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Reshma Aziz Merchant Division of Geriatric Medicine, Department of Medicine, National University Hospital, Singapore, Singapore
Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Michael Wong Wai Kit Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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Jia Yi Lim Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore

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John E Morley Division of Geriatric Medicine, Saint Louis University School of Medicine, St Louis, Missouri, USA

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Objective

To investigate the association of normal BMI with central obesity (CO), high BMI with CO, high BMI without CO, and normal BMI without CO, with function and cognition in older adults.

Methods

Cross-sectional study involving 754 participants ≥ 65 years. Data collected include demographics, cognition, and physical measurements.

Results

Females had a higher prevalence of high BMI with CO and a lower prevalence of high BMI without CO than males (61.0% vs 44.6% and 4.6% vs 15.0%, respectively). Within gender, CO groups, regardless of BMI, had lower mini-mental state examination (MMSE), handgrip strength (HGS), and longer timed-up-and-go (TUG) scores. Overall, the high BMI without CO group had the highest MMSE scores, HGS, and shortest TUG. Amongst males, HGS was significantly lower in the normal BMI with CO group (B −3.28, 95% CI −6.32 to −0.23, P = 0.04). CO, regardless of normal/high BMI, had significantly longer TUG time (B 2.65, 95% CI 0.45 to 4.84, P = 0.02; B 1.07, 95% CI 0.25 to 1.88, P = 0.01, respectively) than normal BMI without CO group. CO was associated with lower MMSE scores in both genders but significant only in males with normal BMI and CO (B −1.60, 95% CI −3.15 to −0.06, P = 0.04).

Conclusion

CO may be a better predictor of obesity and adverse outcomes in older adults. High BMI without CO was associated with better outcomes especially in males but require further validation. Prospective longitudinal studies are needed to ascertain the impact of BMI and/or CO on function, cognition, mortality, and gender differences.

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Sophie van Rijn Clinical Neurodevelopmental Sciences, Leiden University, Wassenaarseweg, Leiden, The Netherlands
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Leiden Institute for Brain and Cognition, Leiden University, Wassenaarseweg, Leiden, The Netherlands

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Kimberly Kuiper Clinical Neurodevelopmental Sciences, Leiden University, Wassenaarseweg, Leiden, The Netherlands
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Leiden Institute for Brain and Cognition, Leiden University, Wassenaarseweg, Leiden, The Netherlands

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Nienke Bouw Clinical Neurodevelopmental Sciences, Leiden University, Wassenaarseweg, Leiden, The Netherlands
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Department of Child and Adolescent Psychiatry/Psychology, Erasmus MC, Sophia Children’s Hospital, Dr. Molewaterplein, Rotterdam, The Netherlands

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Evelien Urbanus Clinical Neurodevelopmental Sciences, Leiden University, Wassenaarseweg, Leiden, The Netherlands
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Department of Clinical, Neuro, and Developmental Psychology, Vrije Universiteit Amsterdam, Van der Boechorststraat, Amsterdam, The Netherlands

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Hanna Swaab Clinical Neurodevelopmental Sciences, Leiden University, Wassenaarseweg, Leiden, The Netherlands
TRIXY Center of Expertise, Leiden University Treatment and Expertise Centre (LUBEC), Sandifortdreef, Leiden, The Netherlands
Leiden Institute for Brain and Cognition, Leiden University, Wassenaarseweg, Leiden, The Netherlands

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Investigating sex chromosome trisomies (SCTs) may help in understanding neurodevelopmental pathways underlying the risk for neurobehavioral problems and psychopathology. Knowledge about the neurobehavioral phenotype is needed to improve clinical care and early intervention for children with SCT. This is especially relevant considering the increasing number of early diagnosed children with the recent introduction of noninvasive prenatal screening. The TRIXY Early Childhood Study is a longitudinal study designed to identify early neurodevelopmental risks in children with SCT, aged 1–7 years. This review summarizes the results from the TRIXY Early Childhood Study, focusing on early behavioral symptoms in areas of autism spectrum disorder, attention-deficit hyperactivity disorder, and communication disorders, and underlying neurocognitive mechanisms in domains of language, emotion regulation, executive functioning, and social cognition. Behavioral symptoms were assessed through structured behavior observation and parental questionnaires. Neurocognition was measured using performance tests, eyetracking, and psychophysiological measures of arousal. In total, 209 children aged 1–7 years were included: 107 children with SCT (33 XXX, 50 XXY, and 24 XYY) and 102 age-matched population controls. Study outcomes showed early behavioral symptoms in young children with SCT, and neurocognitive vulnerabilities, already from an early age onward. Neurobehavioral and neurocognitive difficulties tended to become more pronounced with increasing age and were rather robust, independent of specific karyotype, pre/postnatal diagnosis, or ascertainment strategy. A more longitudinal perspective on neurodevelopmental ‘at-risk’ pathways is warranted, also including studies assessing the effectiveness of targeted early interventions. Neurocognitive markers that signal differences in neurodevelopment may prove to be helpful in this. Focusing on early development of language, social cognition, emotion regulation, and executive functioning may help in uncovering early essential mechanisms of (later) neurobehavioral outcome, allowing for more targeted support and early intervention.

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Izabelle Lövgren Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK

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Azadeh Abravan Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK
Radiotherapy Related Research, The Christie NHS Foundation Trust, Manchester, UK

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Abigail Bryce-Atkinson Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK

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Marcel van Herk Division of Cancer Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, The University of Manchester, Manchester, UK
Radiotherapy Related Research, The Christie NHS Foundation Trust, Manchester, UK

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Brain tumours make up nearly one-third of paediatric malignancies. Over time, advancements in oncological treatments like radiotherapy have helped reduce normal-tissue toxicity when treating cancers in the brain. However, clinicians are still facing a trade-off between treatment efficacy and potential side effects. The aim of this review is to address the late effects of cranial irradiation on the neuroendocrine system and to identify factors that make patients more vulnerable to radiation-induced endocrine sequelae. Radiation damage to the hypothalamic–pituitary axis, which orchestrates hormone release, can lead to endocrinopathy; up to 48.8% of children who have undergone cranial irradiation develop a hormone deficiency. This may lead to further health complications that can appear up to decades after the last treatment, lowering the patients’ quality of life and increasing long-term costs as lifelong hormone replacement therapy may be required. Growth hormone deficiency is the most common sequelae, followed by either thyroid or gonadotropic hormone deficiency. Adrenocorticotropic hormone deficiency tends to be the least common. Identified factors that increase the risk of late endocrine deficiency include total radiation dose, age at treatment, and time since last treatment. However, as there are various other factors that may potentiate the damage, a universal solution proven to be most effective in sparing the endocrine tissues is yet to be identified. Until then, accounting for the identified risk factors during treatment planning may in some cases help reduce the development of endocrine sequelae in childhood cancer survivors.

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J Gebauer Department of Internal Medicine I, University Hospital of Schleswig-Holstein, Campus Luebeck and Institute for Endocrinology and Diabetes, University of Luebeck, Luebeck, Germany

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R Skinner Department of Paediatric and Adolescent Haematology and Oncology and Children’s BMT Unit, Great North Children’s Hospital, Newcastle upon Tyne Hospitals NHS Foundation Trust, and Translational and Clinical Research Institute, Newcastle University Centre for Cancer, Newcastle University, Newcastle upon Tyne, UK

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R Haupt DOPO Clinic, Department of Hematology/Oncolgy, IRCCS Istituto Giannina Gaslini, Genova, Italy

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L Kremer Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands
Amsterdam UMC, Emma’s Children’s Hospital, Amsterdam, The Netherlands

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H van der Pal Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands

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G Michel Department of Health Sciences and Medicine, University of Lucerne, Luzern, Switzerland

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G T Armstrong Department of Epidemiology and Cancer Control, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA

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M M Hudson Department of Oncology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA

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L Hjorth Department of Clinical Sciences Lund, Paediatrics, Lund University, Skane University Hospital, Lund, Sweden

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H Lehnert Paris Lodron University of Salzburg, Salzburg, Austria

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T Langer Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, Campus Luebeck, Luebeck, Germany

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Many long-term childhood cancer survivors suffer from treatment-related late effects, which may occur in any organ and include a wide spectrum of conditions. Long-term follow-up (LTFU) is recommended to facilitate early diagnosis and to ensure better health outcomes. Due to the heterogeneity of these sequelae, different specialists work together in the diagnosis and treatment of these conditions. Experts from both pediatric and internal medicine are involved in age-appropriate care by providing a transition process. Hence, LTFU of childhood cancer survivors is a prototypic example of multidisciplinary care for patients with complex needs treated in a specialized setting. International collaborations of healthcare professionals and scientists involved in LTFU of childhood cancer survivors, such as the International Guideline Harmonization Group, compile surveillance recommendations that can be clinically adopted all over the world. These global networks of clinicians and researchers make a joint effort to address gaps in knowledge, increase visibility and awareness of cancer survivorship and provide an excellent example of how progress in clinical care and scientific research may be achieved by international and multidisciplinary collaboration.

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Patricia Iozzo Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy

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Maria Angela Guzzardi Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy

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The prevalence of obesity has reached epidemic proportions and keeps growing. Obesity seems implicated in the pathogenesis of cognitive dysfunction, Alzheimer’s disease and dementia, and vice versa. Growing scientific efforts are being devoted to the identification of central mechanisms underlying the frequent association between obesity and cognitive dysfunction. Glucose brain handling undergoes dynamic changes during the life-course, suggesting that its alterations might precede and contribute to degenerative changes or signaling abnormalities. Imaging of the glucose analog 18F-labeled fluorodeoxyglucose (18FDG) by positron emission tomography (PET) is the gold-standard for the assessment of cerebral glucose metabolism in vivo. This review summarizes the current literature addressing brain glucose uptake measured by PET imaging, and the effect of insulin on brain metabolism, trying to embrace a life-course vision in the identification of patterns that may explain (and contribute to) the frequent association between obesity and cognitive dysfunction. The current evidence supports that brain hypermetabolism and brain insulin resistance occur in selected high-risk conditions as a transient phenomenon, eventually evolving toward normal or low values during life or disease progression. Associative studies suggest that brain hypermetabolism predicts low BDNF levels, hepatic and whole body insulin resistance, food desire and an unfavorable balance between anticipated reward from food and cognitive inhibitory control. Emerging mechanistic links involve the microbiota and the metabolome, which correlate with brain metabolism and cognition, deserving attention as potential future prevention targets.

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Richard H Tuligenga INSERM U1018, Université Paris Sud, Centre for Research in Epidemiology and Population Health, Hôpital Paul Brousse, Bât 15/16, 16 Avenue Paul Vaillant Couturier, 94807 Paris, Villejuif Cedex, France
INSERM U1018, Université Paris Sud, Centre for Research in Epidemiology and Population Health, Hôpital Paul Brousse, Bât 15/16, 16 Avenue Paul Vaillant Couturier, 94807 Paris, Villejuif Cedex, France

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The aim of this meta-analysis was to compare the effect of intensive vs standard glycaemic control on cognitive decline in type 2 diabetic patients. A systematic search of PubMed and ALOIS was conducted from inception up to October 30, 2014. Randomised controlled trials (RCTs) of type 2 diabetic patients comparing the rate of change in cognitive function among participants assigned to intensive vs standard glycaemic control were included. An inverse-variance-weighted random effects model was used to calculate standardised mean differences (SMDs) and 95% CIs. A total of 24 297 patients from five RCTs were included in the meta-analysis. Follow-up ranged from 3.3 to 6.2 years. The result from the pooled analysis showed that intensive glycaemic control was not associated with a slower rate of cognitive decline in patients with type 2 diabetes, compared with standard glycaemic control (SMD=0.02; 95% CI=−0.03 to 0.08) although there was some heterogeneity across individual studies (I 2=68%, P for heterogeneity=0.01). There are few diabetes control trials including cognitive endpoints and a small number of trials comparing intensive and standard treatment strategies. Currently, intensive glycaemic control should not be recommended for prevention of cognitive decline in patients with type 2 diabetes because there is no evidence of its effectiveness. Moreover, the use of intensive diabetes treatment results in an increase of risk of hypoglycaemia, which is linked to a greater risk of poor cognition.

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Ru-Xuan Zhao Department of Endocrinology, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Ting-Ting Shi Department of Endocrinology, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Sha Luo Department of Nuclear Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Yun-Fu Liu Department of Radiology, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Zhong Xin Department of Endocrinology, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Jin-Kui Yang Department of Endocrinology, Beijing Diabetes Institute, Beijing Tongren Hospital, Capital Medical University, Beijing, China

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Background

Graves’ orbitopathy (GO) is an autoimmune disease with mechanical impairment of orbital muscles and lacrimal gland dysfunction. The frequently used methods of assessing GO activity include Clinical Activity Score (CAS), CT, and MRI. These approaches are mainly associated with orbital muscles; however, there are not many studies that focus on the lacrimal gland inflammation of GO patients.

Objective

The aim of this study is to assess the usefulness of 99mTc-DTPA single-photon emission (SPE) CT/CT in evaluating the lacrimal gland inflammation in GO, as compared with other methods.

Methods

A retrospective analysis of 48 patients with active GO compared with 33 controls was conducted. All subjects underwent clinical–endocrinological analyses, CAS evaluation, CT scans, and SPECT/CT examination. Lacrimal gland dimensions were determined and analyzed.

Results

The lacrimal glands in patients with GO were significantly larger in all measured dimensions (P  < 0.001) on CT scans relative to those in controls. Increased lacrimal gland diethylene triamine pentaacetic acid (DTPA) uptake ratios (P  < 0.001) were displayed in active GO patients compared to controls and were also correlated with thyrotropin receptor antibody levels. The cut-off value for discriminating active and inactive disease was calculated to be 1.735, with specificity of 82.6% and sensitivity of 74.2%. SPECT/CT uptake ratios and CAS values were positively correlated in all GO patients. SPECT/CT uptake ratios were also positively correlated with CT measurements including lacrimal gland volume and coronal width in GO patients.

Conclusions

These data indicated that lacrimal gland SPECT/CT images can serve as a good tool for assessing the inflammation and disease activity of GO.

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Maria Stelmachowska-Banaś Department of Endocrinology, The Centre of Postgraduate Medical Education, Warsaw, Polska, Poland

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Izabella Czajka-Oraniec Department of Endocrinology, The Centre of Postgraduate Medical Education, Warsaw, Polska, Poland

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Immune checkpoint inhibitors (ICIs) belong to a new group of anticancer drugs targeting T-cell proteins involved in the activation of immune response toward malignancies. Their introduction into clinical practice was a milestone in modern cancer treatment. However, the significant advantage of ICIs over conventional chemotherapy in terms of therapeutic efficacy is accompanied by new challenges related to specific side effects. ICI-induced immune system activation could lead to the loss of self-tolerance, presenting as autoimmune inflammation and dysfunction of various tissues and organs. Thus, the typical side effects of ICIs include immune-related adverse events (irAEs), among which endocrine irAEs, affecting numerous endocrine glands, have been commonly recognized. This review aimed to outline the current knowledge regarding ICI-induced endocrine disorders from a clinical perspective. We present updated information on the incidence and clinical development of ICI-induced endocrinopathies, including the most frequent thyroiditis and hypophysitis, the rarely observed insulin-dependent diabetes mellitus and primary adrenal insufficiency, and the recently described cases of hypoparathyroidism and lipodystrophy. Practical guidelines for monitoring, diagnosis, and treatment of ICI-related endocrine toxicities are also offered. Rising awareness of endocrine irAEs among oncologists, endocrinologists, and other health professionals caring for patients receiving ICIs could contribute to better safety and efficacy. As immunotherapy becomes widespread and approved for new types of malignancies, increased incidences of endocrine irAEs are expected in the future.

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A Rouland Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France

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J-C Chauvet-Gelinier Psychiatry Unit, Department of Neurosciences, Dijon University Hospital, Dijon, France
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France

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A-L Sberna Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France

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E Crevisy Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France

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P Buffier Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France

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T Mouillot Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France

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J-M Petit Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France

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B Vergès Endocrinology Diabetics and Metabolic Disorders Department, Dijon University Hospital, Dijon, France
INSERM Unit, LNC-UMR 1231, University of Burgundy, Dijon, France

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Objective

The Type A personality, characterized by impatience, strong career ambition and competitiveness, is associated with greater sensitivity to external stress. Type 1 diabetes (T1D) is an auto-immune disease, which is potentially influenced by stress, unlike type 2 diabetes (T2D). The aim of this study was to assess whether individuals with T1D and T2D exhibited significant differences on the Type A personality scale. We also assessed personality in patients with thyroid auto-immune diseases to validate potential links between auto-immune disease and Type A personality.

Design and methods

The Bortner questionnaire was used to assess Type A personality in 188 patients with T1D, 430 patients with T2D and 85 patients with auto-immune thyroid disease (Graves’ disease or Hashimoto’s thyroiditis).

Results

Type A Bortner scores were significantly higher in T1D patients than in T2D patients (188 ± 34 vs 177 ± 36, P < 0.0001). Patients with auto-immune thyroid diseases and T1D patients had similar Type A Bortner scores (189 ± 33 vs 188 ± 34, P = 0.860).

Conclusion

Patients with auto-immune T1D have higher Type A scores than T2D patients. Furthermore, patients with auto-immune thyroid disease also have elevated Type A scores similar to those observed in type 1 diabetes, suggesting that an elevated Type A score in T1D is potentially related to its auto-immune origin. This suggests a possible link between Type A personality and auto-immune diseases via stress-triggering psychobiological pathways. The different personality score between T1D and T2D is an important factor, which could influence self-care coping strategies in diabetes and long-term prognosis.

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Justyna Modrzynska Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Christine F Klein Department of Cardiology, Herlev Gentofte Hospital, Herlev, Denmark

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Kasper Iversen Department of Clinical Medicine, Herlev Gentofte Hospital, Herlev, Denmark

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Henning Bundgaard Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Bolette Hartmann Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Maike Mose Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark

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Nikolaj Rittig Steno Diabetes Center Aarhus, Aarhus University Hospital, Aarhus, Denmark

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Niels Møller Department of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark

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Jens J Holst Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Nicolai J Wewer Albrechtsen Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Objective

Glucagon and glucagon-like peptide-1 (GLP-1) originate from the common precursor, proglucagon, and their plasma concentrations have been reported to be increased during inflammatory conditions. Increased blood glucose levels are frequently observed in septic patients, and therefore we hypothesized that glucagon, but not GLP-1, is increased in individuals with inflammation.

Design

Prospective longitudinal cohort study.

Materials and methods

We measured glucagon and GLP-1 in plasma sampled consecutively in three cohorts consisting of patients with infective endocarditis (n = 16), urosepsis (n = 28) and post-operative inflammation following percutaneous aortic valve implantation or thoracic endovascular aortic repair (n = 5). Correlations between C-reactive protein (CRP), a marker of systemic inflammation, and glucagon and GLP-1 concentrations were investigated. Additionally, glucagon and GLP-1 concentrations were measured after a bolus infusion of lipopolysaccharide (LPS, 1 ng/kg) in nine healthy young males.

Results

Glucagon and CRP were positively and significantly correlated (r = 0.27; P = 0.0003), whereas no significant association between GLP-1 and CRP was found (r = 0.08, P = 0.30). LPS infusion resulted in acute systemic inflammation reflected by increased temperature, pulse, tumor necrosis factor-α (TNFα), interleukin-6 (IL-6) and concomitantly increased concentrations of glucagon (P < 0.05) but not GLP-1.

Conclusions

Systemic inflammation caused by bacterial infections or developed as a non-infected condition is associated with increased plasma concentration of glucagon, but not GLP-1. Hyperglucagonemia may contribute to the impaired glucose control in patients with systemic inflammatory diseases.

Open access