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Oldenburg, Germany

Conzelmann L.O.,Johannes Gutenberg University Mainz | Hoffmann I.,Johannes Gutenberg University Mainz | Blettner M.,Johannes Gutenberg University Mainz | Kallenbach K.,Task Force for Aortic Surgery and Interventional Vascular Surgery | And 7 more authors.
European Journal of Cardio-thoracic Surgery | Year: 2012

Objectives: Acute aortic dissection type A (AADA) is associated with major adverse events, such as transient or persistent neurological dysfunction (ND), which may be patient-, disease- or surgery-related. There is a lack of consensus regarding risk factors for ND in AADA patients. The aim of this study was to analyse and identify risk factors for new postoperative ND after aortic repair for AADA. Methods: Between July 2006 and June 2010, 2137 AADA patients were enrolled in the multi-centre, prospective German Registry of AADA (GERAADA). Perioperative data were prospectively gathered from 50 institutes in Austria, Switzerland and Germany, and multivariate logistic regression analysis was performed to determine the independent predictors of new onset ND. Results: ND occurred in 20.3% of all patients prior to surgery, 12.6% of which resolved postoperatively and 7.7% persisted. New ND after AADA surgery occurred in 9.5% of patients. Risk factors for an increased rate of postoperative new ND were malperfusion syndrome of three or more territories prior to surgery [odds ratio (OR) = 2.206, P = 0.0065], dissection of the supraaortic vessels (OR = 1.468, P = 0.0103) and longer operating time (OR = 1.002 per min, P = 0.0001). New postoperative ND was associated with an increased rate of mortality (22.5 vs. 16.1%, P = 0.0087). Arterial cannulation site had no statistically significant impact on neurological outcomes. Conclusions: Neurological complications are associated with increased mortality post-AADA repair. New onset ND is associated with extensive malperfusion syndrome, supraaortic vessel dissection and operative time and does not seem to be affected by choice of arterial cannulation site. © The Author 2012. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.

Krille L.,University Medical Center Mainz | Krille L.,International Agency for Research on Cancer | Dreger S.,University of Bremen | Schindel R.,University Medical Center Mainz | And 29 more authors.
Radiation and Environmental Biophysics | Year: 2015

The aim of this cohort study was to assess the risk of developing cancer, specifically leukaemia, tumours of the central nervous system and lymphoma, before the age of 15 years in children previously exposed to computed tomography (CT) in Germany. Data for children with at least one CT between 1980 and 2010 were abstracted from 20 hospitals. Cancer cases occurring between 1980 and 2010 were identified by stochastic linkage with the German Childhood Cancer Registry (GCCR). For all cases and a sample of non-cases, radiology reports were reviewed to assess the underlying medical conditions at time of the CT. Cases were only included if diagnosis occurred at least 2 years after the first CT and no signs of cancer were recorded in the radiology reports. Standardised incidence ratios (SIR) using incidence rates from the general population were estimated. The cohort included information on 71,073 CT examinations in 44,584 children contributing 161,407 person-years at risk with 46 cases initially identified through linkage with the GCCR. Seven cases had to be excluded due to signs possibly suggestive of cancer at the time of first CT. Overall, more cancer cases were observed (O) than expected (E), but this was mainly driven by unexpected and possibly biased results for lymphomas. For leukaemia, the SIR (SIR = O/E) was 1.72 (95 % CI 0.89–3.01, O = 12), and for CNS tumours, the SIR was 1.35 (95 % CI 0.54–2.78, O = 7). Despite careful examination of the medical information, confounding by indication or reverse causation cannot be ruled out completely and may explain parts of the excess. Furthermore, the CT exposure may have been underestimated as only data from the participating clinics were available. This should be taken into account when interpreting risk estimates. © 2015, Springer-Verlag Berlin Heidelberg.

Roth C.L.,Seattle Childrens Hospital Research Institute | Gebhardt U.,Klinikum Oldenburg GmbH | Muller H.L.,Klinikum Oldenburg GmbH
Obesity | Year: 2011

Patients with craniopharyngioma (CP), an embryological tumor located in the hypothalamic and/or pituitary region, often suffer from uncontrolled eating and severe obesity. We aimed to compare peripherally secreted hormones involved in controlling food intake in normal weight and obese children and adolescents with CP vs. controls. Plasma insulin, glucose, total ghrelin, and peptide-YY (PYY) levels were assessed under fasting conditions as well as 60min after liquid mixed meal in four groups: Normal weight (n = 12) and obese (n = 15) CP patients, and 12 normal weight and 15 obese otherwise healthy BMI-, gender- and age-matched controls. Homeostasis model assessment of insulin resistance (HOMA IR), as well as quantitative insulin sensitivity check index (QUICKI) were calculated. Obese CP subjects had significantly higher HOMA IR, higher baseline and postmeal insulin but lower ghrelin levels, weaker postmeal changes for PYY, and lower QUICKI compared to obese controls. QUICKI data from all CP patients correlated positively with ghrelin and PYY % postmeal changes (ghrelin: r = 0.38, P = 0.023; PYY r = 0.40, P = 0.017) and negatively with standard deviation score-BMI (SDS-BMI: r = 0.49, P = 0.002). Tumor growth of 87% obese and 58% of normal weight CP patients affected the hypothalamic area which was associated with higher SDS-BMI and weaker % postmeal ghrelin changes (P = 0.014) compared to CP patients without hypothalamic tumor involvement. Blunted postmeal ghrelin and PYY responses in obese CP subjects are likely due to their higher degree of insulin resistance and lower insulin sensitivity compared to matched obese controls. Thus, insulin resistance in CP patients seems to affect eating behavior by affecting meal responses of gut peptides. © 2010 The Obesity Society.

Roth C.L.,Seattle Childrens Hospital Research Institute | Enriori P.J.,Oregon Health And Science University | Enriori P.J.,Monash University | Gebhardt U.,Klinikum Oldenburg GmbH | And 6 more authors.
Metabolism: Clinical and Experimental | Year: 2010

Relationships of blood circulating melanocortins to childhood obesity are not well established. We evaluated serum α-melanocyte-stimulating hormone (α-MSH) in lean children and different study groups of childhood obesity. We examined serum α-MSH in 52 otherwise healthy children with childhood obesity (Ob; mean age, 11 years; 32 girls/20 boys), 27 normal-weight children of same age, 7 additional obese patients with reduced melanocortin-4 receptor function (MC4Rmut), and 22 patients with craniopharyngioma (CP). Fasting serum α-MSH and leptin were measured by radioimmunoassay. Serum α-MSH was also evaluated 1 hour after 500-kcal liquid meal (CP and Ob) and at the end of 1-year lifestyle intervention in 24 Ob patients. The α-MSH levels were similar in obese vs lean children but significantly lower in CP (P< .001) and significantly higher (P < .05) in MC4Rmut patients compared with Ob. One hour after liquid meal, α-MSH increased in patients with Ob but not with CP. After 1 year, α-MSH levels increased significantly in the successful weight reduction Ob subgroup despite unchanged cortisol levels. The α-MSH changes correlated to weight status changes (r = 0.67, P = .0003) but not to changes of cortisol, insulin, or homeostasis model assessment of insulin resistance index. Persistently low α-MSH levels in CP patients are suspected to be due to pituitary or hypothalamic damage. High peripheral levels in MC4Rmut carriers indicate up-regulation of α-MSH. Changes of weight status are associated with changes of peripheral α-MSH. © 2010 Elsevier Inc. All rights reserved.

Roth C.L.,Seattle Childrens Hospital Research Institute | Elfers C.,Seattle Childrens Hospital Research Institute | Gebhardt U.,Klinikum Oldenburg GmbH | Muller H.L.,Klinikum Oldenburg GmbH | Reinehr T.,Witten/Herdecke University
Metabolism: Clinical and Experimental | Year: 2013

Objective: Brain-derived neurotrophic factor (BDNF) is a regulator of energy homeostasis and food intake through hypothalamic signaling. Currently, data regarding BDNF in children with obesity are lacking. We evaluated serum BDNF concentrations in obese children, both before and after lifestyle intervention, in reference to those of lean children. Methods: A total of 90 (24 normal weight; 66 obese) children were studied utilizing a cross-sectional clinical outpatient study design. In addition, longitudinal data analysis was performed in 30 obese children participating in a lifestyle intervention for one year. Results: Fasting serum BDNF concentrations were higher in obese vs. normal weight children (BDNF 20.3 ± 1.0 vs. 12.5 ± 1.7 ng/mL, respectively, mean ± SEM, p < 0.001) and correlated significantly to BMI standard deviation score (r = 0.426, p < 0.001), and leptin (r = 0.414, p < 0.01). BDNF concentrations were not regulated in response to food, 60 min after ingestion of a liquid test meal. After one year lifestyle intervention, delta BDNF correlated significantly to delta leptin (r = 0.475, p < 0.01), but not to changes of insulin resistance index HOMA-IR, systolic and diastolic blood pressure, HDL, LDL, and triglycerides. In a multiple stepwise linear regression adjusted for pubertal stage, age, sex, and BMI, delta BDNF correlated significantly (p < 0.05) to delta leptin and delta triceps skinfold and in tendency to delta subscapularis skinfold thickness (p = 0.050). Conclusions: Our results in children do not indicate a significant relationship between BDNF and insulin resistance or cardiovascular risk factors. However, the correlation between changes of BDNF and changes of leptin suggests a relationship between BDNF and fat mass. © 2013 Elsevier Inc.

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