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  • Abstract: Adrenal x
  • Abstract: Adrenaline x
  • Abstract: Androgens x
  • Abstract: Catecholamines x
  • Abstract: hyperplasia x
  • Abstract: Cortex x
  • Abstract: Cushings x
  • Abstract: Glucocorticoids x
  • Abstract: Noradrenaline x
  • Hormones and Cancer x
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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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Vita Birzniece School of Medicine, Western Sydney University, New South Wales, Australia
Department of Diabetes and Endocrinology, Blacktown Hospital, New South Wales, Australia
Garvan Institute of Medical Research, New South Wales, Australia
School of Medical Sciences, University of New South Wales, New South Wales, Australia

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Teresa Lam School of Medicine, Western Sydney University, New South Wales, Australia
Department of Diabetes and Endocrinology, Blacktown Hospital, New South Wales, Australia
Department of Diabetes and Endocrinology, Westmead Hospital, New South Wales, Australia

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Mark McLean School of Medicine, Western Sydney University, New South Wales, Australia
Department of Diabetes and Endocrinology, Blacktown Hospital, New South Wales, Australia

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Navneeta Reddy Department of Diabetes and Endocrinology, Blacktown Hospital, New South Wales, Australia

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Haleh Shahidipour School of Medicine, Western Sydney University, New South Wales, Australia
Department of Diabetes and Endocrinology, Blacktown Hospital, New South Wales, Australia

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Amy Hayden School of Medicine, Western Sydney University, New South Wales, Australia
Faculty of Medicine, Health and Human Sciences, Macquarie University, New South Wales, Australia
Crown Princess Mary Cancer Centre, Westmead Hospital, New South Wales, Australia

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Howard Gurney Crown Princess Mary Cancer Centre, Westmead Hospital, New South Wales, Australia

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Glenn Stone School of Computing, Engineering and Mathematics, Western Sydney University, New South Wales, Australia

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Rikke Hjortebjerg Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
Endocrine Research Unit, Department of Endocrinology, Odense University Hospital & Department of Clinical Research, Faculty of Health, University of Southern Denmark, Odense, Denmark
Steno Diabetes Center Odense, Odense University Hospital & Department of Clinical Research, Faculty of Health, University of Southern Denmark, Odense, Denmark

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Jan Frystyk Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
Endocrine Research Unit, Department of Endocrinology, Odense University Hospital & Department of Clinical Research, Faculty of Health, University of Southern Denmark, Odense, Denmark

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Objective

Androgen deprivation therapy (ADT), a principal therapy in patients with prostate cancer, is associated with the development of obesity, insulin resistance, and hyperinsulinemia. Recent evidence indicates that metformin may slow cancer progression and improves survival in prostate cancer patients, but the mechanism is not well understood. Circulating insulin-like growth factors (IGFs) are bound to high-affinity binding proteins, which not only modulate the bioavailability and signalling of IGFs but also have independent actions on cell growth and survival. The aim of this study was to investigate whether metformin modulates IGFs, IGF-binding proteins (IGFBPs), and the pregnancy-associated plasma protein A (PAPP-A) – stanniocalcin 2 (STC2) axis.

Design and methods

In a blinded, randomised, cross-over design, 15 patients with prostate cancer on stable ADT received metformin and placebo treatment for 6 weeks each. Glucose metabolism along with circulating IGFs and IGFBPs was assessed.

Results

Metformin significantly reduced the homeostasis model assessment as an index of insulin resistance (HOMA IR) and hepatic insulin resistance. Metformin also reduced circulating IGF-2 (P  < 0.05) and IGFBP-3 (P  < 0.01) but increased IGF bioactivity (P  < 0.05). At baseline, IGF-2 correlated significantly with the hepatic insulin resistance (r2= 0.28, P  < 0.05). PAPP-A remained unchanged but STC2 declined significantly (P  < 0.05) following metformin administration. During metformin treatment, change in HOMA IR correlated with the change in STC2 (r2= 0.35, P  < 0.05).

Conclusion

Metformin administration alters many components of the circulating IGF system, either directly or indirectly via improved insulin sensitivity. Reduction in IGF-2 and STC2 may provide a novel mechanism for a potential metformin-induced antineoplastic effect.

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Ruth Percik Institute of Endocrinology, Diabetes and Metabolism, Sheba Medical Centre, Ramat Gan, Israel

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Sherwin Criseno Department of Endocrinology, University Hospital Birmingham, Birmingham, UK

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Safwaan Adam Department of Endocrinology, The Christie NHS Foundation Trust, Manchester, UK

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Kate Young Royal Marsden Hospital, London, UK

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Daniel L Morganstein Department of Endocrinology, Chelsea and Westminster Hospital, London, UK
Royal Marsden Hospital, London, UK

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Checkpoint inhibitors are now widely used in the management of many cancers. Endocrine toxicity is amongst the most common side effects. These endocrinopathies differ from most other immune-related toxicities in frequently being irreversible and rarely requiring cessation of checkpoint inhibitor therapy. This review considers an approach to the presentation and diagnosis of endocrinopathies, compared to classical endocrine diagnosis, suggesting improvements to classification and treatment based on fundamental endocrine principles. These will help to align management with other similar endocrine conditions and standardise the diagnosis and reporting of endocrine toxicity of checkpoint inhibitors to improve both endocrine and oncological care. In particular, the importance of considering any inflammatory phase (such as painful thyroiditis or hypophysitis resulting in the pituitary enlargement), from the endocrine consequences (transient hyperthyroidism followed by hypothyroidism, pan-hypopituitarism or isolated adrenocorticotrophic hormone deficiency), is highlighted. It is also important to consider the potential confounder of exogenous corticosteroids in adrenal suppression.

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Hélène Singeisen Department of Internal Medicine, Endocrinology, Cantonal Hospital Thurgau, Münsterlingen, Switzerland

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Mariko Melanie Renzulli Institute of Radiology, Cantonal Hospital Thurgau, Frauenfeld, Switzerland

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Vojtech Pavlicek Department of Internal Medicine, Endocrinology, Cantonal Hospital Thurgau, Münsterlingen, Switzerland

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Pascal Probst Department of Surgery, Cantonal Hospital Thurgau, Frauenfeld, Switzerland

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Fabian Hauswirth Department of Surgery, Cantonal Hospital Thurgau, Münsterlingen, Switzerland

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Markus K Muller Department of Surgery, Cantonal Hospital Thurgau, Frauenfeld, Switzerland

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Magdalene Adamczyk Department of Pathology and Molecular Pathology, University Hospital Zurich and University of Zurich, Zurich, Switzerland

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Achim Weber Department of Pathology and Molecular Pathology, University Hospital Zurich and University of Zurich, Zurich, Switzerland

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Reto Martin Kaderli Department of Visceral Surgery and Medicine, Bern University Hospital, University of Bern, Bern, Switzerland

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Pietro Renzulli Department of Surgery, Cantonal Hospital Thurgau, Münsterlingen, Switzerland

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Objective

Multiple endocrine neoplasia type 4 (MEN4) is caused by a CDKN1B germline mutation first described in 2006. Its estimated prevalence is less than one per million. The aim of this study was to define the disease characteristics.

Methods

A systematic review was performed according to the PRISMA 2020 criteria. A literature search from January 2006 to August 2022 was done using MEDLINE® and Web of ScienceTM.

Results

Forty-eight symptomatic patients fulfilled the pre-defined eligibility criteria. Twenty-eight different CDKN1B variants, mostly missense (21/48, 44%) and frameshift mutations (17/48, 35%), were reported. The majority of patients were women (36/48, 75%). Men became symptomatic at a median age of 32.5 years (range 10–68, mean 33.7 ± 23), whereas the same event was recorded for women at a median age of 49.5 years (range 5–76, mean 44.8 ± 19.9) (P  = 0.25). The most frequently affected endocrine organ was the parathyroid gland (36/48, 75%; uniglandular disease 31/36, 86%), followed by the pituitary gland (21/48, 44%; hormone-secreting 16/21, 76%), the endocrine pancreas (7/48, 15%), and the thyroid gland (4/48, 8%). Tumors of the adrenal glands and thymus were found in three and two patients, respectively. The presenting first endocrine pathology concerned the parathyroid (27/48, 56%) and the pituitary gland (11/48, 23%). There were one (27/48, 56%), two (13/48, 27%), three (3/48, 6%), or four (5/48, 10%) syn- or metachronously affected endocrine organs in a single patient, respectively.

Conclusion

MEN4 is an extremely rare disease, which most frequently affects women around 50 years of age. Primary hyperparathyroidism as a uniglandular disease is the leading pathology.

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