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Eleftherios E Deiktakis Laboratory of Clinical Chemistry, School of Medicine, University of Crete, Heraklion, Greece

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Eleftheria Ieronymaki Laboratory of Clinical Chemistry, School of Medicine, University of Crete, Heraklion, Greece

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Peter Zarén Department of Translational Medicine, Lund University, Malmö, Sweden

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Agnes Hagsund Department of Translational Medicine, Lund University, Malmö, Sweden

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Elin Wirestrand Department of Translational Medicine, Lund University, Malmö, Sweden

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Johan Malm Department of Translational Medicine, Lund University, Malmö, Sweden

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Christos Tsatsanis Laboratory of Clinical Chemistry, School of Medicine, University of Crete, Heraklion, Greece

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Ilpo T Huhtaniemi Department of Translational Medicine, Lund University, Malmö, Sweden
Imperial College London, Institute of Reproductive and Developmental Biology, London, UK

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Aleksander Giwercman Department of Translational Medicine, Lund University, Malmö, Sweden
Malmö University Hospital, Reproductive Medicine Center, Malmö, Sweden

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Yvonne Lundberg Giwercman Department of Translational Medicine, Lund University, Malmö, Sweden

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Objective

During androgen ablation in prostate cancer by the standard gonadotropin-releasing hormone (GnRH) agonist treatment, only luteinizing hormone (LH) is permanently suppressed while circulating follicle-stimulating hormone (FSH) rebounds. We explored direct prostatic effects of add-back FSH, after androgen ablation with GnRH antagonist, permanently suppressing both gonadotropins.

Methods

The effects of recombinant human (rFSH) were examined in mice treated with vehicle (controls), GnRH antagonist degarelix (dgx), dgx + rFSH, dgx + flutamide, or dgx + rFSH + flutamide for 4 weeks. Prostates and testes size and expression of prostate-specific and/or androgen-responsive genes were measured. Additionally, 33 young men underwent dgx-treatment. Seventeen were supplemented with rFSH (weeks 1–5), and all with testosterone (weeks 4–5). Testosterone, gondotropins, prostate-specific antigen (PSA), and inhibin B were measured.

Results

In dgx and dgx + flutamide treated mice, prostate weight/body weight was 91% lower than in controls, but 41 and 11%, respectively, was regained by rFSH treatment (P = 0.02). The levels of seminal vesicle secretion 6, Pbsn, Nkx3.1, beta-microseminoprotein, and inhibin b were elevated in dgx + rFSH-treated animals compared with only dgx treated (all P < 0.05). In men, serum inhibin B rose after dgx treatment but was subsequently suppressed by testosterone. rFSH add-back had no effect on PSA levels.

Conclusions

These data provide novel evidence for the direct effects of FSH on prostate size and gene expression in chemically castrated mice. However, in chemically castrated men, FSH had no effect on PSA production. Whether FSH effects on the prostate in humans also require suppression of the residual adrenal-derived androgens and/or a longer period of rFSH stimulation, remains to be explored.

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Jiaxin Luo Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Weili Yin Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Qiuxia Lin The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong Province, China

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Juqing Wu Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Pan Chen Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Yuanna Ling Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Jing Wang Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Zhen Li Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Liqin Pan Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Yanying Chen Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Wei Ouyang Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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Huijuan Feng Department of Nuclear Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong Province, China

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To evaluate the locoregional progression-free survival (LPFS) of bone metastatic lesions from differentiated thyroid cancer (DTC) after radioiodine therapy (RAIT) and to define its influencing factors, we performed a retrospective cohort analysis of 89 patients with bone metastases from DTC who received RAIT in our department over a 17-year period. The median follow-up time was calculated using the reverse Kaplan–Meier method. The log-rank test and a multivariate Cox proportional hazards regression model were performed in the analysis of prognostic indicators for LPFS. In this research, the median follow-up time for all patients was 47 (95% CI, 35.752–58.248) months, and that for patients with no progression was 42 months. The longest follow-up time was 109 months. The median LPFS time was 58 (95% CI, 32.602–83.398) months, and the 3- and 5-year LPFS probabilities were 57.8 and 45.1%, respectively. Multivariate analysis revealed bone structural changes as an independent risk factor for LPFS (P= 0.004; hazard ratio, 49.216; 95% CI, 3.558–680.704). Furthermore, the non–total-lesion uptake subgroup presented a worse LPFS than the total-lesion uptake subgroup in patients with structural bone lesions (P = 0.027). RAIT can improve the LPFS of radioiodine-avid bone metastases from DTC, especially those without bone structural changes.

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Margarida Brito Department of Medical Oncology, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Susana Prazeres Department of Clinical Pathology, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Marta Malheiros Department of Clinical Pathology, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Background

Fulvestrant resembles estradiol in its structure. Reports have been published concerning fulvestrant measured as estradiol by the immunoassays. This may induce falsely elevated estradiol results and wrongly impact medical decisions. Our aim was to confirm the interference of fulvestrant on estradiol concentration and test a method to identify the false results.

Methods

Four serum samples with low estradiol levels were spiked with fulvestrant at various concentrations. Estradiol was then measured directly on serum (Dir), after a 1:5 dilution (Dil), and a ratio Dil/Dir was estimated. On the second part of the study, estradiol results (Dir, Dil and ratio Dil/Dir) from 14 women treated with fulvestrant were analysed, as well as from 14 patients not under this treatment.

Results

The addition of exogenous fulvestrant to the serum samples induced a gradual rise on estradiol concentration with a mean ratio for the Dil/Dir samples of 2.1 ± 0.4 (range 1.7–2.9). Patients on fulvestrant treatment experienced a mean ratio for the Dil/Dir estradiol sample of 2.4 ± 0.4 (range 1.6–3.0). In the control group, a mean estradiol ratio Dil/Dir of 1.1 ± 0.1 was observed (range 0.8–1.3). No correlation between the number of days after fulvestrant injection and estradiol result (r = 0.531) was observed.

Conclusion

Our study confirmed the interference of fulvestrant in the estradiol measurement by immunoassay. When fulvestrant was present, the estradiol ratio for Dil/Dir sample was about 2. In the control group, the ratio was around 1. The estradiol Dil/Dir ratio is a simple tool which can be used to identify fulvestrant false immunoassay estradiol results.

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Josephina G Kuiper PHARMO Institute for Drug Outcomes Research, AE Utrecht, Netherlands
Department of Public Health, Erasmus University Medical Center, Rotterdam, Netherlands

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Aline C Fenneman Department of Clinical and Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences (ACS), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands
Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism (AGEM), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands

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Anne H van der Spek Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism (AGEM), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands

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Elena Rampanelli Department of Clinical and Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences (ACS), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands

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Max Nieuwdorp Department of Clinical and Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences (ACS), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands
Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism (AGEM), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands

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Myrthe P P van Herk-Sukel Department of Internal Medicine and Dermatology, University Medical Center Utrecht, Utrecht, Netherlands

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Valery E P P Lemmens Department of Public Health, Erasmus University Medical Center, Rotterdam, Netherlands
Netherlands Comprehensive Cancer Organisation, Utrecht, Netherlands

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Ernst J Kuipers Department of Gastroenterology and Hepatology, Erasmus University Medical Center, Rotterdam, Netherlands

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Ron M C Herings PHARMO Institute for Drug Outcomes Research, AE Utrecht, Netherlands
Department of Epidemiology and Data Science, Amsterdam UMC, Amsterdam, Netherlands

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Eric Fliers Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology Metabolism (AGEM), Amsterdam UMC, University of Amsterdam, Amsterdam, Netherlands

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Objective

Whether an association between oral levothyroxine use, leading to supraphysiological exposure of the colon to thyroid hormones, and risk of colorectal cancer exists in humans is unclear. We therefore aimed to assess whether the use of levothyroxine is associated with a reduced risk of colorectal cancer in a linked cohort of pharmacy and cancer data.

Design

Population-based matched case–control study.

Methods

A total of 28,121 patients diagnosed with colorectal cancer between 1998 and 2014 were matched to 106,086 controls. Multivariable logistic regression was used to estimate the association between levothyroxine use and occurrence of colorectal cancer, adjusted for potential confounders. Results were stratified by gender, age, tumour subtype, and staging, as well as treatment duration and dosing.

Results

A total of 1066 colorectal cancer patients (4%) and 4024 (4%) controls had used levothyroxine at any point before index date (adjusted odds ratio 0.95 (0.88–1.01)). Long-term use of levothyroxine was seen in 323 (30%) colorectal cancer patients and 1111 (28%) controls (adjusted odds ratio 1.00 (0.88–1.13)). Stratification by tumour subsite showed a borderline significant risk reduction of rectal cancer, while this was not seen for proximal colon cancer or distal colon cancer. There was no relationship with treatment duration or with levothyroxine dose.

Conclusions

In this study, no reduced risk of colorectal cancer was seen in levothyroxine users. When stratifying by tumour subsite, a borderline significant risk reduction of rectal cancer was found and may warrant further research.

Open access
Nikolaos Kyriakakis Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK
Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK

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Marilena Giannoudi Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Satish S Kumar Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Khyatisha Seejore Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK
Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK

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Georgios K Dimitriadis Department of Endocrinology, King’s College Hospital NHS Foundation Trust, Denmark Hill, London, UK

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Harpal Randeva Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK

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Adam Glaser Pediatric Oncology, Leeds General Infirmary, Leeds Teaching Hospitals NHS Trust, Leeds, UK
Leeds Institute of Medical Research, University of Leeds, UK

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Michelle Kwok-Williams Clinical Oncology, Leeds Cancer Centre, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Georgina Gerrard Clinical Oncology, Leeds Cancer Centre, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Carmel Loughrey Clinical Oncology, Leeds Cancer Centre, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Ahmed Al-Qaissi Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Ramzi Ajjan Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK

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Julie Lynch Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK

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Robert D Murray Department of Endocrinology, Leeds Centre for Diabetes & Endocrinology, Leeds Teaching Hospitals NHS Trust, Leeds, UK
Leeds Institute for Cardiovascular and Metabolic Medicine (LICAMM), University of Leeds, Leeds, UK

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Background

Survivors of childhood brain tumours (SCBT) and teenage and young adult cancer survivors have an adverse cardiovascular risk profile, which translates into an increased vascular mortality. Data on cardiovascular risk profiles in SCBT are limited, and furthermore, there are no data in adult-onset (AO) brain tumours.

Patients and

methods: Fasting lipids, glucose, insulin, 24-h blood pressure (BP), and body composition were measured in 36 brain tumour survivors (20 AO; 16 childhood-onset (CO)) and 36 age- and gender-matched controls.

Results

Compared with controls, patients had elevated total cholesterol (5.3 ± 1.1 vs 4.6 ± 1.0 mmol/L, P = 0.007), LDL-C (3.1 ± 0.8 vs 2.7 ± 0.9 mmol/L, P = 0.011), insulin (13.4 ± 13.1 vs 7.6 ± 3.3 miu/L, P = 0.014), and increased insulin resistance (homeostatic model assessment for insulin resistance (HOMA-IR) 2.90 ± 2.84 vs 1.66 ± 0.73, P = 0.016). Patients showed adverse body composition, with increased total body fat mass (FM) (24.0 ± 12.2 vs 15.7 ± 6.6 kg, P < 0.001) and truncal FM (13.0 ± 6.7 vs 8.2 ± 3.7 kg, P < 0.001).

After stratification by timing of onset, CO survivors showed significantly increased LDL-C, insulin, and HOMA-IR compared with controls. Body composition was characterized by the increased total body and truncal FM. Truncal fat mass was increased by 84.1% compared with controls. AO survivors showed similar adverse cardiovascular risk profiles, with increased total cholesterol and HOMA-IR. Truncal FM was increased by 41.0% compared with matched controls (P = 0.029). No difference in mean 24-h BP was noted between patients and controls irrespective of the timing of cancer diagnosis.

Conclusion

The phenotype of both CO and AO brain tumour survivors is characterized by an adverse metabolic profile and body composition, putatively placing long-term survivors at increased risk of vascular morbidity and mortality.

Open access