Endocrine Disease Unit, University-Hospital of Padova, Padova, Italy
Department of Neuroscience DNS, University of Padova, Padova, Italy
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Laboratory Medicine, University-Hospital of Padova, Padova, Italy
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Endocrine Disease Unit, University-Hospital of Padova, Padova, Italy
Department of Neuroscience DNS, University of Padova, Padova, Italy
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Laboratory Medicine, University-Hospital of Padova, Padova, Italy
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Endocrine Disease Unit, University-Hospital of Padova, Padova, Italy
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, and drafting the manuscript. They all approved the final version of the paper. References 1 Ceccato F Scaroni C . Central adrenal insufficiency: open issues regarding diagnosis and glucocorticoid treatment . Clinical Chemistry and
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Département de Métabolomique Clinique, Hôpital Saint-Antoine, AP-HP Sorbonne Université, Paris, France
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Département de Métabolomique Clinique, Hôpital Saint-Antoine, AP-HP Sorbonne Université, Paris, France
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Université de Paris, INSERM, Institut IMAGINE, Hôpital Necker-Enfants Malades, AP-HP, Paris, France
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Sorbonne Université, INSERM, Centre de Recherche Saint-Antoine, Paris, France
Hôpital Armand Trousseau, AP-HP Sorbonne Université, Paris, France
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Département de Métabolomique Clinique, Hôpital Saint-Antoine, AP-HP Sorbonne Université, Paris, France
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was eventually positively diagnosed thanks to liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS), which allowed the quantitation of endogenous steroid metabolites and the identification of exogenous glucocorticoid treatment on a
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-line modality to delineate the impact of the route, dose, and duration of glucocorticoid treatment on the clinical, hormonal, radiological outcomes. Methods This retrospective study was conducted after obtaining approval from Institutional Ethics
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concentrations. These data suggested that further augmentation of systemic glucocorticoid availability by exogenous administration amplifies the impaired pituitary processing of POMC into ACTH. However, whether glucocorticoid treatment in critically ill humans
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prednisolone and dexamethasone ( 2 ). The hypothalamic–pituitary–adrenal axis is generally suppressed during and following glucocorticoid treatment in ALL ( 3 ). The duration of adrenal suppression is highly variable. While some studies reported persistence for
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Department of Clinical Medicine, Faculty of Health and Clinical Sciences, Copenhagen University, Copenhagen, Denmark
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Department of Clinical Medicine, Faculty of Health and Clinical Sciences, Copenhagen University, Copenhagen, Denmark
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) and it is not without risk to perform ITT in the perioperative phase. Thus, several approaches have been suggested, ranging from routine use of prophylactic glucocorticoid treatment to glucocorticoid sparing regimens with close observation and only
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Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Ludwig-Maximilians-Universität München, Munich, Germany
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Objective
Patients with non-functioning pituitary adenomas exhibit high morbidity and mortality rates. Growth hormone deficiency and high doses of glucocorticoid substitution therapy have been identified as corresponding risk factors. Interestingly, high levels of endogenous cortisol in, e.g., patients with post-traumatic stress disorder or patients with Cushing’s disease have been linked to shorter telomere length. Telomeres are noncoding DNA regions located at the end of chromosomes consisting of repetitive DNA sequences which shorten with aging and hereby determine cell survival. Therefore, telomere length can serve as a predictor for the onset of disease and mortality in some endocrine disorders (e.g., Cushing’s disease).
Design/methods
Here, we examine telomere length from blood in patients (n = 115) with non-functioning pituitary adenomas (NFPA) in a cross-sectional case–control (n = 106, age-, gender-matched) study using qPCR. Linear regression models were used to identify independent predictors of telomere length.
Results
We show that patients with NFPA exhibited shorter telomeres than controls. No significant association of indices of growth hormone deficiency (IGF-1-level-SDS, years of unsubstituted growth hormone deficiency etc.) with telomere length was detected. Interestingly, linear regression analysis showed that hydrocortisone replacement dosage in patients with adrenal insufficiency (n = 52) was a significant predictor for shorter telomere length (β = 0.377; P = 0.018) independent of potential confounders (gender, age, BMI, arterial hypertension, systolic blood pressure, number of antihypertensive drugs, total leukocyte count, waist-to-hip ratio, waist circumference, diabetes mellitus type 2, HbA1c, current statin use). Median split analysis revealed that higher hydrocortisone intake (>20 mg) was associated with significantly shorter telomeres.
Conclusion
These observations strengthen the importance of adjusted glucocorticoid treatment in NFPA patients with respect to morbidity and mortality rates.
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
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patients who receive chronic exogenous glucocorticoid treatment with doses ≥5 mg prednisolone equivalent for more than 4 weeks. This may also be caused by long-lasting glucocorticoid injections into joints or chronic application of glucocorticoid cream or
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doses of glucocorticoids ( P < 0.001), with the difference remaining significant after surface area adjustment ( P = 0.002) ( Table 2 ). The median duration of glucocorticoid treatment in the entire cohort was 24 (IQR 16 to 46) years. Treatment
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Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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dose (mg), mean (min–max) 247 (83–563) 240 (100–304) 255 (83–563) 259 (150–300) Previous glucocorticoid treatment (%) None 75 (57) 43 (57) 23 (58) 9 (56) In relation to chemotherapy 26 (20) 17 (23) 6 (15
