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Elin Kahlert Clinic of Gastroenterology and Endocrinology, University Medical Center Goettingen, Goettingen, Germany

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Martina Blaschke Clinic of Gastroenterology and Endocrinology, University Medical Center Goettingen, Goettingen, Germany
Endokrinologikum Goettingen, Goettingen, Germany

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Knut Brockmann Interdisciplinary Pediatric Center for Children with Developmental Disabilities and Severe Chronic Disorders, University Medical Center Goettingen, Goettingen, Germany

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Clemens Freiberg Interdisciplinary Pediatric Center for Children with Developmental Disabilities and Severe Chronic Disorders, University Medical Center Goettingen, Goettingen, Germany

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Onno E Janssen Endokrinologikum Hamburg, Hamburg, Germany

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Nikolaus Stahnke Endokrinologikum Hamburg, Hamburg, Germany

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Domenika Strik Endokrinologikum Berlin, Berlin, Germany

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Martin Merkel Endokrinologikum Hannover, Hannover, Germany

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Alexander Mann Endokrinologikum Frankfurt, Frankfurt/Main, Germany

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Klaus-Peter Liesenkötter Endokrinologikum Berlin, Berlin, Germany

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Heide Siggelkow Clinic of Gastroenterology and Endocrinology, University Medical Center Goettingen, Goettingen, Germany
Endokrinologikum Goettingen, Goettingen, Germany

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Objective

Turner syndrome (TS) is characterized by the complete or partial loss of the second sex chromosome and associated with a wide range of clinical manifestations. We aimed to assess the medical care of adult patients with TS in Germany.

Design

Retrospective multicenter observational study.

Methods

Data were collected from medical records of 258 women with TS treated between 2001 and 2017 in five non-university endocrinologic centers in Germany.

Results

Mean age was 29.8 ± 11.6 years, mean height 152 ± 7.7 cm, and mean BMI 26.6 ± 6.3 kg/m2. The karyotype was known in 50% of patients. Information on cholesterol state, liver enzymes, and thyroid status was available in 81–98% of women with TS; autoimmune thyroiditis was diagnosed in 37%. Echocardiography was performed in 42% and cardiac MRI in 8.5%, resulting in a diagnosis of cardiovascular disorder in 28%. Data on growth hormone therapy were available for 40 patients (15%) and data concerning menarche in 157 patients (61%).

Conclusion

In 258 women with TS, retrospective analysis of healthcare data indicated that medical management was focused on endocrine manifestations. Further significant clinical features including cardiovascular disease, renal malformation, liver involvement, autoimmune diseases, hearing loss, and osteoporosis were only marginally if at all considered. Based on this evaluation and in accordance with recent guidelines, we compiled a documentation form facilitating the transition from pediatric to adult care and further medical management of TS patients. The foundation of Turner Centers in March 2019 will improve the treatment of TS women in Germany.

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Elena Izkhakov Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
School of Public Health, Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel

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Joseph Meyerovitch Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Community Division, Clalit Health Services, Tel Aviv, Israel
The Jesse Z and Sara Lea Shafer Institute for Endocrinology and Diabetes, National Center for Childhood Diabetes, Schneider Children’s Medical Center of Israel, Petah Tikva, Israel

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Micha Barchana School of Public Health, Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel

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Yacov Shacham Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Department of Cardiology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel

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Naftali Stern Institute of Endocrinology, Metabolism and Hypertension, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel
Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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Lital Keinan-Boker School of Public Health, Faculty of Social Welfare and Health Sciences, University of Haifa, Haifa, Israel
National Cancer Registry, Israel Center for Disease Control, Ministry of Health, Israel, Ramat Gan, Israel

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Objective

Thyroid cancer (TC) survivors may be at risk of subsequent cardiovascular and cerebrovascular (CaV&CeV) morbidity. The 2009 American Thyroid Association (ATA) guidelines recommended less aggressive treatment for low-risk TC patients. The aim of this study was to assess the atherosclerotic CaV&CeV outcome of Israeli TC survivors compared to individuals with no thyroid disease, and the atherosclerotic CaV&CeV outcome before (2000–2008) and after (2009–2011) implementation of the 2009 ATA guidelines.

Methods

All members of the largest Israeli healthcare organization who were diagnosed with TC from 1/2000 to 12/2014 (study group) and age- and sex-matched members with no thyroid disease (controls) were included. Adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) were calculated using Cox proportional hazards models.

Results

The mean follow-up was 7.6 ± 4.2 and 7.8 ± 4.1 years for the study (n = 5,677, 79% women) and control (n = 23,962) groups, respectively. The former had an increased risk of new atherosclerotic CaV&CeV events (adjusted HR 1.26, 95% CI 1.15–1.39). The 5-year incidence of CaV&CeV was lower (adjusted HR 0.49, 95% CI 0.38–0.62) from 2009 to 2011 compared to 2000 to 2008, but remained higher in the study group than in the control group (adjusted HR 1.5, 95% CI 1.14–1.69).

Conclusions

This large Israeli population-based cohort study showed greater atherosclerotic CaV&CeV morbidity in TC survivors compared to individuals with no thyroid diseases. There was a trend toward a decreased 5-year incidence of atherosclerotic CaV&CeV events among TC survivors following the implementation of the 2009 ATA guidelines, but it remained higher compared to the general population.

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Ananda A Santana-Ribeiro Laboratory of Motor Control and Body Balance, Center for Health Science Research, Federal University of Sergipe, Sergipe, Brazil

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Giulliani A Moreira-Brasileiro Laboratory of Motor Control and Body Balance, Center for Health Science Research, Federal University of Sergipe, Sergipe, Brazil
Department of Physical Therapy and Post-Graduate Program in Health Science, Federal University of Sergipe, The GREAT Group (GRupo de Estudos em ATividade física), Sergipe, Brazil

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Manuel H Aguiar-Oliveira Division of Endocrinology, Federal University of Sergipe, Aracaju, Sergipe, Brazil

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Roberto Salvatori Division of Endocrinology, Diabetes and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

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Vitor O Carvalho Department of Physical Therapy and Post-Graduate Program in Health Science, Federal University of Sergipe, The GREAT Group (GRupo de Estudos em ATividade física), Sergipe, Brazil

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Claudia K Alvim-Pereira Laboratory of Motor Control and Body Balance, Center for Health Science Research, Federal University of Sergipe, Sergipe, Brazil

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Carlos R Araújo-Daniel Department of Statistic and Actuarial Sciences, Federal University of Sergipe, Aracaju, Sergipe, Brazil

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Júlia G Reis-Costa Laboratory of Motor Control and Body Balance, Center for Health Science Research, Federal University of Sergipe, Sergipe, Brazil

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Alana L Andrade-Guimarães Laboratory of Motor Control and Body Balance, Center for Health Science Research, Federal University of Sergipe, Sergipe, Brazil
Department of Physical Therapy and Post-Graduate Program in Health Science, Federal University of Sergipe, The GREAT Group (GRupo de Estudos em ATividade física), Sergipe, Brazil

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Alécia A Oliveira-Santos Division of Endocrinology, Federal University of Sergipe, Aracaju, Sergipe, Brazil

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Edgar R Vieira Department of Physical Therapy and Neuroscience, Wertheims’ College of Nursing and Health Science, Florida International University, Miami, Florida, USA

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Miburge B Gois-Junior Laboratory of Motor Control and Body Balance, Center for Health Science Research, Federal University of Sergipe, Sergipe, Brazil
Department of Physical Therapy and Post-Graduate Program in Health Science, Federal University of Sergipe, The GREAT Group (GRupo de Estudos em ATividade física), Sergipe, Brazil
Department of Physical Therapy and Neuroscience, Wertheims’ College of Nursing and Health Science, Florida International University, Miami, Florida, USA

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Objectives

Walking and postural balance are extremely important to obtain food and to work. Both are critical for quality of life and ability to survive. While walking reflects musculoskeletal and cardiopulmonary systems, postural balance depends on body size, muscle tone, visual, vestibular and nervous systems. Since GH and IGF-I act on all these systems, we decided to study those parameters in a cohort of individuals with severe short stature due to untreated isolated GH deficiency (IGHD) caused by a mutation in the GHRH receptor gene. These IGHD subjects, despite reduction in muscle mass, are very active and have normal longevity.

Methods

In a cross-sectional study, we assessed walking (by a 6-min walk test), postural balance (by force platform) and fall risk (by the 'Timed Up and Go' test) in 31 IGHD and 40 matched health controls.

Results

The percentage of the walked distance measured in relation to the predicted one was similar in groups, but higher in IGHD, when corrected by the leg length. Absolute postural balance data showed similar velocity of unipodal support in the two groups, and better values, with open and closed eyes and unipodal support, in IGHD, but these differences became non-significant when corrected for height and lower-limb length. The time in 'Timed Up and Go' test was higher in IGHD cohort, but still below the cut-off value for fall risk.

Conclusion

IGHD subjects exhibit satisfactory walking and postural balance, without increase in fall risk.

Open access
Shenglong Le Exercise, Health and Technology Centre, Department of Physical Education, Shanghai Jiao Tong University, Shanghai, China
Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland

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Leiting Xu Medical School, Ningbo University, Ningbo, China

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Moritz Schumann Department of Molecular and Cellular Sports Medicine, German Sport University Cologne, Cologne, Germany
The Key Laboratory of Systems Biomedicine, Ministry of Education, and Exercise Translational Medicine Center, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China

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Na Wu Exercise, Health and Technology Centre, Department of Physical Education, Shanghai Jiao Tong University, Shanghai, China
Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland

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Timo Törmäkangas Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland

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Markku Alén Department of Medical Rehabilitation, Oulu University Hospital, Oulu, Finland

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Sulin Cheng Exercise, Health and Technology Centre, Department of Physical Education, Shanghai Jiao Tong University, Shanghai, China
Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland
The Key Laboratory of Systems Biomedicine, Ministry of Education, and Exercise Translational Medicine Center, Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China

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Petri Wiklund Exercise, Health and Technology Centre, Department of Physical Education, Shanghai Jiao Tong University, Shanghai, China
Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland
Department of Epidemiology and Biostatistics, Centre for Environment and Health, School of Public Health, Imperial College London, London, UK
Center for Life Course Health Research, Faculty of Medicine, University of Oulu, Oulu, Finland

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Background

The directional influences between serum sex hormone-binding globulin (SHBG), adiposity and insulin resistance during pubertal growth remain unclear. The aim of this study was to investigate bidirectional associations between SHBG and insulin resistance (HOMA-IR) and adiposity from childhood to early adulthood.

Methods

Participants were 396 healthy girls measured at baseline (age 11.2 years) and at 1, 2, 4 and 7.5 years. Serum concentrations of estradiol, testosterone and SHBG were determined by ELISA, glucose and insulin by enzymatic photometry, insulin-like growth factor 1 (IGF-1) by time-resolved fluoroimmunoassays, whole-body fat mass by dual-energy X-ray absorptiometry and HOMA-IR were determined by homeostatic model assessment. The associations were examined using cross-lagged path models.

Results

In a cross-lagged path model, SHBG predicted HOMA-IR before menarche β = −0.320 (95% CI: −0.552 to −0.089), P = 0.007, independent of adiposity and IGF-1. After menarche, no directional effect was found between SHBG and insulin resistance or adiposity.

Conclusions

Our results suggest that in early puberty, decline in SHBG predicts development of insulin resistance, independent of adiposity. However, after menarche, no directional influences between SHBG, adiposity and insulin resistance were found, suggesting that observational associations between SHBG, adiposity and insulin resistance in pubertal children may be subject to confounding. Further research is needed to understand the underlying mechanisms of the associations between SHBG and cardiometabolic risk markers in peripubertal children.

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Ling-Jun Li Division of O&G, KK Women’s and Children’s Hospital, Singapore, Singapore
O&G ACP, Duke-NUS Graduate Medical School, Singapore, Singapore
Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore

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Izzuddin M Aris Singapore Institute for Clinical Sciences, Agency for Science Technology and Research (A*STAR), Singapore, Singapore

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Lin Lin Su Department of O&G, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Yap Seng Chong Singapore Institute for Clinical Sciences, Agency for Science Technology and Research (A*STAR), Singapore, Singapore
Department of O&G, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Tien Yin Wong O&G ACP, Duke-NUS Graduate Medical School, Singapore, Singapore
Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore

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Kok Hian Tan Division of O&G, KK Women’s and Children’s Hospital, Singapore, Singapore
O&G ACP, Duke-NUS Graduate Medical School, Singapore, Singapore

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Jie Jin Wang O&G ACP, Duke-NUS Graduate Medical School, Singapore, Singapore

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Aims

The cumulative effect of gestational diabetes mellitus (GDM) and hypertensive disorders of pregnancy (HDP) on postpartum cardio-metabolic diseases is equivocal. We aimed to assess the associations of GDM and HDP’s individual and synergic contribution to risks of postpartum cardio-metabolic diseases (metabolic syndrome (MetS), abnormal glucose metabolism and hypertension (HTN)).

Methods

Of participants from a Singapore birth cohort, 276 mothers attending the 5-year postpartum visit were included in this study. During this visit, we collected mothers’ history of GDM and HDP in all live births in a chronicle sequence and assessed the cardio-metabolic risks based on blood pressure, anthropometry and a panel of serum biomarkers. We diagnosed MetS, abnormal glucose metabolism and HTN according to Adult Treatment Panel III 2000 and World Health Organization guidelines.

Results

Of 276 mothers, 157 (56.9%) had histories of GDM while 23 (8.3%) had histories of HDP. After full adjustment, we found associations of GDM episodes with postpartum abnormal glucose metabolism (single episode: relative risk (RR) 2.9 (95% CI: 1.7, 4.8); recurrent episodes (≥2): RR = 3.8 (2.1–6.8)). Also, we found association between histories of HDP and HTN (RR = 3.6 (1.5, 8.6)). Having either (RR 2.6 (1.7–3.9)) or both gestational complications (RR 2.7 (1.6–4.9)) was associated with similar risk of postpartum cardio-metabolic disease.

Conclusions

Mothers with GDM or HDP had a threefold increased risk of postpartum abnormal glucose metabolism or HTN, respectively. Having both GDM and HDP during past pregnancies was not associated with additional risk of postpartum cardio-metabolic diseases beyond that associated with either complication alone.

Open access
Marianne Aa Grytaas Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Kjersti Sellevåg Department of Heart Disease, Haukeland University Hospital, Bergen, Norway

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Hrafnkell B Thordarson Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Eystein S Husebye Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Kristian Løvås Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Terje H Larsen Department of Heart Disease, Haukeland University Hospital, Bergen, Norway
Department of Biomedicine, University of Bergen, Bergen, Norway

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Background

Primary aldosteronism (PA) is associated with increased cardiovascular morbidity, presumably due to left ventricular (LV) hypertrophy and fibrosis. However, the degree of fibrosis has not been extensively studied. Cardiac magnetic resonance imaging (CMR) contrast enhancement and novel sensitive T1 mapping to estimate increased extracellular volume (ECV) are available to measure the extent of fibrosis.

Objectives

To assess LV mass and fibrosis before and after treatment of PA using CMR with contrast enhancement and T1 mapping.

Methods

Fifteen patients with newly diagnosed PA (PA1) and 24 age- and sex-matched healthy subjects (HS) were studied by CMR with contrast enhancement. Repeated imaging with a new scanner with T1 mapping was performed in 14 of the PA1 and 20 of the HS median 18 months after specific PA treatment and in additional 16 newly diagnosed PA patients (PA2).

Results

PA1 had higher baseline LV mass index than HS (69 (53–91) vs 51 (40–72) g/m2; P < 0.001), which decreased significantly after treatment (58 (40–86) g/m2; P < 0.001 vs baseline), more with adrenalectomy (n = 8; −9 g/m2; P = 0.003) than with medical treatment (n = 6; −5 g/m2; P = 0.075). No baseline difference was found in contrast enhancement between PA1 and HS. T1 mapping showed no increase in ECV as a myocardial fibrosis marker in PA. Moreover, ECV was lower in the untreated PA2 than HS 10 min post-contrast, and in both PA groups compared with HS 20 min post-contrast.

Conclusion

Specific treatment rapidly reduced LV mass in PA. Increased myocardial fibrosis was not found and may not represent a common clinical problem.

Open access
Charlotte Höybye Patient Area Endocrinology and Nephrology, Infection and Inflammation Theme, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

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Laia Faseh Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

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Christos Himonakos Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden
Department of Medicine, Karlstad Hospital, Karlstad, Sweden

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Tomasz Pielak NUTOPI Sp. z o. o., Poznan, Poland

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Jesper Eugen-Olsen Clinical Research Centre, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark

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Growth hormone deficiency (GHD) syndrome is associated with adverse levels of several risk factors for cardiovascular diseases (CVD), including metabolic inflammation. However, the impact of GHD and GH treatment on low-grade inflammation is unknown. The aim of the study was to establish the level of the low-grade inflammation biomarker soluble urokinase plasminogen activator receptor (suPAR) in adults with GHD and the response to long-term GH treatment. Measurements of suPAR and CRP were performed in bio-bank serum samples from 72 adults, 34 males and 38 females, with GHD before and during at least 5 years of GH treatment. Mean age was 52.5 ± 15.5 years, BMI 27.3 ± 5 kg/m2. Clinical evaluations and blood sampling were performed at routine visits. Data on demography, anthropometry, lab results and clinical events were retrieved from post-marketing surveillance study databases and medical records. suPAR and high-sensitive (hs) CRP were analysed using ELISA and immunochemistry, respectively. At baseline blood pressure, lipid profile and fasting glucose were within the normal reference range. Baseline geometric mean and 95% CI of suPAR was 2.9 (2.7–3.3) ng/mL and of CRP 2.3 (0.6–4.0) mg/L. Mean follow-up was 8 ± 2 years. The suPAR levels remained stable during follow-up, although individual increases were seen on occurrence or presence of co-morbidities. In contrast, levels of CRP decreased. In conclusion, the decrease in CRP and indirectly the absence of an expected increase in suPAR over time indicates a favourable effect of GH on low-grade inflammation.

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Andrea V Haas Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Paul N Hopkins Cardiovascular Genetics, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA

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Nancy J Brown Vanderbilt University Medical Center, Nashville, Tennessee, USA

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Luminita H Pojoga Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Jonathan S Williams Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Gail K Adler Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Gordon H Williams Division of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

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There are conflicting data on whether variations of physiologic cortisol levels associated with cardiovascular risk. We hypothesize that prior discordant findings are related to problems associated with varying sample size, techniques for assessing cardiovascular risk and failure to adequately account for environmental factors. To address these issues, we utilized a large sample size, selected the Framingham risk score to compute cardiovascular risk and performed the study in a highly controlled setting. We had two main objectives: determine whether higher, yet physiologic, cortisol levels associated with increased cardiovascular risk and determine whether caveolin-1 (rs926198) risk allele carriers associated with increased cardiovascular risk. This was a cross-sectional study of 574 non-diabetic individuals who completed a common protocol. Data collection included fasting blood samples, blood pressure measurements and a 24-h urine-free cortisol collection. Five hundred seventeen of these participants also completed caveolin-1 genotyping. Subjects were classified as belonging to either the low-mode or high-mode urine-free cortisol groups, based on the bimodal distribution of urine-free cortisol. In multivariate analysis, Framingham risk score was statistically higher in the high-mode cortisol group (10.22 (mean) ± 0.43 (s.e.m.)) compared to the low-mode cortisol group (7.73 ± 0.34), P < 0.001. Framingham risk score was also statistically higher in the caveolin-1 risk allele carriers (8.91 ± 0.37) compared to caveolin-1 non-risk allele carriers (7.59 ± 0.48), P = 0.034. Overall, the estimated effect on Framingham risk score of carrying the caveolin-1 risk allele was 1.33 ± 0.61, P = 0.029. Both urinary cortisol and caveolin-1 risk allele status are independent predictors of Framingham risk score.

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Marc Blondon Division of Angiology and Hemostasis, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland

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Emmanuel Biver Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland

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Olivia Braillard Division of Primary Care Medicine, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland

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Marc Righini Division of Angiology and Hemostasis, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland

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Pierre Fontana Division of Angiology and Hemostasis, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland

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Alessandro Casini Division of Angiology and Hemostasis, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland

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Objective

Vitamin D deficiency is associated with increased risks of arterial and venous cardiovascular events. Hypothetically, supplementation with vitamin D may lead to a less prothrombotic phenotype, as measured by global coagulation assays and fibrin clot structure.

Methods

In this prospective cohort study, we enrolled adult outpatients attending the Primary Care Division of the Geneva University Hospitals with a severe vitamin D deficiency (25-hydroxyvitamin-D3 (25-OHD) <25 nmol/L), excluding obese patients or with a recent acute medical event. We evaluated changes in coagulation times, thrombin generation assay, clot formation and clot lysis time, 25-OHD and parathormone before and 1–3 months after cholecalciferol oral supplementation with one-time 300,000 IU then 800 IU daily. Paired t-tests with a two-sided alpha of 0.05 compared absolute mean differences.

Results

The 48 participants had a mean age of 43.8 ± 13.8 years. After supplementation, 25-OHD levels increased from 17.9 ± 4.6 nmol/L to 62.5 ± 20.7 nmol/L 6.4 ± 3.0 weeks after inclusion. Endogenous thrombin potential and thrombin generation peak values both decreased significantly (−95.4 nM × min (95%CI −127.9 to −62.8), P < 0.001; −15.1 nM (−23.3 to −6.8), P < 0.001). The maximum absorbance by turbidimetry decreased significantly (P = 0.001) after supplementation. There was no change in clot lysis time, coagulation times or plasminogen activator inhibitor-1 and homocysteine levels.

Conclusions

In severe vitamin D deficiency, a high-dose cholecalciferol supplementation was associated with a reduction in thrombin generation and an average decreased number of fibrin protofibrils per fibers and fibrin fiber size measured by turbidimetry. This suggests that severe vitamin D deficiency may be associated with a potentially reversible prothrombotic profile.

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T L C Wolters Division of Endocrinology, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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C D C C van der Heijden Division of Experimental Internal Medicine, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands
Division of Vascular Medicine, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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N van Leeuwen Department of Physiology, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands

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B T P Hijmans-Kersten Department of Physiology, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands

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M G Netea Division of Experimental Internal Medicine, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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J W A Smit Division of Endocrinology, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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D H J Thijssen Department of Physiology, Radboud Institute for Health Sciences, Radboud University Medical Center, Nijmegen, The Netherlands
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK

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A R M M Hermus Division of Endocrinology, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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N P Riksen Division of Vascular Medicine, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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R T Netea-Maier Division of Endocrinology, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands

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Objective

Acromegaly is characterized by an excess of growth hormone (GH) and insulin-like growth factor 1 (IGF1). Cardiovascular disease (CVD) risk factors are common in acromegaly and often persist after treatment. Both acute and long-lasting pro-inflammatory effects have been attributed to IGF1. Therefore, we hypothesized that inflammation persists in treated acromegaly and may contribute to CVD risk.

Methods

In this cross-sectional study, we assessed cardiovascular structure and function, and inflammatory parameters in treated acromegaly patients. Immune cell populations and inflammatory markers were assessed in peripheral blood from 71 treated acromegaly patients (with controlled or uncontrolled disease) and 41 matched controls. Whole blood (WB) was stimulated with Toll-like receptor ligands. In a subgroup of 21 controls and 33 patients with controlled disease, vascular ultrasound measurements were performed.

Results

Leukocyte counts were lower in patients with controlled acromegaly compared to patients with uncontrolled acromegaly and controls. Circulating IL18 concentrations were lower in patients; concentrations of other inflammatory mediators were comparable with controls. In stimulated WB, cytokine production was skewed toward inflammation in patients, most pronounced in those with uncontrolled disease. Vascular measurements in controlled patients showed endothelial dysfunction as indicated by a lower flow-mediated dilatation/nitroglycerine-mediated dilatation ratio. Surprisingly, pulse wave analysis and pulse wave velocity, both markers of endothelial dysfunction, were lower in patients, whereas intima-media thickness did not differ.

Conclusions

Despite treatment, acromegaly patients display persistent inflammatory changes and endothelial dysfunction, which may contribute to CVD risk and development of CVD.

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