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Henrik H Thomsen Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Holger J Møller Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Christian Trolle Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Kristian A Groth Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Anne Skakkebæk Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Anders Bojesen Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Christian Høst Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Claus H Gravholt Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark
Medical Research Laboratories, Departments of Clinical Biochemistry, Molecular Medicine, Department of Clinical Genetics, Department of Endocrinology and Internal Medicine, Clinical Institute, Aarhus University Hospital, Nørrebrogade 44, DK-8000 Aarhus C, Denmark

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Soluble CD163 (sCD163) is a novel marker linked to states of low-grade inflammation such as diabetes, obesity, liver disease, and atherosclerosis, all prevalent in subjects with Turner syndrome (TS) and Klinefelter syndrome (KS). We aimed to assess the levels of sCD163 and the regulation of sCD163 in regards to treatment with sex hormone therapy in males with and without KS and females with and without TS. Males with KS (n=70) and age-matched controls (n=71) participating in a cross-sectional study and 12 healthy males from an experimental hypogonadism study. Females with TS (n=8) and healthy age-matched controls (n=8) participating in a randomized crossover trial. The intervention comprised of treatment with sex steroids. Males with KS had higher levels of sCD163 compared with controls (1.75 (0.47–6.90) and 1.36 (0.77–3.11) respectively, P<0.001) and the levels correlated to plasma testosterone (r=−0.31, P<0.01), BMI (r=0.42, P<0.001), and homeostasis model of assessment insulin resistance (r=0.46, P<0.001). Treatment with testosterone did not significantly lower sCD163. Females with TS not receiving hormone replacement therapy (HRT) had higher levels of sCD163 than those of their age-matched healthy controls (1.38±0.44 vs 0.91±0.40, P=0.04). HRT and oral contraceptive therapy decreased sCD163 in TS by 22% (1.07±0.30) and in controls by 39% (0.55±0.36), with significance in both groups (P=0.01 and P=0.04). We conclude that levels of sCD163 correlate with endogenous testosterone in KS and are higher in KS subjects compared with controls, but treatment did not significantly lower levels. Both endogenous and exogenous estradiol in TS was associated with lower levels of sCD163.

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Ghazala Zaidi Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Vijayalakshmi Bhatia Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Saroj K Sahoo Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Aditya Narayan Sarangi Departments of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Niharika Bharti Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Li Zhang Department of Immunology, Barbara Davis Centre for Childhood Diabetes, Denver, USA

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Liping Yu Department of Immunology, Barbara Davis Centre for Childhood Diabetes, Denver, USA

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Daniel Eriksson Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden

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Sophie Bensing Department of Molecular Medicine and Surgery, Karolinska Institutet, and Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden

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Olle Kämpe Department of Medicine (Solna), Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
Science for Life Laboratory, Department of Medical Sciences, Uppsala University, Sweden

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Nisha Bharani Department of Endocrinology, Amrita Institute of Medical Sciences, Kochi, India

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Surendra Kumar Yachha Departments of Paediatric Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Anil Bhansali Department of Endocrinology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

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Alok Sachan Department of Endocrinology, Sri Venkateshwara Institute of Medical Sciences, Tirupathi, India

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Vandana Jain Department of Paediatrics, All India Institute of Medical Sciences, New Delhi, India

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Nalini Shah Department of Endocrinology, King Edward Memorial Hospital, Seth GS Medical College, Mumbai, India

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Rakesh Aggarwal Departments of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Amita Aggarwal Departments of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Muthuswamy Srinivasan Departments of Medical Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Sarita Agarwal Departments of Medical Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Eesh Bhatia Departments of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

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Objective

Autoimmune polyendocrine syndrome type 1 (APS1) is a rare autosomal recessive disorder characterized by progressive organ-specific autoimmunity. There is scant information on APS1 in ethnic groups other than European Caucasians. We studied clinical aspects and autoimmune regulator (AIRE) gene mutations in a cohort of Indian APS1 patients.

Design

Twenty-three patients (19 families) from six referral centres in India, diagnosed between 1996 and 2016, were followed for [median (range)] 4 (0.2–19) years.

Methods

Clinical features, mortality, organ-specific autoantibodies and AIRE gene mutations were studied.

Results

Patients varied widely in their age of presentation [3.5 (0.1–17) years] and number of clinical manifestations [5 (2–11)]. Despite genetic heterogeneity, the frequencies of the major APS1 components (mucocutaneous candidiasis: 96%; hypoparathyroidism: 91%; primary adrenal insufficiency: 55%) were similar to reports in European series. In contrast, primary hypothyroidism (23%) occurred more frequently and at an early age, while kerato-conjunctivitis, urticarial rash and autoimmune hepatitis were uncommon (9% each). Six (26%) patients died at a young age [5.8 (3–23) years] due to septicaemia, hepatic failure and adrenal/hypocalcaemic crisis from non-compliance/unexplained cause. Interferon-α and/or interleukin-22 antibodies were elevated in all 19 patients tested, including an asymptomatic infant. Eleven AIRE mutations were detected, the most common being p.C322fsX372 (haplotype frequency 37%). Four mutations were novel, while six others were previously described in European Caucasians.

Conclusions

Indian APS1 patients exhibited considerable genetic heterogeneity and had highly variable clinical features. While the frequency of major manifestations was similar to that of European Caucasians, other features showed significant differences. A high mortality at a young age was observed.

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Fahim Ebrahimi Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, University of Basel Hospital, Basel, Switzerland
Department of Clinical Research, University of Basel Hospital, Basel, Switzerland

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Sandrine A Urwyler Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, University of Basel Hospital, Basel, Switzerland
Department of Clinical Research, University of Basel Hospital, Basel, Switzerland

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Philipp Schuetz Department of Clinical Research, University of Basel Hospital, Basel, Switzerland
Division of Endocrinology, Diabetes and Metabolism, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland

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Beat Mueller Department of Clinical Research, University of Basel Hospital, Basel, Switzerland
Division of Endocrinology, Diabetes and Metabolism, University Department of Medicine, Kantonsspital Aarau, Aarau, Switzerland

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Luca Bernasconi Department of Laboratory Medicine, Kantonsspital Aarau, Aarau, Switzerland

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Peter Neyer Department of Laboratory Medicine, Kantonsspital Aarau, Aarau, Switzerland

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Marc Y Donath Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, University of Basel Hospital, Basel, Switzerland
Department of Clinical Research, University of Basel Hospital, Basel, Switzerland

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Mirjam Christ-Crain Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, University of Basel Hospital, Basel, Switzerland
Department of Clinical Research, University of Basel Hospital, Basel, Switzerland

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Background

Anti-inflammatory treatment with interleukin-1 (IL-1) antagonism decreases both cortisol and adrenocorticotropin hormone (ACTH) levels in individuals with obesity in short term. However, it remains unknown whether these effects persist upon prolonged treatment.

Methods

In this double-blind, parallel-group trial involving patients with features of the metabolic syndrome, 33 patients were randomly assigned to receive 100 mg of anakinra (recombinant human IL-1 receptor antagonist) subcutaneously twice-daily and 34 patients to receive placebo for 4 weeks. For this analysis, change in cortisol and ACTH levels from baseline to 4 weeks were predefined end points of the trial.

Results

The mean age was 54 years, baseline cortisol levels were 314 nmol/L (IQR 241–385) and C-reactive protein (CRP) levels were 3.4 mg/L (IQR 1.7–4.8). Treatment with anakinra led to a significant decrease in cortisol levels at day 1 when compared to placebo with an adjusted between-group difference of 28 nmol/L (95% CI, −7 to −43; P = 0.03). After 4 weeks, the cortisol-lowering effect of anakinra was attenuated and overall was statistically not significant (P = 0.72). Injection-site reactions occurred in 21 patients receiving anakinra and were associated with higher CRP and cortisol levels.

Conclusions

IL-1 antagonism decreases cortisol levels in male patients with obesity and chronic low-grade inflammation on the short term. After prolonged treatment, this effect is attenuated, probably due to injection-site reactions (ClinicalTrials.gov, NCT02672592).

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Angela Köninger
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Philippos Edimiris
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Laura Koch
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Antje Enekwe
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Claudia Lamina Department of Gynecology and Obstetrics, Division of Genetic Epidemiology, Vitateq Biotechnology GmbH, University of Duisburg-Essen, D-45122 Essen, Germany

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Sabine Kasimir-Bauer
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Rainer Kimmig
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Hans Dieplinger Department of Gynecology and Obstetrics, Division of Genetic Epidemiology, Vitateq Biotechnology GmbH, University of Duisburg-Essen, D-45122 Essen, Germany
Department of Gynecology and Obstetrics, Division of Genetic Epidemiology, Vitateq Biotechnology GmbH, University of Duisburg-Essen, D-45122 Essen, Germany

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Oxidative stress seems to be present in patients with polycystic ovary syndrome (PCOS). The aim of this study was to evaluate the correlation between characteristics of PCOS and serum concentrations of afamin, a novel binding protein for the antioxidant vitamin E. A total of 85 patients with PCOS and 76 control subjects were investigated in a pilot cross-sectional study design between 2009 and 2013 in the University Hospital of Essen, Germany. Patients with PCOS were diagnosed according to the Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group. Afamin and diagnostic parameters of PCOS were determined at early follicular phase. Afamin concentrations were significantly higher in patients with PCOS than in controls (odds ratio (OR) for a 10 mg/ml increase in afamin=1.3, 95% CI=1.08–1.58). This difference vanished in a model adjusting for age, BMI, free testosterone index (FTI), and sex hormone-binding globulin (SHBG) (OR=1.05, 95% CI=0.80–1.38). In patients with PCOS, afamin correlated significantly with homeostatic model assessment-insulin resistance (HOMA-IR), fasting glucose, BMI, FTI, and SHBG (P<0.001), but in a multivariate linear model, only HOMA-IR remained significantly associated with afamin (P=0.001). No correlation was observed between afamin and androgens, LH, FSH, LH/FSH ratio, antral follicle count, ovarian volume, or anti-Müllerian hormone. In conclusion, elevated afamin values may indicate a state of oxidative stress and inflammation, strongly associated with IR and offering an indicator of impaired glucose tolerance in patients with PCOS irrespective of obesity.

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Mengxue Yang Department of Endocrinology, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai, China
Department of Endocrinology, Zunyi Medical University, Zunyi, China

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Bowen Sun Department of Endocrinology, Zunyi Medical University, Zunyi, China

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Jianhui Li Department of Endocrinology, Ningbo No. 2 Hospital, Ningbo, China

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Bo Yang Department of Endocrinology, Zunyi Medical University, Zunyi, China

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Jie Xu School of Public Health, Zunyi Medical University, Zunyi, China

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Xue Zhou Department of Endocrinology, Zunyi Medical University, Zunyi, China

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Jie Yu School of Public Health, Zunyi Medical University, Zunyi, China

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Xuan Zhang Department of Endocrinology, Zunyi Medical University, Zunyi, China

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Qun Zhang Department of Endocrinology, Ningbo No. 2 Hospital, Ningbo, China

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Shan Zhou Department of Endocrinology, Ningbo No. 2 Hospital, Ningbo, China

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Xiaohua Sun Department of Endocrinology, Ningbo No. 2 Hospital, Ningbo, China

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Objectives

The pathogenesis of Graves’ disease (GD) remains unclear. In terms of environmental factors, GD development may be associated with chronic inflammation caused by alteration of the intestinal flora. This study explored the association of intestinal flora alteration with the development of GD among the Han population in southwest China.

Design and methods

Fifteen GD patients at the Affiliated Hospital of Zunyi Medical College between March 2016 and March 2017 were randomly enrolled. Additionally, 15 sex- and age-matched healthy volunteers were selected as the control group during the same period. Fresh stool samples were collected, and bacterial 16S RNA was extracted and amplified for gene sequencing with the Illumina MiSeq platform. The sequencing results were subjected to operational taxonomic unit-based classification, classification verification, alpha diversity analysis, taxonomic composition analysis and partial least squares-discriminant analysis (PLS-DA).

Results

The diversity indices for the GD group were lower than those for the control group. The GD group showed significantly higher abundances of Firmicutes, Proteobacteria and Actinobacillus and a higher Firmicutes/Bacteroidetes ratio than the control group. PLS-DA suggested the satisfactory classification of the flora between the GD group and the control group. The abundances of the genera Oribacterium, Mogibacterium, Lactobacillus, Aggregatibacter and Mogibacterium were significantly higher in the GD group than in the control group (P < 0.05).

Conclusions

The intestinal flora of GD patients was significantly different from that of the healthy population. Thus, alteration of intestinal flora may be associated with the development of GD.

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Ermina Bach Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark

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Niels Møller Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark

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Jens Otto L Jørgensen Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark

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Mads Buhl The Neonatal Intensive Care Unit, Aarhus University Hospital, Aarhus, Denmark

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Holger Jon Møller Department of Clinical Biochemistry, Aarhus University Hospital, Aarhus, Denmark

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Aims/hypothesis

The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low-grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as a result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aim of this study was to investigate if low-grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner.

Methods

We studied eight male hypopituitary patients and eight age- and gender-matched healthy controls during intravenous low-dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360-min infusion with saline and low-dose LPS in each leg respectively.

Results:

Systemic low-grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65 ± 0.51 mg/L (placebo) to 1.92 ± 0.46 mg/L (LPS) at 220 min, P = 0.005 and from 1.66 ± 0.42 mg/L (placebo) to 2.19 ± 0.56 mg/L (LPS) at 340 min, P = 0.006. A very similar response was observed in hypopituitary patients: from 1.59 ± 0.53 mg/L (placebo) to 1.83 ± 0.45 mg/L (LPS) at 220 min, P = 0.021 and from 1.52 ± 0.53 mg/L (placebo) to 2.03 ± 0.44 mg/L (LPS) at 340 min, P < 0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163.

Conclusion:

Systemic low-grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.

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Amar Osmancevic School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Kristin Ottarsdottir School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Margareta Hellgren School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Ulf Lindblad School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Bledar Daka School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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Context

Obesity seems to decrease levels of testosterone. It is still unknown what role inflammation plays in the secretion of testosterone in men.

Objective

The objective is to study the association between levels of C-reactive protein and testosterone and its role in predicting biochemical hypogonadism in men.

Design

This was a longitudinal observational study between 2002 and 2014 in Sweden.

Patients or other participants

At the first visit, a random population sample of 1400 men was included, and 645 men fulfilled a similar protocol at a 10-year follow-up visit. After exclusion, 625 men remained to be included in the final analyses.

Main outcome measure(s)

Serum concentrations of testosterone and C-reactive protein (CRP) were measured at both visits. Bioavailable testosterone was calculated. Biochemical hypogonadism was defined as total testosterone levels <8 nmol/L.

Results

At the first visit and in the longitudinal analyses, a strong association was found between high levels of CRP and low levels of calculated bioavailable testosterone even after adjustments for age, waist–hip ratio, hypertension, smoking, type 2 diabetes, and leisuretime physical activity (B = −0.31, 95% CI −0.49 to −0.13, P = 0.001, B = −0.26, 95% CI −0.41 to −0.11, P = 0.001). Similarly, increase with one s. d. in CRP was associated with increased risk of having hypogonadism after adjustment in the final model (odds ratio (OR) 1.76, 95% CI 1.12–2.78, P = 0.015, OR 1.80, 95% CI 1.16–2.78, P =0.008).

Conclusions

In this representative cohort of men in southwestern Sweden, high levels of CRP were longitudinally associated with low concentrations of calculated bioavailable testosterone and increased risk of biochemical hypogonadism.

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Jiaxin Zhang Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Jinlan Jiang Wenzhou Institute, University of Chinese Academy of Sciences, Wenzhou, Zhejiang, China

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Yao Qin School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China

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Yihui Zhang Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Yungang Wu Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Huadong Xu School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China

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Purpose

This study aims to investigate the associations of the systemic immune-inflammation index (SII) with bone mineral density (BMD) and osteoporosis in adult females from a nationally representative sample.

Methods

A cross-sectional study was performed among 4092 females aged ≥20 years from the National Health and Nutrition Examination Survey 2007–2010. Linear and logistic regressions were applied to explore the relationships of SII with BMD and the risk of osteoporosis, respectively.

Results

Linear regression analyses found that a doubling of SII levels was significantly correlated with a 1.39% (95% CI: 0.57%, 2.20%) decrease in total femur BMD, a 1.16% (95% CI: 0.31%, 2.00%) decrease in femur neck BMD, a 1.73% (95% CI: 0.78%, 2.66%) decrease in trochanter BMD, and a 1.35% (95% CI: 0.50%, 2.20%) decrease in intertrochanteric BMD among postmenopausal women, after adjusting for covariates. Logistic regression analyses showed that compared with postmenopausal women in the lowest SII quartile, those in the highest quartile had higher risks of osteoporosis in the total femur (odds ratio (OR) = 1.70, 95% CI: 1.04, 2.76), trochanter (OR = 1.86, 95% CI: 1.07, 3.38), intertrochanter (OR = 2.01, 95% CI: 1.05, 4.04) as well as overall osteoporosis (OR = 1.57, 95% CI: 1.04, 2.37). In contrast, there was no significant association between SII and BMD in premenopausal women.

Conclusions

SII levels were negatively associated with BMD levels in postmenopausal women but not in premenopausal women. Elevated SII levels could be a potential risk factor for osteoporosis in postmenopausal women.

Open access
Clara Lundetoft Clausen Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital – Amager and Hvidovre, Hvidovre, Denmark
Department of Infectious Diseases, Copenhagen University Hospital – Amager and Hvidovre, Hvidovre, Denmark

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Trine Holm Johannsen Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

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Niels Erik Skakkebæk Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

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Hanne Frederiksen Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

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Camilla Koch Ryrsø Department of Pulmonary and Infectious Diseases, Copenhagen University Hospital – Nordsjælland, Hillerød, Denmark
Centre for Physical Activity Research, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

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Arnold Matovu Dungu Department of Pulmonary and Infectious Diseases, Copenhagen University Hospital – Nordsjælland, Hillerød, Denmark

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Maria Hein Hegelund Department of Pulmonary and Infectious Diseases, Copenhagen University Hospital – Nordsjælland, Hillerød, Denmark

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Daniel Faurholt-Jepsen Department of Infectious Diseases, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

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Rikke Krogh-Madsen Department of Infectious Diseases, Copenhagen University Hospital – Amager and Hvidovre, Hvidovre, Denmark
Centre for Physical Activity Research, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark

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Birgitte Lindegaard Department of Pulmonary and Infectious Diseases, Copenhagen University Hospital – Nordsjælland, Hillerød, Denmark
Centre for Physical Activity Research, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Allan Linneberg Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Center for Clinical Research and Prevention, Copenhagen University Hospital – Bispebjerg and Frederiksberg, Copenhagen, Denmark

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Line Lund Kårhus Center for Clinical Research and Prevention, Copenhagen University Hospital – Bispebjerg and Frederiksberg, Copenhagen, Denmark

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Anders Juul Department of Growth and Reproduction, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Thomas Benfield Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital – Amager and Hvidovre, Hvidovre, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Aim

To explore pituitary–gonadal hormone concentrations and assess their association with inflammation, severe respiratory failure, and mortality in hospitalized men and women with COVID-19, and compare these to hormone concentrations in hospitalized patients with bacterial community-acquired pneumonia (CAP) and influenza virus CAP and to concentrations in a reference group of healthy individuals.

Methods

Serum concentrations of testosterone, estrone sulfate, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and interleukin-6 (IL-6) were measured within 4 days of admission. Associations were assessed by logistic regression analysis in patients with COVID-19, and results were reported as odds ratio with 95% CI per two-fold reduction after adjustment for age, comorbidities, days to sample collection, and IL-6 concentrations.

Results

In total, 278 patients with COVID-19, 21 with influenza virus CAP, and 76 with bacterial CAP were included. Testosterone concentrations were suppressed in men hospitalized with COVID-19, bacterial and influenza virus CAP, and moderately suppressed in women. Reductions in testosterone (OR: 3.43 (1.14–10.30), P = 0.028) and LH (OR: 2.51 (1.28–4.92), P = 0.008) were associated with higher odds of mehanical ventilation (MV) in men with COVID-19. In women with COVID-19, reductions in LH (OR: 3.34 (1.02–10-90), P = 0.046) and FSH (OR: 2.52 (1.01–6.27), P = 0.047) were associated with higher odds of MV.

Conclusion

Low testosterone and LH concentrations were predictive of severe respiratory failure in men with COVID-19, whereas low concentrations of LH and FSH were predictive of severe respiratory failure in women with COVID-19.

Open access
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