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"text": "\n4439\nSerum osteoprotegerin levels in patients after liver transplantation and correlation to bone turnover, bone mineral density and fracture status.\n\nFahrleitner, A\n\nPrenner, G\n\nKniepeiss, D\n\nIberer, F\n\nTscheliessnigg, KH\n\nPiswanger-Sölkner, C\n\nObermayer-Pietsch, B\n\nLeb, G\n\nDobnig, H\n\nBeiträge in Fachzeitschriften\nISI:000177884000012\n12602117.0\nNone\nNone\nThe aim of this cross sectional study was to evaluate the prevalence of osteoporosis, vertebral fracture status and possible risk factors of bone loss including serum osteoprotegerin, a novel key regulator of osteoclast proliferation and activity in the posttransplantation period. We investigated 15 patients (10 male, 5 female) 20 +/- 6 (SE) months after orthotopic liver transplantation (OLT). All patients received immunosuppressive therapy and non were on calcium and/or vitamin D supplements at the time of admission to our osteoporosis outpatient clinic. Examinations included a bone densitometry measurement at the femoral neck, a standardized spinal X-ray and a morning blood sample. According to WHO criteria, osteoporosis at the femoral neck was present in 67% (10/15) of the patients with a mean T-score of -2.55 +/- 0.35. Vertebral fractures were seen in 33% and the mean number of fractures was 2.4 per patient. Secondary hyperparathyroidism (33%), vitamin D deficiency (53%) as well as impaired renal function (47%) were frequent findings in the patients. Low serum calcium was associated with elevated PTH- (r = -0.75, p = 0.001), serum cross laps- (r = -0.61, p = 0.01), osteocalcin levels (r = -0.49, p = 0.05), was an independent predictor of femoral neck bone mass (r = 0.57, p = 0.02) and accounted for 36% of this variance. Similarly, serum magnesium levels were also independently correlated to femoral neck Z-scores (r = -0.68, p = 0.0005). Two-thirds of the patients had elevated serum cross-laps, osteocalcin and bone specific alkaline phosphatase levels reflecting increased bone turnover. Serum osteoprotegerin (OPG) in liver transplant recipients was not significantly different when compared to healthy, matched controls (84.7 +/- 6.6 vs. 97.3 +/- 9.4 pg/ml, p = 0.50) and similar when fractured/non-fractured or osteoporotic/non-osteoporotic patients were compared. Serum OPG was, however, significantly correlated to serum cross laps (r = 0.71, p = 0.003), osteocalcin (r = 0.63, p = 0.01), serum parathyroid hormone (r = 0.61, p = 0.01) and serum creatinine levels (r = 0.53, p = 0.04) and showed only a weak and non-significant correlation to femoral neck Z-scores (r = -0.38, p = 0.16). Multiple regression analysis revealed that serum OPG was correlated independently of PTH, serum calcium and creatinine to serum cross-laps concentrations (r = 0.63, p = 0.04). In summary, we found a high prevalence of osteoporosis and vertebral fractures in liver transplant recipients with many of the patients showing evidence of vitamin D deficiency, secondary hyperparathyroidism and accelerated bone turnover. We conclude that secondary hyperparathyroidism and possibly serum magnesium seems to contribute significantly to the changes in bone mass during the posttransplantation period. Serum OPG was not correlated to bone mass or fracture status in this cross sectional setting but was elevated together with other bone resorption and -formation markers.\n\nFahrleitner-Pammer, Astrid\n\nKniepeiss, Daniela\n\nObermayer-Pietsch, Barbara\n\nPiswanger-Solkner, Claudia\n\nPrenner, Günther\n\n\n"
},
{
"text": "\n175349\nMendelian randomization evaluation of causal effects of fibrinogen on incident coronary heart disease.\n\nWard-Caviness, CK\n\nde Vries, PS\n\nWiggins, KL\n\nHuffman, JE\n\nYanek, LR\n\nBielak, LF\n\nGiulianini, F\n\nGuo, X\n\nKleber, ME\n\nKacprowski, T\n\nGroß, S\n\nPetersman, A\n\nDavey Smith, G\n\nHartwig, FP\n\nBowden, J\n\nHemani, G\n\nMüller-Nuraysid, M\n\nStrauch, K\n\nKoenig, W\n\nWaldenberger, M\n\nMeitinger, T\n\nPankratz, N\n\nBoerwinkle, E\n\nTang, W\n\nFu, YP\n\nJohnson, AD\n\nSong, C\n\nde Maat, MPM\n\nUitterlinden, AG\n\nFranco, OH\n\nBrody, JA\n\nMcKnight, B\n\nChen, YI\n\nPsaty, BM\n\nMathias, RA\n\nBecker, DM\n\nPeyser, PA\n\nSmith, JA\n\nBielinski, SJ\n\nRidker, PM\n\nTaylor, KD\n\nYao, J\n\nTracy, R\n\nDelgado, G\n\nTrompet, S\n\nSattar, N\n\nJukema, JW\n\nBecker, LC\n\nKardia, SLR\n\nRotter, JI\n\nMärz, W\n\nDörr, M\n\nChasman, DI\n\nDehghan, A\n\nO'Donnell, CJ\n\nSmith, NL\n\nPeters, A\n\nMorrison, AC\n\nBeiträge in Fachzeitschriften\nISI:000467556300017\n31075152.0\n10.1371/journal.pone.0216222\nPMC6510421\nFibrinogen is an essential hemostatic factor and cardiovascular disease risk factor. Early attempts at evaluating the causal effect of fibrinogen on coronary heart disease (CHD) and myocardial infraction (MI) using Mendelian randomization (MR) used single variant approaches, and did not take advantage of recent genome-wide association studies (GWAS) or multi-variant, pleiotropy robust MR methodologies.\n We evaluated evidence for a causal effect of fibrinogen on both CHD and MI using MR. We used both an allele score approach and pleiotropy robust MR models. The allele score was composed of 38 fibrinogen-associated variants from recent GWAS. Initial analyses using the allele score used a meta-analysis of 11 European-ancestry prospective cohorts, free of CHD and MI at baseline, to examine incidence CHD and MI. We also applied 2 sample MR methods with data from a prevalent CHD and MI GWAS. Results are given in terms of the hazard ratio (HR) or odds ratio (OR), depending on the study design, and associated 95% confidence interval (CI). In single variant analyses no causal effect of fibrinogen on CHD or MI was observed. In multi-variant analyses using incidence CHD cases and the allele score approach, the estimated causal effect (HR) of a 1 g/L higher fibrinogen concentration was 1.62 (CI = 1.12, 2.36) when using incident cases and the allele score approach. In 2 sample MR analyses that accounted for pleiotropy, the causal estimate (OR) was reduced to 1.18 (CI = 0.98, 1.42) and 1.09 (CI = 0.89, 1.33) in the 2 most precise (smallest CI) models, out of 4 models evaluated. In the 2 sample MR analyses for MI, there was only very weak evidence of a causal effect in only 1 out of 4 models.\n A small causal effect of fibrinogen on CHD is observed using multi-variant MR approaches which account for pleiotropy, but not single variant MR approaches. Taken together, results indicate that even with large sample sizes and multi-variant approaches MR analyses still cannot exclude the null when estimating the causal effect of fibrinogen on CHD, but that any potential causal effect is likely to be much smaller than observed in epidemiological studies.\n\nMärz, Winfried\n\n\n"
},
{
"text": "\n182874\nGeneral and Disease-Specific Health Indicator Changes Associated with Inpatient Rehabilitation.\n\nGrote, V\n\nUnger, A\n\nBöttcher, E\n\nMuntean, M\n\nPuff, H\n\nMarktl, W\n\nMur, E\n\nKullich, W\n\nHolasek, S\n\nHofmann, P\n\nLackner, HK\n\nGoswami, N\n\nMoser, M\n\nBeiträge in Fachzeitschriften\nISI:000595574700046\n32736990.0\n10.1016/j.jamda.2020.05.034\nNone\nRehabilitation plays a vital role in the mitigation and improvement of functional limitations associated with aging and chronic conditions. Moderating factors such as sex, age, the medical diagnosis, and rehabilitation timing for admission status, as well as the expected change related to inpatient rehabilitation, are examined to provide a valid basis for the routine assessment of the quality of medical outcomes.\n An observational study was carried out, placing a focus on general and disease-specific health measurements, to assess representative results of multidisciplinary inpatient rehabilitation. Aspects that were possibly confounding and introduced bias were controlled based on data from a quasi-experimental (waiting) control group.\n Existing data or general health indicators were extracted from medical records. The indicators included blood pressure, resting heart rate, self-assessed health, and pain, as well as more disease-specific indicators of physical function and performance (eg, activities of daily living, walking tests, blood lipids). These are used to identify moderating factors related to health outcomes.\n A standardized collection of routine data from 16, 66 patients [61.5 ± 12.5 years; 7871 (46%) women, 9095 (54%) men] with different medical diagnoses before and after rehabilitation were summarized using a descriptive evaluation in terms of a content and factor analysis.\n Without rehabilitation, general health indicators did not improve independently and remained stable at best [odds ratio (OR) = 0.74], whereas disease-specific indicators improved noticeably after surgery (OR = 3.20). Inpatient rehabilitation was shown to reduce the risk factors associated with certain lifestyles, optimize organ function, and improve well-being in most patients (>70%; cutoff: z-difference >0.20), with a standardized mean difference (SMD) seen in overall medical quality outcome of -0.48 ± 0.37 [pre- vs post-rehabilitation: ηp2 = 0.622; dCohen = -1.22; 95% confidence interval (95% CI) -1.24 to -1.19]. The baseline medical values obtained at the beginning of rehabilitation were influenced by indication, age, and sex (all P < .001); however, these factors have less significant effects on improvements in general health indicators (ηp2 < 0.01). According to the disease-specific results, the greatest improvements were found in older patients (SMD for patients >60 vs ≤60 years: 95% CI 0.08-0.11) and during the early rehabilitation stage (ηp2 = 0.063).\n Compared with those who received no inpatient rehabilitation, patients who received rehabilitation showed greater improvements in 2 independent areas, general and disease-specific health measures, regardless of their diagnosis, age, and sex. Due to the study design and the use of a nonrandomized waiting group, causal conclusions must be drawn with caution. However, the comparability and stability of the presented results strongly support the validity of the observed improvements associated with inpatient rehabilitation.\n Copyright © 2020 AMDA – The Society for Post-Acute and Long-Term Care Medicine. Published by Elsevier Inc. All rights reserved.\n\nGoswami, Nandu\n\nHolasek, Sandra Johanna\n\nLackner, Helmut Karl\n\nMoser, Maximilian\n\n\n"
},
{
"text": "\n129870\nAssessment of Response to Lithium Maintenance Treatment in Bipolar Disorder: A Consortium on Lithium Genetics (ConLiGen) Report.\n\nManchia, M\n\nAdli, M\n\nAkula, N\n\nArdau, R\n\nAubry, JM\n\nBacklund, L\n\nBanzato, CE\n\nBaune, BT\n\nBellivier, F\n\nBengesser, S\n\nBiernacka, JM\n\nBrichant-Petitjean, C\n\nBui, E\n\nCalkin, CV\n\nCheng, AT\n\nChillotti, C\n\nCichon, S\n\nClark, S\n\nCzerski, PM\n\nDantas, C\n\nZompo, MD\n\nDepaulo, JR\n\nDetera-Wadleigh, SD\n\nEtain, B\n\nFalkai, P\n\nFrisén, L\n\nFrye, MA\n\nFullerton, J\n\nGard, S\n\nGarnham, J\n\nGoes, FS\n\nGrof, P\n\nGruber, O\n\nHashimoto, R\n\nHauser, J\n\nHeilbronner, U\n\nHoban, R\n\nHou, L\n\nJamain, S\n\nKahn, JP\n\nKassem, L\n\nKato, T\n\nKelsoe, JR\n\nKittel-Schneider, S\n\nKliwicki, S\n\nKuo, PH\n\nKusumi, I\n\nLaje, G\n\nLavebratt, C\n\nLeboyer, M\n\nLeckband, SG\n\nLópez Jaramillo, CA\n\nMaj, M\n\nMalafosse, A\n\nMartinsson, L\n\nMasui, T\n\nMitchell, PB\n\nMondimore, F\n\nMonteleone, P\n\nNallet, A\n\nNeuner, M\n\nNovák, T\n\nO'Donovan, C\n\nOsby, U\n\nOzaki, N\n\nPerlis, RH\n\nPfennig, A\n\nPotash, JB\n\nReich-Erkelenz, D\n\nReif, A\n\nReininghaus, E\n\nRichardson, S\n\nRouleau, GA\n\nRybakowski, JK\n\nSchalling, M\n\nSchofield, PR\n\nSchubert, OK\n\nSchweizer, B\n\nSeemüller, F\n\nGrigoroiu-Serbanescu, M\n\nSeverino, G\n\nSeymour, LR\n\nSlaney, C\n\nSmoller, JW\n\nSquassina, A\n\nStamm, T\n\nSteele, J\n\nStopkova, P\n\nTighe, SK\n\nTortorella, A\n\nTurecki, G\n\nWray, NR\n\nWright, A\n\nZandi, PP\n\nZilles, D\n\nBauer, M\n\nRietschel, M\n\nMcMahon, FJ\n\nSchulze, TG\n\nAlda, M\n\nBeiträge in Fachzeitschriften\nISI:000322361200028\n23840348.0\n10.1371/journal.pone.0065636\nPMC3686769\nThe assessment of response to lithium maintenance treatment in bipolar disorder (BD) is complicated by variable length of treatment, unpredictable clinical course, and often inconsistent compliance. Prospective and retrospective methods of assessment of lithium response have been proposed in the literature. In this study we report the key phenotypic measures of the "Retrospective Criteria of Long-Term Treatment Response in Research Subjects with Bipolar Disorder" scale currently used in the Consortium on Lithium Genetics (ConLiGen) study.\n Twenty-nine ConLiGen sites took part in a two-stage case-vignette rating procedure to examine inter-rater agreement [Kappa (κ)] and reliability [intra-class correlation coefficient (ICC)] of lithium response. Annotated first-round vignettes and rating guidelines were circulated to expert research clinicians for training purposes between the two stages. Further, we analyzed the distributional properties of the treatment response scores available for 1, 08 patients using mixture modeling.\n Substantial and moderate agreement was shown across sites in the first and second sets of vignettes (κ = 0.66 and κ = 0.54, respectively), without significant improvement from training. However, definition of response using the A score as a quantitative trait and selecting cases with B criteria of 4 or less showed an improvement between the two stages (ICC1 = 0.71 and ICC2 = 0.75, respectively). Mixture modeling of score distribution indicated three subpopulations (full responders, partial responders, non responders).\n We identified two definitions of lithium response, one dichotomous and the other continuous, with moderate to substantial inter-rater agreement and reliability. Accurate phenotypic measurement of lithium response is crucial for the ongoing ConLiGen pharmacogenomic study.\n\nBengesser, Susanne\n\nReininghaus, Eva\n\n\n"
},
{
"text": "\n149805\nTreating rheumatoid arthritis to target: 2014 update of the recommendations of an international task force.\n\nSmolen, JS\n\nBreedveld, FC\n\nBurmester, GR\n\nBykerk, V\n\nDougados, M\n\nEmery, P\n\nKvien, TK\n\nNavarro-Compán, MV\n\nOliver, S\n\nSchoels, M\n\nScholte-Voshaar, M\n\nStamm, T\n\nStoffer, M\n\nTakeuchi, T\n\nAletaha, D\n\nAndreu, JL\n\nAringer, M\n\nBergman, M\n\nBetteridge, N\n\nBijlsma, H\n\nBurkhardt, H\n\nCardiel, M\n\nCombe, B\n\nDurez, P\n\nFonseca, JE\n\nGibofsky, A\n\nGomez-Reino, JJ\n\nGraninger, W\n\nHannonen, P\n\nHaraoui, B\n\nKouloumas, M\n\nLandewe, R\n\nMartin-Mola, E\n\nNash, P\n\nOstergaard, M\n\nÖstör, A\n\nRichards, P\n\nSokka-Isler, T\n\nThorne, C\n\nTzioufas, AG\n\nvan Vollenhoven, R\n\nde Wit, M\n\nvan der Heijde, D\n\nBeiträge in Fachzeitschriften\nISI:000366402400043\n25969430.0\n10.1136/annrheumdis-2015-207524\nPMC4717393\nReaching the therapeutic target of remission or low-disease activity has improved outcomes in patients with rheumatoid arthritis (RA) significantly. The treat-to-target recommendations, formulated in 2010, have provided a basis for implementation of a strategic approach towards this therapeutic goal in routine clinical practice, but these recommendations need to be re-evaluated for appropriateness and practicability in the light of new insights.\n To update the 2010 treat-to-target recommendations based on systematic literature reviews (SLR) and expert opinion.\n A task force of rheumatologists, patients and a nurse specialist assessed the SLR results and evaluated the individual items of the 2010 recommendations accordingly, reformulating many of the items. These were subsequently discussed, amended and voted upon by >40 experts, including 5 patients, from various regions of the world. Levels of evidence, strengths of recommendations and levels of agreement were derived.\n The update resulted in 4 overarching principles and 10 recommendations. The previous recommendations were partly adapted and their order changed as deemed appropriate in terms of importance in the view of the experts. The SLR had now provided also data for the effectiveness of targeting low-disease activity or remission in established rather than only early disease. The role of comorbidities, including their potential to preclude treatment intensification, was highlighted more strongly than before. The treatment aim was again defined as remission with low-disease activity being an alternative goal especially in patients with long-standing disease. Regular follow-up (every 1-3 months during active disease) with according therapeutic adaptations to reach the desired state was recommended. Follow-up examinations ought to employ composite measures of disease activity that include joint counts. Additional items provide further details for particular aspects of the disease, especially comorbidity and shared decision-making with the patient. Levels of evidence had increased for many items compared with the 2010 recommendations, and levels of agreement were very high for most of the individual recommendations (≥9/10).\n The 4 overarching principles and 10 recommendations are based on stronger evidence than before and are supposed to inform patients, rheumatologists and other stakeholders about strategies to reach optimal outcomes of RA.\n Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/\n\nGraninger, Winfried\n\n\n"
},
{
"text": "\n187374\nManagement of anaphylaxis due to COVID-19 vaccines in the elderly.\n\nBousquet, J\n\nAgache, I\n\nBlain, H\n\nJutel, M\n\nVentura, MT\n\nWorm, M\n\nDel Giacco, S\n\nBenetos, A\n\nBilo, MB\n\nCzarlewski, W\n\nAbdul Latiff, AH\n\nAl-Ahmad, M\n\nAngier, E\n\nAnnesi-Maesano, I\n\nAtanaskovic-Markovic, M\n\nBachert, C\n\nBarbaud, A\n\nBedbrook, A\n\nBennoor, KS\n\nBerghea, EC\n\nBindslev-Jensen, C\n\nBonini, S\n\nBosnic-Anticevich, S\n\nBrockow, K\n\nBrussino, L\n\nCamargos, P\n\nCanonica, GW\n\nCardona, V\n\nCarreiro-Martins, P\n\nCarriazo, A\n\nCasale, T\n\nCaubet, JC\n\nCecchi, L\n\nCherubini, A\n\nChristoff, G\n\nChu, DK\n\nCruz, AA\n\nDokic, D\n\nEl-Gamal, Y\n\nEbisawa, M\n\nEberlein, B\n\nFarrell, J\n\nFernandez-Rivas, M\n\nFokkens, WJ\n\nFonseca, JA\n\nGao, Y\n\nGavazzi, G\n\nGawlik, R\n\nGelincik, A\n\nGemicioğlu, B\n\nGotua, M\n\nGuérin, O\n\nHaahtela, T\n\nHoffmann-Sommergruber, K\n\nHoffmann, HJ\n\nHofmann, M\n\nHrubisko, M\n\nlenaIllario, M\n\nIrani, C\n\nIspayeva, Z\n\nIvancevich, JC\n\nJulge, K\n\nKaidashev, I\n\nKhaitov, M\n\nKnol, E\n\nKraxner, H\n\nKuna, P\n\nKvedariene, V\n\nLauerma, A\n\nLe, LT\n\nLe Moing, V\n\nLevin, M\n\nLouis, R\n\nLourenco, O\n\nMahler, V\n\nMartin, FC\n\nMatucci, A\n\nMilenkovic, B\n\nMiot, S\n\nMontella, E\n\nMorais-Almeida, M\n\nMortz, CG\n\nMullol, J\n\nNamazova-Baranova, L\n\nNeffen, H\n\nNekam, K\n\nNiedoszytko, M\n\nOdemyr, M\n\nO'Hehir, RE\n\nOkamoto, Y\n\nOllert, M\n\nPalomares, O\n\nPapadopoulos, NG\n\nPanzner, P\n\nPassalacqua, G\n\nPatella, V\n\nPetrovic, M\n\nPfaar, O\n\nPham-Thi, N\n\nPlavec, D\n\nPopov, TA\n\nRecto, MT\n\nRegateiro, FS\n\nReynes, J\n\nRoller-Winsberger, RE\n\nRolland, Y\n\nRomano, A\n\nRondon, C\n\nRottem, M\n\nRouadi, PW\n\nSalles, N\n\nSamolinski, B\n\nSantos, AF\n\nSerpa, FS\n\nSastre, J\n\nSchols, JMGA\n\nScichilone, N\n\nSediva, A\n\nShamji, MH\n\nSheikh, A\n\nSkypala, I\n\nSmolinska, S\n\nSokolowska, M\n\nSousa-Pinto, B\n\nSova, M\n\nStelmach, R\n\nSturm, G\n\nSuppli Ulrik, C\n\nTodo-Bom, AM\n\nToppila-Salmi, S\n\nTsiligianni, I\n\nTorres, M\n\nUntersmayr, E\n\nUrrutia Pereira, M\n\nValiulis, A\n\nVitte, J\n\nVultaggio, A\n\nWallace, D\n\nWalusiak-Skorupa, J\n\nWang, DY\n\nWaserman, S\n\nYorgancioglu, A\n\nYusuf, OM\n\nZernotti, M\n\nZidarn, M\n\nChivato, T\n\nAkdis, CA\n\nZuberbier, T\n\nKlimek, L\n\nBeiträge in Fachzeitschriften\nNone\n33811358.0\n10.1111/all.14838\nNone\nOlder adults, especially men and/or those with diabetes, hypertension and/or obesity, are prone to severe COVID-19. In some countries, older adults, particularly those residing in nursing homes, have been prioritised to receive COVID-19 vaccines due to high risk of death. In very rare instances, he COVID-19 vaccines can induce anaphylaxis, and the management of anaphylaxis in older people should be considered carefully. An ARIA-EAACI-EuGMS (Allergic Rhinitis and its Impact on Asthma, European Academy of Allergy and Clinical Immunology, and European Geriatric Medicine Society)Working Group has proposed some recommendations for older adults receiving the COVID-19 vaccines. Anaphylaxis to COVID-19 vaccines is extremely rare (from 1 per 100, 00 to 5 per million injections). Symptoms are similar in younger and older adults but they tend to be more severe in the older patients. Adrenaline is the mainstay treatment and should be readily available. A flowchart is proposed to manage anaphylaxis in the older patients.\n This article is protected by copyright. All rights reserved.\n\nRoller-Wirnsberger, Regina\n\nSturm, Gunter\n\n\n"
},
{
"text": "\n877\nEffects of the bradykinin antagonist, icatibant (Hoe 140), on pancreas and liver functions during and after caerulein-induced pancreatitis in rats.\n\nGriesbacher, T\n\nKolbitsch, C\n\nTiran, B\n\nLembeck, F\n\nBeiträge in Fachzeitschriften\nISI:A1995TG10200014\n8751086.0\n10.1007%2FBF00169391\nNone\nIt has been found earlier that the bradykinin antagonist, icatibant (Hoe 140), prevents the pancreatic oedema and the ensuing hypotension and haemoconcentration, and facilitates the removal of activated enzymes form the tissue during caerulein-induced acute pancreatitis. For a potential therapeutic use of the compound in clinical situations it is essential to investigate whether the associated increase in enzyme activities in the blood serum has any adverse effects on the pancreas itself or on other organs. Normal amylase secretion into the biliopancreatic duct stimulated by a low dose of caerulein (0.4 nmol kg-1 h-1, i.v.) was not affect by icatibant (100 nmol kg-1, s.c.) Acute pancreatitis, induced by a high dose of caerulein (4 nmol kg-1 h-1 for 2 h, i.v.), resulted in elevations in the activities of amylase and lipase in the pancreatic tissue and in the blood serum lasting for at least 4 h after the end of the caerulein infusion. While the rise in enzyme activities in the blood serum was augmented in icatibant-treated rats only at the end of the caerulein-infusion, the enzyme accumulation in the pancreas was significantly reduced by icatibant for at least 4 h after the end of the caerulein infusion. The secretion of amylase and lipase into the biliopancreatic duct was significantly increased only during the first 20 min of acute pancreatitis; in rats pre-treated with icatibant, no significant increase could be observed. Twenty-four hours after induction of pancreatitis, a low-dose caerulein stimulation of the exocrine function of the pancreas led to a reduced but sustained secretion of amylase regardless of whether the animals had received icatibant or not. During the first 45 min of pancreatitis, blood glucose concentrations were significantly reduced, but returned to values not different from those obtained in saline-infused controls. This effect was not affected by icatibant. No changes in the response to an i.v. glucose tolerance test were found on the day after induction of acute pancreatitis. The serum activities of glutamic pyruvic transaminase and gamma-glutamyl transpeptidase determined up to 24 h after induction of pancreatitis were not different from saline controls. icatibant had no effect on the activities of these enzymes. It is concluded that during caerulein-induced acute pancreatitis normal exocrine secretion of pancreatic enzymes into the pancreatic duct ceases almost immediately. Pre-treatment with icatibant significantly reduces the accumulation of activated enzymes in the pancreatic tissue for several hours after induction of pancreatitis while a concomitant augmentation in enzyme activities in the blood serum lasts much shorter. There is no indication of adverse effects on the function of the endocrine or exocrine pancreas and that of the liver, either during the acute stages of pancreatitis or during the recovery period.\n\nGriesbacher, Thomas\n\nTiran, Beate\n\n\n"
},
{
"text": "\n92418\nEffect of home-based telemonitoring using mobile phone technology on the outcome of heart failure patients after an episode of acute decompensation: randomized controlled trial.\n\nScherr, D\n\nKastner, P\n\nKollmann, A\n\nHallas, A\n\nAuer, J\n\nKrappinger, H\n\nSchuchlenz, H\n\nStark, G\n\nGrander, W\n\nJakl, G\n\nSchreier, G\n\nFruhwald, FM\n\nMOBITEL Investigators\n\nBeiträge in Fachzeitschriften\nISI:000274632900014\n19687005.0\n10.2196/jmir.1252\nPMC2762855\nTelemonitoring of patients with chronic heart failure (CHF) is an emerging concept to detect early warning signs of impending acute decompensation in order to prevent hospitalization.\n The goal of the MOBIle TELemonitoring in Heart Failure Patients Study (MOBITEL) was to evaluate the impact of home-based telemonitoring using Internet and mobile phone technology on the outcome of heart failure patients after an episode of acute decompensation.\n Patients were randomly allocated to pharmacological treatment (control group) or to pharmacological treatment with telemedical surveillance for 6 months (tele group). Patients randomized into the tele group were equipped with mobile phone-based patient terminals for data acquisition and data transmission to the monitoring center. Study physicians had continuous access to the data via a secure Web portal. If transmitted values went outside individually adjustable borders, study physicians were sent an email alert. Primary endpoint was hospitalization for worsening CHF or death from cardiovascular cause.\n The study was stopped after randomization of 120 patients (85 male, 35 female); median age was 66 years (IQR 62-72). The control group comprised 54 patients (39 male, 15 female) with a median age of 67 years (IQR 61-72), and the tele group included 54 patients (40 male, 14 female) with a median age of 65 years (IQR 62-72). There was no significant difference between groups with regard to baseline characteristics. Twelve tele group patients were unable to begin data transmission due to the inability of these patients to properly operate the mobile phone ("never beginners"). Four patients did not finish the study due to personal reasons. Intention-to-treat analysis at study end indicated that 18 control group patients (33%) reached the primary endpoint (1 death, 17 hospitalizations), compared with 11 tele group patients (17%, 0 deaths, 11 hospitalizations; relative risk reduction 50%, 95% CI 3-74%, P = .06). Per-protocol analysis revealed that 15% of tele group patients (0 deaths, 8 hospitalizations) reached the primary endpoint (relative risk reduction 54%, 95% CI 7-79%, P= .04). NYHA class improved by one class in tele group patients only (P< .001). Tele group patients who were hospitalized for worsening heart failure during the study had a significantly shorter length of stay (median 6.5 days, IQR 5.5-8.3) compared with control group patients (median 10.0 days, IQR 7.0-13.0; P= .04). The event rate of never beginners was not higher than the event rate of control group patients.\n Telemonitoring using mobile phones as patient terminals has the potential to reduce frequency and duration of heart failure hospitalizations. Providing elderly patients with an adequate user interface for daily data acquisition remains a challenging component of such a concept.\n\nFruhwald, Friedrich\n\nScherr, Daniel\n\n\n"
},
{
"text": "\n485\nClinical course, early diagnosis, treatment, and prevention of disease in glutaryl-CoA dehydrogenase deficiency.\n\nHoffmann, GF\n\nAthanassopoulos, S\n\nBurlina, AB\n\nDuran, M\n\nde Klerk, JB\n\nLehnert, W\n\nLeonard, JV\n\nMonavari, AA\n\nMüller, E\n\nMuntau, AC\n\nNaughten, ER\n\nPlecko-Starting, B\n\nSuperti-Furga, A\n\nZschocke, J\n\nChristensen, E\n\nBeiträge in Fachzeitschriften\nISI:A1996UY46500001\n8837070.0\n10.1055/s-2007-973761\nNone\nBACKGROUND: Glutaryl-CoA dehydrogenase deficiency (GDD) is a recessively inherited neurometabolic disorder associated with encephalopathic crises and severe extrapyramidal symptoms. Treatment regimens including glucose and electrolyte infusions during acute illnesses, oral carnitine supplementation and/or a low-protein or lysine-restricted diet have been recommended, but their efficacy has been documented only on an anecdotal basis. SUBJECTS AND METHODS: We conducted a retrospective analysis of 57 patients with proven GDD-relating appearance and severity of neurological disease to age and clinical status at diagnosis, glutaric acid levels in body fluids, and different treatment regimens. RESULTS: Thirty-six patients were diagnosed after the onset of neurological disease (symptomatic group), twenty-one before (presymptomatic group). Carnitine levels were found to be reduced in all patients at diagnosis. In the symptomatic group, macrocephaly had been present around birth and was followed by rapid postnatal head growth in 70% of the children. The patients often showed symptoms such as hypotonia, irritability, and jitteriness followed by an acute encephalopathic crisis occurring on average at 12 months of age. Common neuroimaging findings included frontotemporal atrophy, subependymal pseudocysts, delayed myelination, basal ganglia atrophy, chronic subdural effusions and hematomas. In four patients the latter two findings were initially misinterpreted as resulting from child abuse. Other important misdiagnoses in older siblings who were affected and went undiagnosed include postencephalitic cerebral palsy, dystonic cerebral palsy and sudden infant death syndrome. Metabolic treatment did not convincingly improve the neurological disease, although it may have prevented further deterioration. Symptomatic treatment with baclofen or benzodiazepines was effective in reducing muscle spasms. Children in the presymptomatic group were diagnosed because of familiarity for the disease (n = 13), macrocephaly and/or additional minor neurological signs in infancy (n = 6), or acute encephalopathy, which was fully reversible after prompt treatment (n = 2). After diagnosis, all children were treated with oral carnitine, fluid infusion during intercurrent illnesses and, in addition, a diet was started in 13 of the 21 children. All 21 children except one (born prematurely at 31 weeks) have continued to develop normally up to now. Mean age at report is 6.3 years with a range from 6 months to 14.8 years. In older patients, the neuroradiological changes, present in infancy as in the symptomatic patients, became less prominent and in one girl disappeared. CONCLUSIONS: In presymptomatic children with GDD, the onset of neurological disease can be prevented by vigorous treatment of catabolic crises during illnesses together with carnitine supplementation. The importance of dietary therapy remains unclear and needs further evaluation. The potential treatability of GDD calls for increased attention to early presenting signs in order to recognize the disorder and to initiate treatment before the onset of irreversible neurological disease.\n\nPlecko, Barbara\n\n\n"
},
{
"text": "\n1080\nFirst-year results of CABRI (Coronary Angioplasty versus Bypass Revascularisation Investigation). CABRI Trial Participants.\n\nRICKARDS, AF\n\nILSLEY, C\n\nSIMON, R\n\nPROBST, P\n\nDANCHIN, N\n\nBOWKER, T\n\nSERRUYS PW, BERTRAND M, DECKERS J, BREEMAN A, BOERSMA E, CUNNINGHAM D, PORENTA G, HOFIG M, WAHRBORG P, RODLER S, GOTTSAUNERWOLF M, WOLNER E, MAST EG, PLOKKER HWM, MARTUSCELLI E, SINATRA R, ROMEO F, NIGRI A, MARINO B, CASSACCIA M, MARRA S, PENNONE M, DAMICO M, HERRMANN G, REGENSBURGER D, RICKARDS A, SIGWART U, BULLER N, SHORE D, BEURET P, GOY JJ, KAPPENBERGER L, HURNI M, SADEGHI H, HEYNDRICKX GR, DEBRUYNE B, NELLENS P, GOETHALS M, VANERMEN H, ALBRECHTSSON U, STAHL E, JOHANSSON S, BEATT KJ, VENN G, JULIARD JM, HVASS U, KLEIN W, SCHUMACHER M, LUHA O, EMANUELSSON H, ALBERTSSON P, LEGRAND V, SMEETS S, VANDAMME H, LIMET R, YACOUB M, REES A, DEFEYTER P, DEJAGERE P, VANDENBRAND M, ROELANDT J, PIOVACCARI G, MARZOCCHI A, MARROZZINI C, MAGNANI B, TURINETTO B, BERTRAND ME, LABLANCHE JM, STANKOWIAK C, WAREMBOURG H, HEIKKILA J, JARVINEN A, SCHROEDER E, CHENU P, MARCHANDISE B, LOUAGIE Y, BUCHE M, SCHOEVAERDTS JC, BONNIER JJ, MICHELS HR, BERREKLOUW E, HIEJMEN E, VONASPERDT F, JUILLIERE Y, VILLEMOT JP, DUBOISRANDE JL, APTECAR E, CASTAIGNE A, LOISANCE D, MACHECOURT J, VANZETTO G, BLIN D, FOUCALT JP, POTIER JC, GROLLIER G, SEABRAGOMES R, MELO JQ, VENTOSA A\n\n\n\nBeiträge in Fachzeitschriften\nISI:A1995TC97600006\n7475656.0\nNone\nNone\nThe Coronary Angioplasty versus Bypass Revascularisation Investigation (CABRI) is a multinational, multicentre randomised trial comparing the strategies of revascularisation by CABG (coronary artery bypass grafting) and PTCA (percutaneous transluminal coronary angioplasty) in patients with symptomatic multivessel coronary disease. 1054 patients (820 men and 234 women) were recruited from 26 European cardiac centres. The average age was 60 years and 62% presented with angina of class 3 or greater. 513 patients were randomised to CABG and 541 to PTCA, and 93% and 96%, respectively, of those randomised underwent the allocated procedure. This first report presents data analysed by intention to treat and documents all deaths, major cardiac events, and the symptom status of the patients 1 year after randomisation. After 1 year of follow-up, 14 (2.7%) of those randomised to CABG and 21 (3.9%) of those randomised to PTCA had died. The PTCA group's relative risk (RR) of death was 1.42 (95% CI 0.73-2.76). Patients randomised to PTCA required significantly more reinterventions; only 66.4% reached 1 year with a single revascularisation procedure compared with 93.5% of patients randomised to CABG (RR = 5.23 [3.90-7.03], p < 0.001). The patients in the PTCA group took significantly more medication at 1 year (RR = 1.30 [1.18-1.43], p < 0.001). They were also more likely to have clinically significant angina (RR = 1.54 [1.09-2.16], p = 0.012); this association was present in both sexes but was significant only in females. CABRI is the largest trial of CABG versus PTCA to be reported so far. Its findings are consistent with previous studies, and add to the weight of information that clinicians need to discuss with patients when options for the management of severe angina are under consideration.\n\n\n"
},
{
"text": "\n92545\nStandard graft-versus-host disease prophylaxis with or without anti-T-cell globulin in haematopoietic cell transplantation from matched unrelated donors: a randomised, open-label, multicentre phase 3 trial.\n\nFinke, J\n\nBethge, WA\n\nSchmoor, C\n\nOttinger, HD\n\nStelljes, M\n\nZander, AR\n\nVolin, L\n\nRuutu, T\n\nHeim, DA\n\nSchwerdtfeger, R\n\nKolbe, K\n\nMayer, J\n\nMaertens, JA\n\nLinkesch, W\n\nHoller, E\n\nKoza, V\n\nBornhäuser, M\n\nEinsele, H\n\nKolb, HJ\n\nBertz, H\n\nEgger, M\n\nGrishina, O\n\nSocié, G\n\nATG-Fresenius Trial Group\n\nBeiträge in Fachzeitschriften\nISI:000269953400014\n19695955.0\n10.1016/S1470-2045(09)70225-6\nNone\nBACKGROUND: Graft-versus-host disease (GVHD) is a major cause of morbidity and mortality after allogeneic haematopoietic cell transplantation from unrelated donors. Anti-T-cell globulins (ATGs) might lower the incidence of GVHD. We did a prospective, randomised, multicentre, open-label, phase 3 trial to compare standard GVHD prophylaxis with ciclosporin and methotrexate with or without anti-Jurkat ATG-Fresenius (ATG-F). METHODS: Between May 26, 2003, and Feb 8, 2007, 202 patients with haematological malignancies were centrally randomly assigned using computer-generated centre-stratified block randomisation between treatment groups receiving ciclosporin and methotrexate with or without additional ATG-F. One patient in the ATG-F group did not undergo transplantation, thus 201 patients who underwent transplantation with peripheral blood (n=164; 82%) or bone marrow (n=37; 18%) grafts from unrelated donors after myeloablative conditioning were included in the full analysis set, and were analysed according to their randomly assigned treatment (ATG-F n=103, control n=98). The primary endpoint was severe acute GVHD (aGVHD) grade III-IV or death within 100 days of transplantation. The trial is registered with the numbers DRKS00000002 and NCT00655343. FINDINGS: The number of patients in the ATG-F group who had severe aGVHD grade III-IV or who died within 100 days of transplantation was 12 and 10 (21.4%, 95% CI 13.4-29.3), respectively, compared with 24 and nine (33.7%, 24.3-43.0) patients, respectively, in the control group (adjusted odds ratio 0.59, 95% CI 0.30-1.17; p=0.13). The cumulative incidence of aGVHD grade III-IV was 11.7% (95% CI 6.8-19.8) in the ATG-F group versus 24.5% (17.3-34.7) in the control group (adjusted hazard ratio [HR] 0.50, 95% CI 0.25-1.01; p=0.054), and cumulative incidence of aGVHD grade II-IV was 33.0% (n=34; 95% CI 25.1-43.5) in the ATG-F group versus 51.0% (n=50; 95% CI 42.0-61.9) in the control group (adjusted HR 0.56, 0.36-0.87; p=0.011). The 2-year cumulative incidence of extensive chronic GVHD was 12.2% (n=11; 95% CI 7.0-21.3) versus 42.6% (n=34; 95% CI 33.0-55.0; adjusted HR 0.22, 0.11-0.43; p<0.0001). There were no differences between treatment groups with regard to relapse, non-relapse mortality, overall survival, and mortality from infectious causes. INTERPRETATION: The addition of ATG-F to GVHD prophylaxis with ciclosporin and methotrexate resulted in decreased incidence of acute and chronic GVHD without an increase in relapse or non-relapse mortality, and without compromising overall survival. The use of ATG-F is safe for patients who are going to receive a haematopoietic cell transplantation from matched unrelated donors. FUNDING: Fresenius Biotech GmbH.\n\n\n"
},
{
"text": "\n155463\nPosition paper on screening for breast cancer by the European Society of Breast Imaging (EUSOBI) and 30 national breast radiology bodies from Austria, Belgium, Bosnia and Herzegovina, Bulgaria, Croatia, Czech Republic, Denmark, Estonia, Finland, France, Germany, Greece, Hungary, Iceland, Ireland, Italy, Israel, Lithuania, Moldova, The Netherlands, Norway, Poland, Portugal, Romania, Serbia, Slovakia, Spain, Sweden, Switzerland and Turkey.\n\nSardanelli, F\n\nAase, HS\n\nÁlvarez, M\n\nAzavedo, E\n\nBaarslag, HJ\n\nBalleyguier, C\n\nBaltzer, PA\n\nBeslagic, V\n\nBick, U\n\nBogdanovic-Stojanovic, D\n\nBriediene, R\n\nBrkljacic, B\n\nCamps Herrero, J\n\nColin, C\n\nCornford, E\n\nDanes, J\n\nde Geer, G\n\nEsen, G\n\nEvans, A\n\nFuchsjaeger, MH\n\nGilbert, FJ\n\nGraf, O\n\nHargaden, G\n\nHelbich, TH\n\nHeywang-Köbrunner, SH\n\nIvanov, V\n\nJónsson, Á\n\nKuhl, CK\n\nLisencu, EC\n\nLuczynska, E\n\nMann, RM\n\nMarques, JC\n\nMartincich, L\n\nMortier, M\n\nMüller-Schimpfle, M\n\nOrmandi, K\n\nPanizza, P\n\nPediconi, F\n\nPijnappel, RM\n\nPinker, K\n\nRissanen, T\n\nRotaru, N\n\nSaguatti, G\n\nSella, T\n\nSlobodníková, J\n\nTalk, M\n\nTaourel, P\n\nTrimboli, RM\n\nVejborg, I\n\nVourtsis, A\n\nForrai, G\n\nBeiträge in Fachzeitschriften\nISI:000403366700010\n27807699.0\n10.1007/s00330-016-4612-z\nPMC5486792\nEUSOBI and 30 national breast radiology bodies support mammography for population-based screening, demonstrated to reduce breast cancer (BC) mortality and treatment impact. According to the International Agency for Research on Cancer, the reduction in mortality is 40 % for women aged 50-69 years taking up the invitation while the probability of false-positive needle biopsy is <1 % per round and overdiagnosis is only 1-10 % for a 20-year screening. Mortality reduction was also observed for the age groups 40-49 years and 70-74 years, although with "limited evidence". Thus, we firstly recommend biennial screening mammography for average-risk women aged 50-69 years; extension up to 73 or 75 years, biennially, is a second priority, from 40-45 to 49 years, annually, a third priority. Screening with thermography or other optical tools as alternatives to mammography is discouraged. Preference should be given to population screening programmes on a territorial basis, with double reading. Adoption of digital mammography (not film-screen or phosphor-plate computer radiography) is a priority, which also improves sensitivity in dense breasts. Radiologists qualified as screening readers should be involved in programmes. Digital breast tomosynthesis is also set to become "routine mammography" in the screening setting in the next future. Dedicated pathways for high-risk women offering breast MRI according to national or international guidelines and recommendations are encouraged.\n • EUSOBI and 30 national breast radiology bodies support screening mammography. • A first priority is double-reading biennial mammography for women aged 50-69 years. • Extension to 73-75 and from 40-45 to 49 years is also encouraged. • Digital mammography (not film-screen or computer radiography) should be used. • DBT is set to become "routine mammography" in the screening setting in the next future.\n\nFuchsjäger, Michael\n\n\n"
},
{
"text": "\n157764\nSymmetry of the arcuate fasciculus and its impact on language performance of patients with brain tumors in the language-dominant hemisphere.\n\nJehna, M\n\nBecker, J\n\nZaar, K\n\nvon Campe, G\n\nMahdy Ali, K\n\nReishofer, G\n\nPayer, F\n\nSynowitz, M\n\nFazekas, F\n\nEnzinger, C\n\nDeutschmann, H\n\nBeiträge in Fachzeitschriften\nISI:000416895700025\n28128689.0\n10.3171/2016.9.JNS161281\nNone\nOBJECTIVE Cerebral damage in frontal, parietal, and temporal brain areas and, probably more importantly, their interconnections can lead to deficits in language. However, neural plasticity and repair allow the brain to partly compensate for neural injury, mediated by both functional and structural changes. In this study, the authors sought to systematically investigate the relationship between language performance in brain tumor patients and structural perisylvian pathways (i.e., the arcuate fasciculus [AF]) using probabilistic fiber tracking on diffusion tensor imaging. The authors used a previously proposed model in which the AF is divided into anterior, long, and posterior segments. The authors hypothesized that right-handed patients with gliomas in the language-dominant (left) hemisphere would benefit from a more symmetrical or right-lateralized language pathway in terms of better preservation of language abilities. Furthermore, they investigated to what extent specific tumor characteristics, including proximity to the AF, affect language outcome in such patients. METHODS Twenty-seven right-handed patients (12 males and 15 females; mean age 52 ± 16 years) with 11 low-grade and 16 high-grade gliomas of the left hemisphere underwent 3-T diffusion-weighted MRI (30 directions) and language assessment as part of presurgical planning. For a systematic quantitative evaluation of the AF, probabilistic fiber tracking with a 2 regions of interest approach was carried out. Volumes of the 3 segments of both hemispheric AFs were evaluated by quantifying normalized and thresholded pathways. Resulting values served to generate the laterality index of the AFs. RESULTS Patients without language deficits tended to have an AF that was symmetric or lateralized to the right, whereas patients with deficits in language significantly more often demonstrated a left-lateralized posterior segment of the AF. Patients with high-grade gliomas had more severe language deficits than those with low-grade gliomas. Backward logistic regression revealed the laterality index of the posterior AF segment and tumor grade as the only independent statistically significant predictors for language deficits in this cohort. CONCLUSIONS In addition to the well-known fact that tumor entity influences behavioral outcome, the authors' findings suggest that the right homologs of structural language-associated pathways could be supportive for language function and facilitate compensation mechanisms after brain damage in functionally eloquent areas. This further indicates that knowledge about preoperative functional redistribution (identified by neurofunctional imaging) increases the chance for total or near-total resections of tumors in eloquent areas. In the future, longitudinal studies with larger groups are mandatory to overcome the methodological limitations of this cross-sectional study and to map neuroplastic changes associated with language performance and rehabilitation in brain tumor patients.\n\nDeutschmann, Hannes\n\nEnzinger, Christian\n\nFazekas, Franz\n\nJehna, Margit\n\nMahdy Ali, Kariem\n\nReishofer, Gernot\n\nvon Campe, Gord\n\n\n"
},
{
"text": "\n160726\nMedical diagnostics for indoor mold exposure.\n\nHurraß, J\n\nHeinzow, B\n\nAurbach, U\n\nBergmann, KC\n\nBufe, A\n\nBuzina, W\n\nCornely, OA\n\nEngelhart, S\n\nFischer, G\n\nGabrio, T\n\nHeinz, W\n\nHerr, CEW\n\nKleine-Tebbe, J\n\nKlimek, L\n\nKöberle, M\n\nLichtnecker, H\n\nLob-Corzilius, T\n\nMerget, R\n\nMülleneisen, N\n\nNowak, D\n\nRabe, U\n\nRaulf, M\n\nSeidl, HP\n\nSteiß, JO\n\nSzewszyk, R\n\nThomas, P\n\nValtanen, K\n\nWiesmüller, GA\n\nBeiträge in Fachzeitschriften\nISI:000401215300001\n27986496.0\n10.1016/j.ijheh.2016.11.012\nNone\nIn April 2016, the German Society of Hygiene, Environmental Medicine and Preventative Medicine (Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin (GHUP)) together with other scientific medical societies, German and Austrian medical societies, physician unions and experts has provided an AWMF (Association of the Scientific Medical Societies) guideline 'Medical diagnostics for indoor mold exposure'. This guideline shall help physicians to advise and treat patients exposed indoors to mold. Indoor mold growth is a potential health risk, even without a quantitative and/or causal association between the occurrence of individual mold species and health effects. Apart from the allergic bronchopulmonary aspergillosis (ABPA) and the mycoses caused by mold, there is only sufficient evidence for the following associations between moisture/mold damages and different health effects: Allergic respiratory diseases, asthma (manifestation, progression, exacerbation), allergic rhinitis, exogenous allergic alveolitis and respiratory tract infections/bronchitis. In comparison to other environmental allergens, the sensitizing potential of molds is estimated to be low. Recent studies show a prevalence of sensitization of 3-10% in the total population of Europe. The evidence for associations to mucous membrane irritation and atopic eczema (manifestation, progression, exacerbation) is classified as limited or suspected. Inadequate or insufficient evidence for an association is given for COPD, acute idiopathic pulmonary hemorrhage in children, rheumatism/arthritis, sarcoidosis, and cancer. The risk of infections from indoor molds is low for healthy individuals. Only molds that are capable to form toxins can cause intoxications. The environmental and growth conditions and especially the substrate determine whether toxin formation occurs, but indoor air concentrations are always very low. In the case of indoor moisture/mold damages, everyone can be affected by odor effects and/or impairment of well-being. Predisposing factors for odor effects can be given by genetic and hormonal influences, imprinting, context and adaptation effects. Predisposing factors for impairment of well-being are environmental concerns, anxieties, conditioning and attributions as well as a variety of diseases. Risk groups that must be protected are patients with immunosuppression and with mucoviscidosis (cystic fibrosis) with regard to infections and individuals with mucoviscidosis and asthma with regard to allergies. If an association between mold exposure and health effects is suspected, the medical diagnosis includes medical history, physical examination, conventional allergy diagnosis, and if indicated, provocation tests. For the treatment of mold infections, it is referred to the AWMF guidelines for diagnosis and treatment of invasive Aspergillus infections. Regarding mycotoxins, there are currently no validated test methods that could be used in clinical diagnostics. From the perspective of preventive medicine, it is important that mold damages cannot be tolerated in indoor environments.\n Copyright © 2016 Elsevier GmbH. All rights reserved.\n\nBuzina, Walter\n\n\n"
},
{
"text": "\n5052\nAntimicrobial therapy of unexplained fever in neutropenic patients--guidelines of the Infectious Diseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO), Study Group Interventional Therapy of Unexplained Fever, Arbeitsgemeinschaft Supportivmassnahmen in der Onkologie (ASO) of the Deutsche Krebsgesellschaft (DKG-German Cancer Society).\n\nLink, H\n\nBöhme, A\n\nCornely, OA\n\nHöffken, K\n\nKellner, O\n\nKern, WV\n\nMahlberg, R\n\nMaschmeyer, G\n\nNowrousian, MR\n\nOstermann, H\n\nRuhnke, M\n\nSezer, O\n\nSchiel, X\n\nWilhelm, M\n\nAuner, HW\n\nDiseases Working Party (AGIHO) of the German Society of Hematology and Oncology (DGHO)\n\nGroup Interventional Therapy of Unexplained Fever, Arbeitsgemeinschaft Supportivmassnahmen in der Onkologie (ASO) of the Deutsche Krebsgesellschaft (DKG-German Cancer Society)\n\nBeiträge in Fachzeitschriften\nISI:000185602900002\n13680173.0\n10.1007/s00277-003-0764-4\nNone\nCytostatic chemotherapy of hematological malignancies is often complicated by neutropenia, which increases the risk of infections, especially if the neutrophil count is below 500/microl. Frequently, fever is the first, and in most patients the only, sign of an infection. Unexplained fever is defined as follows: temperature of >/=38.3 degrees C or >/=38.0 degrees C for at least 1 h, or measured twice within 12 h, if the neutrophil count is <500/microl or <1000/microl with predicted decline to 500/microl. Different risk categories can be identified according to the duration of neutropenia: low risk =5 days, intermediate risk 6-9 days, high risk >/=10 days. An empirical mono- or duotherapy with antipseudomonal and antistreptococcal agents should be initiated immediately. In the low risk patient group, oral therapy with cipro-, levo-, or ofloxacin combined with amoxicillin/clavulanic acid is permissible. For standard and high risk patients, monotherapy can be carried out with either ceftazidime, cefepime, piperacillin with tazobactam or a carbapenem. In duotherapy, a single dose of an aminoglycoside is combined with acylaminopenicillin or a cephalosporin of the third or fourth generation. The addition of glycopeptides in empirical therapy should only be considered in the presence of severe mucositis, or if a catheter-associated infection is suspected. If fever persists after 72-96 h of first-line therapy with antibiotics, the regimen should be modified (with the exception of e.g. coagulase-negative staphylococci infections, because these infections take longer to respond). Intermediate risk patients should additionally receive an aminoglycoside after monotherapy (penicillin or a cephalosporin). If a carbapenem was administered for monotherapy, this can be followed by a quinolone and/or a glycopeptide. In the high risk group, the same modifications should be made as in the intermediate risk group but with additional systemic antifungal treatment. In the presence of unexplained fever, fluconazole can be administered at first, but if this fails, amphotericin B (conventional or liposomal), itraconazole, voriconazole or caspofungin should be started. After defervescence to <38 degrees C, treatment should be continued for 7 days if the neutrophil count is <1000/microl, and for 2 days if the neutrophil count is >1000/microl.\n\n\n"
},
{
"text": "\n151946\nPP141. The lipid transporters ABCA1 and ABCG1 are differentially expressed in preeclamptic and IUGR placentas.\n\nKörner, M\n\nWenger, F\n\nNikitina, L\n\nBaumann, M\n\nSurbek, D\n\nAlbrecht, C\n\nBeiträge in Fachzeitschriften\nNone\n26105462.0\n10.1016/j.preghy.2012.04.252\nNone\nThe ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 are highly expressed in the placenta in various compartments, including the villous syncytiotrophoblast (V-STB) and foetal endothelial cells. Among other not yet characterized functions, they play a role in the foeto-maternal transport of cholesterol and other lipophilic molecules. In humans, preliminary data suggest expressional changes of ABCA1 and ABCG1 in pathologic gestation, particularly under hypoxic conditions, but a systematic expression analysis in common human pregnancy diseases has never been performed.\n The aim of the present study was to characterize ABCA1 and ABCG1 expression in a large series of pathologic placentas, in particular from preeclampsia (PE) and intrauterine growth restriction (IUGR) which are associated with placental hypoxia.\n Placentas from 152 pathological pregnancies, including PE and/or HELLP (n=24) and IUGR (n=21), and 20 normal control placentas were assessed for their ABCA1 and ABCG1 mRNA and protein expression with quantitative RT-PCR and semi-quantitative immunohistochemical analysis, respectively.\n ABCA1 protein expression in the V-STB was significantly less extensive in PE compared with normal controls (<10% of V-STB stained for ABCA1 in 58% PE placentas vs. 25% controls; p=0.035). Conversely, it was significantly more wide-spread in IUGR (>75% of V-STB stained in 57% IUGR placentas vs. 15% controls; p=0.009). Moreover, there was an insignificant trend for increased ABCA1 expression in fetal endothelial cells of stem villi in PE (p=0.0588). ABCA1 staining levels in V-STB were significantly associated with placental histopathological features related with hypoxia: they were decreased in placentas exhibiting syncytial knotting (p=0.033) and decidual vasculopathy (p=0.0437) and increased in low weight placentas (p=0.015). The significant and specific alterations in ABCA1 protein expression found at a specific cellular level were not paralleled by changes in ABCA1 mRNA abundance of total placental tissue. ABCG1 staining was universally extensive in the V-STB of normal placentas, always affecting more than 90% of V-STB surface. In comparison, ABCG1 staining of the V-STB was generally often reduced in pregnancy diseases. In particular, less than 90% of V-STB exhibited ABCG1 staining in 26% of PE placentas (p=0.022) and 35% of IUGR placentas (p=0.003). Similarly to ABCA1, ABCG1 mRNA expression in total placental tissue was not significantly different between controls and PE or IUGR.\n ABCA1 and ABCG1 proteins are differentially expressed, with either down- or up-regulation, in the V-STB of placentas exhibiting features of chronic hypoxia, such as in PE and IUGR. This suggests that other factors in addition to hypoxia regulate the expression of placental lipid transporters. The specific changes on a cellular level were masked when only total tissue mRNA was analysed underlining the importance of cell specific expression analysis. The potential effects of decreased placental ABCA1 and ABCG1 expression on foetal nutrition and development remain to be elucidated.\n Copyright © 2012. Published by Elsevier B.V.\n\n\n"
},
{
"text": "\n181081\nHDL-related biomarkers are robust predictors of survival in patients with chronic liver failure.\n\nTrieb, M\n\nRainer, F\n\nStadlbauer, V\n\nDouschan, P\n\nHorvath, A\n\nBinder, L\n\nTrakaki, A\n\nKnuplez, E\n\nScharnagl, H\n\nStojakovic, T\n\nHeinemann, Á\n\nMandorfer, M\n\nPaternostro, R\n\nReiberger, T\n\nPitarch, C\n\nAmorós, A\n\nGerbes, A\n\nCaraceni, P\n\nAlessandria, C\n\nMoreau, R\n\nClària, J\n\nMarsche, G\n\nStauber, RE\n\nBeiträge in Fachzeitschriften\nISI:000563494500015\n32061870.0\n10.1016/j.jhep.2020.01.026\nNone\nHigh-density lipoprotein cholesterol (HDL-C) levels are reduced in patients with chronic liver disease and inversely correlate with disease severity. During acute conditions such as sepsis, HDL-C levels decrease rapidly and HDL particles undergo profound changes in their composition and function. We aimed to determine whether indices of HDL quantity and quality associate with progression and survival in patients with advanced liver disease.\n HDL-related biomarkers were studied in 508 patients with compensated or decompensated cirrhosis (including acute-on-chronic liver failure [ACLF]) and 40 age- and gender-matched controls. Specifically, we studied levels of HDL-C, its subclasses HDL2-C and HDL3-C, and apolipoprotein A1 (apoA-I), as well as HDL cholesterol efflux capacity as a metric of HDL functionality.\n Baseline levels of HDL-C and apoA-I were significantly lower in patients with stable cirrhosis compared to controls and were further decreased in patients with acute decompensation (AD) and ACLF. In stable cirrhosis (n = 228), both HDL-C and apoA-I predicted the development of liver-related complications independently of model for end-stage liver disease (MELD) score. In patients with AD, with or without ACLF (n = 280), both HDL-C and apoA-I were MELD-independent predictors of 90-day mortality. On ROC analysis, both HDL-C and apoA-I had high diagnostic accuracy for 90-day mortality in patients with AD (AUROCs of 0.79 and 0.80, respectively, similar to that of MELD 0.81). On Kaplan-Meier analysis, HDL-C <17 mg/dl and apoA-I <50 mg/dl indicated poor short-term survival. The prognostic accuracy of HDL-C was validated in a large external validation cohort of 985 patients with portal hypertension due to advanced chronic liver disease (AUROCs HDL-C: 0.81 vs. MELD: 0.77).\n HDL-related biomarkers are robust predictors of disease progression and survival in chronic liver failure.\n People who suffer from cirrhosis (scarring of the liver) have low levels of cholesterol carried by high-density lipoproteins (HDL-C). These alterations are connected to inflammation, which is a problem in severe liver disease. Herein, we show that reduced levels of HDL-C and apolipoprotein A-I (apoA-I, the main protein carried by HDL) are closely linked to the severity of liver failure, its complications and survival. Both HDL-C and apoA-I can be easily measured in clinical laboratories and are as good as currently used prognostic scores calculated from several laboratory values by complex formulas.\n Copyright © 2020 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.\n\nBinder, Lukas\n\nDouschan, Philipp\n\nGruden, Eva\n\nHeinemann, Akos\n\nHorvath, Angela\n\nMarsche, Gunther\n\nRainer, Florian\n\nScharnagl, Hubert\n\nStadlbauer-Köllner, Vanessa\n\nStauber, Rudolf\n\nTrakaki, Athina\n\n\n"
},
{
"text": "\n140498\nThe nitric oxide donor, S-nitroso human serum albumin, as an adjunct to HTK-N cardioplegia improves protection during cardioplegic arrest after myocardial infarction in rats.\n\nTrescher, K\n\nDzilic, E\n\nKreibich, M\n\nGasser, H\n\nAumayr, K\n\nKerjaschki, D\n\nPelzmann, B\n\nHallström, S\n\nPodesser, BK\n\nBeiträge in Fachzeitschriften\nISI:000350196400016\n25468794.0\n10.1093/icvts/ivu383\nNone\nCurrently available cardioplegic solutions provide excellent protection in patients with normal surgical risk; in high-risk patients, however, such as in emergency coronary artery bypass surgery, there is still room for improvement. As most of the cardioplegic solutions primarily protect myocytes, the addition of substances for protection of the endothelium might improve their protective potential. The nitric oxide donor, S-nitroso human serum albumin (S-NO-HSA), which has been shown to prevent endothelial nitric oxide synthase uncoupling, was added to the newly developed histidine-tryptophan-ketoglutarat (HTK-N) cardioplegia in an isolated heart perfusion system after subjecting rats to acute myocardial infarction (MI) and reperfusion.\n In male Sprague-Dawley rats, acute MI was induced by ligation for 1 h of the anterior descending coronary artery. After 2 h of in vivo reperfusion hearts were evaluated on an isolated erythrocyte-perfused working heart model. Cold ischaemia (4°C) for 60 min was followed by 45 min of reperfusion. Cardiac arrest was induced either with HTK (n = 10), HTK-N (n = 10) or HTK-N + S-NO-HSA (n = 10). In one group (HTK-N + S-NO-HSA plus in vivo S-NO-HSA; n = 9) an additional in vivo infusion of S-NO-HSA was performed.\n Post-ischaemic recovery of cardiac output (HTK: 77 ± 4%, HTK-N: 86 ± 7%, HTK-N + S-NO-HSA: 101 ± 5%, in vivo S-NO-HSA: 93 ± 8%), external heart work (HTK: 79 ± 5%, HTK-N: 83 ± 3%, HTK-N + S-NO-HSA: 101 ± 8%, in vivo S-NO-HSA: 109 ± 13%), coronary flow (HTK: 77 ± 4%, HTK-N: 94 ± 6%, HTK-N + S-NO-HSA: 118 ± 15%, in vivo S-NO-HSA: 113 ± 3.17%) [HTK-N + S-NO-HSA vs HTK P < 0.001; HTK-N + S-NO-HSA vs HTK-N P < 0.05] and left atrial diastolic pressure (HTK: 122 ± 31%, HTK-N: 159 ± 43%, HTK-N + S-NO-HSA: 88 ± 30, in vivo S-NO-HSA: 62 ± 10%) [HTK-N + S-NO-HSA vs HTK P < 0.05; in vivo S-NO-HSA vs HTK-N P < 0.05] were significantly improved in both S-NO-HSA-treated groups compared with HTK and HTK-N, respectively. This was accompanied by better preservation of high-energy phosphates (adenosine triphosphate; energy charge) and ultrastructural integrity on transmission electron microscopy. However, no additional benefit of in vivo S-NO-HSA infusion was observed.\n Addition of the NO donor, S-NO-HSA refines the concept of HTK-N cardioplegia in improving post-ischaemic myocardial perfusion. HTK-N with S-NO-HSA is a possible therapeutic option for patients who have to be operated on for acute MI.\n © The Author 2014. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.\n\nHallström, Seth\n\nPelzmann, Brigitte\n\n\n"
},
{
"text": "\n152138\nImpact of errors in paper-based and computerized diabetes management with decision support for hospitalized patients with type 2 diabetes. A post-hoc analysis of a before and after study.\n\nDonsa, K\n\nBeck, P\n\nHöll, B\n\nMader, JK\n\nSchaupp, L\n\nPlank, J\n\nNeubauer, KM\n\nBaumgartner, C\n\nPieber, TR\n\nBeiträge in Fachzeitschriften\nISI:000375155200008\n27103198.0\n10.1016/j.ijmedinf.2016.03.007\nNone\nMost preventable adverse drug events and medication errors occur during medication ordering. Medication order entry and clinical decision support are available on paper or as computerized systems. In this post-hoc analysis we investigated frequency and clinical impact of blood glucose (BG) documentation- and user-related calculation errors as well as workflow deviations in diabetes management. We aimed to compare a paper-based protocol to a computerized medication management system combined with clinical workflow and decision support.\n Seventy-nine hospitalized patients with type 2 diabetes mellitus were treated with an algorithm driven basal-bolus insulin regimen. BG measurements, which were the basis for insulin dose calculations, were manually entered either into the paper-based workflow protocol (PaperG: 37 patients) or into GlucoTab(®)-a mobile tablet PC based system (CompG: 42 patients). We used BG values from the laboratory information system as a reference. A workflow simulator was used to determine user calculation errors as well as workflow deviations and to estimate the effect of errors on insulin doses. The clinical impact of insulin dosing errors and workflow deviations on hypo- and hyperglycemia was investigated.\n The BG documentation error rate was similar for PaperG (4.9%) and CompG group (4.0%). In PaperG group, 11.1% of manual insulin dose calculations were erroneous and the odds ratio (OR) of a hypoglycemic event following an insulin dosing error was 3.1 (95% CI: 1.4-6.8). The number of BG values influenced by insulin dosing errors was eightfold higher than in the CompG group. In the CompG group, workflow deviations occurred in 5.0% of the tasks which led to an increased likelihood of hyperglycemia, OR 2.2 (95% CI: 1.1-4.6).\n Manual insulin dose calculations were the major source of error and had a particularly strong influence on hypoglycemia. By using GlucoTab(®), user calculation errors were entirely excluded. The immediate availability and automated handling of BG values from medical devices directly at the point of care has a high potential to reduce errors. Computerized systems facilitate the safe use of more complex insulin dosing algorithms without compromising usability. In CompG group, missed or delayed tasks had a significant effect on hyperglycemia, while in PaperG group insufficient precision of documentation times limited analysis. The use of old BG measurements was clinically less relevant.\n Insulin dosing errors and workflow deviations led to measurable changes in clinical outcome. Diabetes management systems including decision support should address nurses as well as physicians in a computerized way. Our analysis shows that such systems reduce the frequency of errors and therefore decrease the probability of hypo- and hyperglycemia.\n Copyright © 2016. Published by Elsevier Ireland Ltd.\n\nLichtenegger, Katharina\n\nMader, Julia\n\nPieber, Thomas\n\n\n"
},
{
"text": "\n162225\nDEVOTE 3: temporal relationships between severe hypoglycaemia, cardiovascular outcomes and mortality.\n\nPieber, TR\n\nMarso, SP\n\nMcGuire, DK\n\nZinman, B\n\nPoulter, NR\n\nEmerson, SS\n\nPratley, RE\n\nWoo, V\n\nHeller, S\n\nLange, M\n\nBrown-Frandsen, K\n\nMoses, A\n\nBarner Lekdorf, J\n\nLehmann, L\n\nKvist, K\n\nBuse, JB\n\nDEVOTE Study Group\n\nBeiträge in Fachzeitschriften\nISI:000417272300008\n28913543.0\n10.1007/s00125-017-4422-0\nPMC6002964\nThe double-blind Trial Comparing Cardiovascular Safety of Insulin Degludec vs Insulin Glargine in Patients with Type 2 Diabetes at High Risk of Cardiovascular Events (DEVOTE) assessed the cardiovascular safety of insulin degludec. The incidence and rates of adjudicated severe hypoglycaemia, and all-cause mortality were also determined. This paper reports a secondary analysis investigating associations of severe hypoglycaemia with cardiovascular outcomes and mortality.\n In DEVOTE, patients with type 2 diabetes were randomised to receive either insulin degludec or insulin glargine U100 (100 units/ml) once daily (between dinner and bedtime) in an event-driven, double-blind, treat-to-target cardiovascular outcomes trial. The primary outcome was the first occurrence of an adjudicated major adverse cardiovascular event (MACE; cardiovascular death, non-fatal myocardial infarction or non-fatal stroke). Adjudicated severe hypoglycaemia was the pre-specified secondary outcome. In the present analysis, the associations of severe hypoglycaemia with both MACE and all-cause mortality was evaluated in the pooled trial population using time-to-event analyses, with severe hypoglycaemia as a time-dependent variable and randomised treatment as a fixed factor. An investigation with interaction terms indicated that the effect of severe hypoglycaemia on the risk of MACE and all-cause mortality were the same for both treatment arms, and so the temporal association for severe hypoglycaemia with subsequent MACE and all-cause mortality is reported for the pooled population.\n There was a non-significant difference in the risk of MACE for individuals who had vs those who had not experienced severe hypoglycaemia during the trial (HR 1.38, 95% CI 0.96, 1.96; p = 0.080) and therefore there was no temporal relationship between severe hypoglycaemia and MACE. There was a significantly higher risk of all-cause mortality for patients who had vs those who had not experienced severe hypoglycaemia during the trial (HR 2.51, 95% CI 1.79, 3.50; p < 0.001). There was a higher risk of all-cause mortality 15, 30, 60, 90, 180 and 365 days after experiencing severe hypoglycaemia compared with not experiencing severe hypoglycaemia in the same time interval. The association between severe hypoglycaemia and all-cause mortality was maintained after adjustment for the following baseline characteristics: age, sex, HbA1c, BMI, diabetes duration, insulin regimen, hepatic impairment, renal status and cardiovascular risk group.\n The results from these analyses demonstrate an association between severe hypoglycaemia and all-cause mortality. Furthermore, they indicate that patients who experienced severe hypoglycaemia were particularly at greater risk of death in the short term after the hypoglycaemic episode. These findings indicate that severe hypoglycaemia is associated with higher subsequent mortality; however, they cannot answer the question as to whether severe hypoglycaemia serves as a risk marker for adverse outcomes or whether there is a direct causal effect.\n ClinicalTrials.gov NCT01959529.\n\nPieber, Thomas\n\n\n"
}
]
}