Search Results
Search for other papers by T L C Wolters in
Google Scholar
PubMed
Division of Vascular Medicine, Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands
Search for other papers by C D C C van der Heijden in
Google Scholar
PubMed
Search for other papers by N van Leeuwen in
Google Scholar
PubMed
Search for other papers by B T P Hijmans-Kersten in
Google Scholar
PubMed
Search for other papers by M G Netea in
Google Scholar
PubMed
Search for other papers by J W A Smit in
Google Scholar
PubMed
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK
Search for other papers by D H J Thijssen in
Google Scholar
PubMed
Search for other papers by A R M M Hermus in
Google Scholar
PubMed
Search for other papers by N P Riksen in
Google Scholar
PubMed
Search for other papers by R T Netea-Maier in
Google Scholar
PubMed
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.
Search for other papers by Elizabeth J de Koster in
Google Scholar
PubMed
Division of Medical Oncology, Netherlands Cancer Institute, Amsterdam, The Netherlands
Division of Clinical Studies, Institute of Cancer Research, London, UK
Search for other papers by Olga Husson in
Google Scholar
PubMed
Search for other papers by Eveline W C M van Dam in
Google Scholar
PubMed
Search for other papers by G Sophie Mijnhout in
Google Scholar
PubMed
Search for other papers by Romana T Netea-Maier in
Google Scholar
PubMed
Department of Radiology and Nuclear Medicine, Rijnstate Hospital, Arnhem, The Netherlands
Department of Biomedical Sciences and Humanitas Clinical and Research Centre, Department of Nuclear Medicine, Humanitas University, Milan, Italy
Search for other papers by Wim J G Oyen in
Google Scholar
PubMed
Search for other papers by Marieke Snel in
Google Scholar
PubMed
Department of Radiology, Section of Nuclear Medicine, Leiden University Medical Center, Leiden, The Netherlands
Biomedical Photonic Imaging Group, University of Twente, Enschede, The Netherlands
Search for other papers by Lioe-Fee de Geus-Oei in
Google Scholar
PubMed
Search for other papers by Dennis Vriens in
Google Scholar
PubMed
Search for other papers by for the EfFECTS trial study group in
Google Scholar
PubMed
Objective
This study assessed the health-related quality of life (HRQoL) in patients undergoing 2-[18F]fluoro-2-deoxy-D-glucose (FDG)-PET/CT for an indeterminate (Bethesda III/IV) thyroid nodule. FDG-PET/CT accurately rules out malignancy and prevents 40% of futile diagnostic surgeries in these nodules.
Design
Secondary analyses of HRQoL data from a randomised controlled multicentre trial (NCT02208544) in 126 patients from 15 hospitals in the Netherlands were done.
Methods
Longitudinal HRQoL assessment was performed using the EuroQol 5-dimension 5-level (EQ-5D-5L), the RAND 36-item Health Survey v2.0 (RAND-36), and the Thyroid Patient-Reported Outcome (ThyPRO) questionnaire on baseline, 3, 6, and 12 months, relative to the date of the FDG-PET/CT scan.
Results
Patients who were randomised to active surveillance following an FDG-negative nodule instead of diagnostic surgery reported stable HRQoL scores throughout the year. Univariate analysis indicated better HRQoL for patients undergoing surveillance than surgical patients with benign histopathology on multiple physical and psychosocial domains. Univariate within-group analysis suggested both temporary and continued HRQoL deteriorations in patients with benign histopathology over time. Multivariate within-group analysis demonstrated no significant longitudinal HRQoL changes in patients undergoing active surveillance. In contrast, in patients with benign histopathology, worse HRQoL was observed with regard to ThyPRO cognitive impairment (P = 0.01) and cosmetic complaints (P = 0.02), whereas goitre symptoms (P < 0.001) and anxiety (P = 0.04) improved over time. In patients with malignant histopathology, anxiety also decreased (P = 0.05).
Conclusions
The reassurance of a negative FDG-PET/CT resulted in sustained HRQoL throughout the first year of active surveillance. Diagnostic surgery for a nodule with benign histopathology resulted in more cognitive impairment and physical problems including cosmetic complaints, but improved goitre symptoms and anxiety. Anxiety was also reduced in patients with malignant histopathology.
