\n\nGonzalez, C\n\nSánchez, L\n\nOtín, AP\n\nRequena, L\n\nRodríguez-Peralto, JL\n\nCerroni, L\n\nPiris, MÁ\n\nBeiträge in Fachzeitschriften\nISI:000315095000007\n23348211.0\n10.1097/PAS.0b013e318275d1a2\nNone\nPrimary cutaneous γδ T-cell lymphomas (PCGD-TCLs) are considered a subgroup of aggressive cytotoxic T-cell lymphomas (CTCLs). We have taken advantage of a new, commercially available antibody that recognizes the T-cell receptor-γ (TCR-γ) subunit of the TCR in paraffin-embedded tissue. We have analyzed a series of 146 primary cutaneous T-cell lymphomas received for consultation or a second opinion in the CNIO Pathology Department. Cases were classified according to the World Health Organization 2008 classification as mycosis fungoides (MF; n=96), PCGD-TCLs (n=5), pagetoid reticulosis (n=6), CD30(+) primary cutaneous anaplastic large cell lymphomas (n=5), primary cutaneous CD8 aggressive epidermotropic CTCLs (n=3), primary cutaneous CTCL, not otherwise specified (n=4), and extranodal nasal-type NK/T-cell lymphomas primarily affecting the skin or subcutaneous tissue (n=11). Sixteen cases of the newly named lymphomatoid papulosis type D (LyP-D; n=16) were also included. In those cases positive for TCR-γ, a further panel of 13 antibodies was used for analysis, including TIA-1, granzyme B, and perforin. Clinical and follow-up data were recorded in all cases. Twelve cases (8.2%) were positive for TCR-γ, including 5 PCGD-TCLs, 2 MFs, and 5 LyP-Ds. All 5 PCGD-TCL patients and 1 MF patient died of the disease, whereas the other MF patient and all those with LyP-D were alive. All cases expressed cytotoxic markers, were frequently CD3(+)/CD8(+), and tended to lose CD5 and CD7 expressions. Eight of 12 and 5 of 11 cases were CD30(+) and CD56(+), respectively. Interestingly, 5/12 TCR-γ-positive cases also expressed TCR-BF1. All cases analyzed were negative for Epstein-Barr virus-encoded RNA. In conclusion, TCR-γ expression seems to be rare and is confined to cytotoxic primary cutaneous TCLs. Nevertheless, its expression is not exclusive to PCGD-TCLs, as TCR-γ protein can be found in other CTCLs. Moreover, its expression does not seem to be associated with bad prognosis by itself, as it can be found in cases with good and bad outcomes.\n\nCerroni, Lorenzo\n\n\n"
},
{
"text": "\n149511\nA Follow-Up of the Multicenter Collaborative Study on HIV-1 Drug Resistance and Tropism Testing Using 454 Ultra Deep Pyrosequencing.\n\nSt John, EP\n\nSimen, BB\n\nTurenchalk, GS\n\nBraverman, MS\n\nAbbate, I\n\nAerssens, J\n\nBouchez, O\n\nGabriel, C\n\nIzopet, J\n\nMeixenberger, K\n\nDi Giallonardo, F\n\nSchlapbach, R\n\nParedes, R\n\nSakwa, J\n\nSchmitz-Agheguian, GG\n\nThielen, A\n\nVictor, M\n\nMetzner, KJ\n\nDäumer, MP\n\n454 HIV-1 Alpha Study Group\n\nBeiträge in Fachzeitschriften\nISI:000367888800027\n26756901.0\n10.1371/journal.pone.0146687\nPMC4710461\nUltra deep sequencing is of increasing use not only in research but also in diagnostics. For implementation of ultra deep sequencing assays in clinical laboratories for routine diagnostics, intra- and inter-laboratory testing are of the utmost importance.\n A multicenter study was conducted to validate an updated assay design for 454 Life Sciences' GS FLX Titanium system targeting protease/reverse transcriptase (RTP) and env (V3) regions to identify HIV-1 drug-resistance mutations and determine co-receptor use with high sensitivity. The study included 30 HIV-1 subtype B and 6 subtype non-B samples with viral titers (VT) of 3, 40-447, 00 copies/mL, two dilution series (52, 29-1, 40 and 25, 30-734 copies/mL), and triplicate samples. Amplicons spanning PR codons 10-99, RT codons 1-251 and the entire V3 region were generated using barcoded primers. Analysis was performed using the GS Amplicon Variant Analyzer and geno2pheno for tropism. For comparison, population sequencing was performed using the ViroSeq HIV-1 genotyping system.\n The median sequencing depth across the 11 sites was 1, 29 reads per position for RTP (IQR 592-3, 88) and 2, 10 for V3 (IQR 786-3, 95). 10 preselected drug resistant variants were measured across sites and showed high inter-laboratory correlation across all sites with data (P<0.001). The triplicate samples of a plasmid mixture confirmed the high inter-laboratory consistency (mean% ± stdev: 4.6 ±0.5, 4.8 ±0.4, 4.9 ±0.3) and revealed good intra-laboratory consistency (mean% range ± stdev range: 4.2-5.2 ± 0.04-0.65). In the two dilutions series, no variants >20% were missed, variants 2-10% were detected at most sites (even at low VT), and variants 1-2% were detected by some sites. All mutations detected by population sequencing were also detected by UDS.\n This assay design results in an accurate and reproducible approach to analyze HIV-1 mutant spectra, even at variant frequencies well below those routinely detectable by population sequencing.\n\n\n"
},
{
"text": "\n154825\nTwo-year follow-up of outcomes related to scarring and distress in children with severe burns.\n\nWurzer, P\n\nForbes, AA\n\nHundeshagen, G\n\nAndersen, CR\n\nEpperson, KM\n\nMeyer, WJ\n\nKamolz, LP\n\nBranski, LK\n\nSuman, OE\n\nHerndon, DN\n\nFinnerty, CC\n\nBeiträge in Fachzeitschriften\nISI:000401704500010\n27685196.0\n10.1080/09638288.2016.1209579\nPMC5465822\nWe assessed the perception of scarring and distress by pediatric burn survivors with burns covering more than one-third of total body surface area (TBSA) for up to 2 years post-burn.\n Children with severe burns were admitted to our hospital between 2004 and 2012, and consented to this IRB-approved-study. Subjects completed at least one Scars Problems and/or Distress questionnaire between discharge and 24 months post burn. Outcomes were modeled with generalized estimating equations or using mixed linear models. Significance was accepted at p < 0.01.\n Responses of 167 children with a mean age of 7 ± 5 years and burns covering an average 54 ± 14% of TBSA were analyzed. Significant improvements over the 2-year period were seen in reduction of pain, itching, sleeping disturbance, tightness, range of motion, and strength (p < 0.01). There was a significantly increased persistent desire to hide the scarred body areas over time (p < 0.01). The perception of mouth scarring, inability to portray accurate facial expressions, and skin coloration did not improve over the follow-up period.\n According to self-assessment questionnaires, severely burned children exhibit significant improvements in their overall perception of scarring and distress. However, these patients remain self-conscious with respect to their body image even 2 years after burn injury. Implications for Rehabilitation According to self-assessment questionnaires, severely burned children perceive significant improvements in scarring and distress during the first 2 years post burn. Significant improvements were seen in reduction of pain, itching, sleeping disturbances, tightness, range of motion, and strength (p < 0.01). Burn care providers should improve the treatment of burns surrounding the mouth that with result in scarring, and develop strategies to prevent skin discoloration. Careful evaluation of pain and sleeping disorders during the first year post burn are warranted to improve the patient rehabilitation. Overall, significantly more female patients expressed a persistent desire to hide their scarred body areas. The rehabilitation team should provide access to wigs or other aids to pediatric burn survivors to address these needs.\n\nBranski, Ludwik\n\nKamolz, Lars-Peter\n\nWurzer, Paul\n\n\n"
},
{
"text": "\n160113\nWidespread cortical demyelination of both hemispheres can be induced by injection of pro-inflammatory cytokines via an implanted catheter in the cortex of MOG-immunized rats.\n\nÜçal, M\n\nHaindl, MT\n\nAdzemovic, MZ\n\nStrasser, J\n\nTheisl, L\n\nZeitelhofer, M\n\nKraitsy, K\n\nRopele, S\n\nSchäfer, U\n\nFazekas, F\n\nHochmeister, S\n\nBeiträge in Fachzeitschriften\nISI:000404076700004\n28457906.0\n10.1016/j.expneurol.2017.04.014\nNone\nCortical demyelination is a common finding in patients with chronic multiple sclerosis (MS) and contributes to disease progression and overall disability. The exact pathomechanism that leads to cortical lesions is not clear. Research is limited by the fact that standard animal models of multiple sclerosis do not commonly affect the cortex, or if they do in some variants, the cortical demyelination is rather sparse and already remyelinated within a few days. In an attempt to overcome these limitations we implanted a tissue-compatible catheter into the cortex of Dark Agouti rats. After 14days the rats were immunized with 5μg myelin oligodendrocyte glycoprotein (MOG) in incomplete Freund's Adjuvant, which did not cause any clinical signs but animals developed a stable anti-MOG antibody titer. Then the animals received an injection of proinflammatory cytokines through the catheter. This led to a demyelination of cortical and subcortical areas starting from day 1 in a cone-like pattern spreading from the catheter area towards the subarachnoid space. On day 3 cortical demyelination already expanded to the contralateral hemisphere and reached its peak between days 9-15 after cytokine injection with a widespread demyelination of cortical and subcortical areas of both hemispheres. Clinically the animals showed only discrete signs of fatigue and recovered completely after day 15. Even on day 30 we still were able to detect demyelination in subpial and intracortical areas along with areas of partial and complete remyelination. Loss of cortical myelin was accompanied with marked microglia activation. A second injection of cytokines through the catheter on day 30 led to a second demyelination phase with the same symptoms, but again no detectable motor dysfunction. Suffering of the animals appeared minor compared to standard Experimental Autoimmune Encephalomyelitis and therefore, even long-term observation and repeated demyelination phases seem ethically acceptable.\n Copyright © 2017 Elsevier Inc. All rights reserved.\n\nFazekas, Franz\n\nHaindl, Michaela\n\nHochmeister, Sonja\n\nRopele, Stefan\n\nSchäfer, Ute\n\nStrasser, Johannes\n\nÜcal, Muammer\n\n\n"
},
{
"text": "\n162554\nGenetic Interactions with Age, Sex, Body Mass Index, and Hypertension in Relation to Atrial Fibrillation: The AFGen Consortium.\n\nWeng, LC\n\nLunetta, KL\n\nMüller-Nurasyid, M\n\nSmith, AV\n\nThériault, S\n\nWeeke, PE\n\nBarnard, J\n\nBis, JC\n\nLyytikäinen, LP\n\nKleber, ME\n\nMartinsson, A\n\nLin, HJ\n\nRienstra, M\n\nTrompet, S\n\nKrijthe, BP\n\nDörr, M\n\nKlarin, D\n\nChasman, DI\n\nSinner, MF\n\nWaldenberger, M\n\nLauner, LJ\n\nHarris, TB\n\nSoliman, EZ\n\nAlonso, A\n\nParé, G\n\nTeixeira, PL\n\nDenny, JC\n\nShoemaker, MB\n\nVan Wagoner, DR\n\nSmith, JD\n\nPsaty, BM\n\nSotoodehnia, N\n\nTaylor, KD\n\nKähönen, M\n\nNikus, K\n\nDelgado, GE\n\nMelander, O\n\nEngström, G\n\nYao, J\n\nGuo, X\n\nChristophersen, IE\n\nEllinor, PT\n\nGeelhoed, B\n\nVerweij, N\n\nMacfarlane, P\n\nFord, I\n\nHeeringa, J\n\nFranco, OH\n\nUitterlinden, AG\n\nVölker, U\n\nTeumer, A\n\nRose, LM\n\nKääb, S\n\nGudnason, V\n\nArking, DE\n\nConen, D\n\nRoden, DM\n\nChung, MK\n\nHeckbert, SR\n\nBenjamin, EJ\n\nLehtimäki, T\n\nMärz, W\n\nSmith, JG\n\nRotter, JI\n\nvan der Harst, P\n\nJukema, JW\n\nStricker, BH\n\nFelix, SB\n\nAlbert, CM\n\nLubitz, SA\n\nBeiträge in Fachzeitschriften\nISI:000410297900017\n28900195.0\n10.1038/s41598-017-09396-7\nPMC5595875\nIt is unclear whether genetic markers interact with risk factors to influence atrial fibrillation (AF) risk. We performed genome-wide interaction analyses between genetic variants and age, sex, hypertension, and body mass index in the AFGen Consortium. Study-specific results were combined using meta-analysis (88, 83 individuals of European descent, including 7, 92 with AF). Variants with nominal interaction associations in the discovery analysis were tested for association in four independent studies (131, 41 individuals, including 5, 22 with AF). In the discovery analysis, the AF risk associated with the minor rs6817105 allele (at the PITX2 locus) was greater among subjects ≤ 65 years of age than among those > 65 years (interaction p-value = 4.0 × 10-5). The interaction p-value exceeded genome-wide significance in combined discovery and replication analyses (interaction p-value = 1.7 × 10-8). We observed one genome-wide significant interaction with body mass index and several suggestive interactions with age, sex, and body mass index in the discovery analysis. However, none was replicated in the independent sample. Our findings suggest that the pathogenesis of AF may differ according to age in individuals of European descent, but we did not observe evidence of statistically significant genetic interactions with sex, body mass index, or hypertension on AF risk.\n\nMärz, Winfried\n\n\n"
},
{
"text": "\n177144\nSudden cardiac death in dialysis patients: different causes and management strategies.\n\nGenovesi, S\n\nBoriani, G\n\nCovic, A\n\nVernooij, RWM\n\nCombe, C\n\nBurlacu, A\n\nDavenport, A\n\nKanbay, M\n\nKirmizis, D\n\nSchneditz, D\n\nvan der Sande, F\n\nBasile, C\n\nEUDIAL Working Group of ERA-EDTA\n\nBeiträge in Fachzeitschriften\nISI:000646227900005\n31538192.0\n10.1093/ndt/gfz182\nNone\nSudden cardiac death (SCD) represents a major cause of death in end-stage kidney disease (ESKD). The precise estimate of its incidence is difficult to establish because studies on the incidence of SCD in ESKD are often combined with those related to sudden cardiac arrest (SCA) occurring during a haemodialysis (HD) session. The aim of the European Dialysis Working Group of ERA-EDTA was to critically review the current literature examining the causes of extradialysis SCD and intradialysis SCA in ESKD patients and potential management strategies to reduce the incidence of such events. Extradialysis SCD and intradialysis SCA represent different clinical situations and should be kept distinct. Regarding the problem, numerically less relevant, of patients affected by intradialysis SCA, some modifiable risk factors have been identified, such as a low concentration of potassium and calcium in the dialysate, and some advantages linked to the presence of automated external defibrillators in dialysis units have been documented. The problem of extra-dialysis SCD is more complex. A reduced left ventricular ejection fraction associated with SCD is present only in a minority of cases occurring in HD patients. This is the proof that SCD occurring in ESKD has different characteristics compared with SCD occurring in patients with ischaemic heart disease and/or heart failure and not affected by ESKD. Recent evidence suggests that the fatal arrhythmia in this population may be due more frequently to bradyarrhythmias than to tachyarrhythmias. This fact may partly explain why several studies could not demonstrate an advantage of implantable cardioverter defibrillators in preventing SCD in ESKD patients. Electrolyte imbalances, frequently present in HD patients, could explain part of the arrhythmic phenomena, as suggested by the relationship between SCD and timing of the HD session. However, the high incidence of SCD in patients on peritoneal dialysis suggests that other risk factors due to cardiac comorbidities and uraemia per se may contribute to sudden mortality in ESKD patients.\n © The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.\n\nSchneditz, Daniel\n\n\n"
}
]
}