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      Glucocorticoid-induced diabetes in patients with metastatic spinal cord compression

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          Abstract

          Background

          The risk of developing diabetes mellitus (DM) during treatment with high-dose glucocorticoids is unknown and monitoring of glucose is random in many settings.

          Objective

          To determine incidence of and risk factors for induction of DM during high-dose glucocorticoid therapy of metastatic spinal cord compression (MSCC) in patients referred to radiotherapy. Furthermore, to describe the time course of development of DM.

          Subjects and methods

          140 patients were recruited (131 were included in the analysis) with MSCC receiving high-dose glucocorticoid ≥100 mg prednisolone per day were included in a prospective, observational cohort study. The primary endpoint was development of DM defined by two or more plasma glucose values ≥11.1 mmol/L. Plasma glucose was monitored on a daily basis for 12 days during radiotherapy.

          Results

          Fifty-six of the patients (43%; 95% CI 35–52%) were diagnosed with DM based on plasma glucose measurements during the study period. Sixteen patients, 12% (95% CI 6–18%), were treated with insulin. At multivariate analysis, only high baseline HbA1c predicted the development of insulin-treated DM. An HbA1c-value <39 mmol/mol was associated with a negative predictive value of 96% for not developing DM needing treatment with insulin. The diagnosis of diabetes with need for insulin treatment was made within 7 days in 14 of the 16 (88%; 95% CI 72–100%) patients.

          Conclusion

          The risk of developing DM during treatment with high-dose glucocorticoids in patients with MSCC referred to radiotherapy is high in the first treatment week. Only referral HbA1c predicts the development of DM.

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          Most cited references14

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          The high incidence of steroid-induced hyperglycaemia in hospital.

          The objective of this study was to systematically evaluate the incidence of steroid-induced hyperglycaemia in a tertiary referral hospital. We conducted a glucometric audit of a prospective protocol where glucose monitoring was routinely performed on patients treated with high-dose steroids.
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            Steroid diabetes: from mechanism to treatment?

            Glucocorticoids (GCs) are frequently prescribed anti-inflammatory and immunosuppressive drugs. In addition to their beneficial effects on disease activity, GCs have an extensive side effect profile, including adverse effects on metabolism resulting in the development of glucose intolerance and overt diabetes. Recent developments have led to renewed interest in the mechanisms underlying these diabetogenic effects of GCs. First, dissociated glucocorticoid receptor (GR) agonists were developed which are designed to segregate the anti-inflammatory and metabolic actions of GCs, potentially rendering compounds with a higher therapeutic index. Second, at present, 11-beta hydroxysteroid dehydrogenase type-1 inhibitors are under development. These compounds may lower tissue GC concentrations by inhibiting cortisone to cortisol conversion and are being evaluated in clinical trials as a novel treatment modality for the metabolic syndrome. Here, we provide an up-to-date overview of the current insights regarding the mechanisms responsible for the adverse metabolic effects of GCs that may lead to steroid diabetes. Particularly, we will focus on GC-related induction of insulin resistance and pancreatic islet-cell dysfunction. Finally, we will discuss how increased knowledge concerning the pathophysiology of steroid diabetes may result in improved treatment strategies.
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              Glucocorticoid-Induced Diabetes Mellitus: Prevalence and Risk Factors in Primary Renal Diseases

              Background/Aims: In patients with primary renal diseases the current knowledge of hyperglycemia associated with corticosteroid therapy is limited. We therefore examined the prevalence and risk factors of glucocorticoid-induced diabetes mellitus (DM) in primary renal diseases. Methods: Patients were recruited with primary renal diseases who were started on corticosteroids between April 2002 and June 2005. In patients with DM, an impaired fasting glucose level and/or positive urinary glucose analyses before corticosteroids therapy were excluded. Results: During corticosteroid therapy (initial dose: prednisolone 0.75 ± 0.10 mg/kg/day), DM was newly diagnosed in 17 (40.5%) of 42 patients. All of the 17 patients were diagnosed as having DM by postprandial hyperglycemia at 2 h after lunch, although they had normal fasting blood glucose levels. Age (OR 1.40, 95% CI 1.06–1.84) and body mass index (OR 1.87, 95% CI 1.03–3.38) were determined as independent risk factors for glucocorticoid-induced DM. Conclusion: Over 40% of patients with primary renal disease developed DM during treatment with corticosteroids. A high age and high body mass index are the independent risk factors for glucocorticoid-induced DM. 24-hour urinary glucose analyses and postprandial plasma glucose are useful for detecting glucocorticoid-induced DM.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                May 2018
                18 April 2018
                : 7
                : 5
                : 719-726
                Affiliations
                [1 ]Department of Cardiology Nephrology and Endocrinology, Nordsjællands Hospital, Hillerød, Denmark
                [2 ]Department of Radiation Oncology Rigshospitalet, Copenhagen, Denmark
                [3 ]Faculty of Health and Medical Sciences University of Copenhagen, Copenhagen, Denmark
                [4 ]Department of Oncology and Palliation Nordsjællands Hospital, Hillerød, Denmark
                Author notes
                Correspondence should be addressed to P L Kristensen: peter.lommer.kristensen.01@ 123456regionh.dk
                Article
                EC180088
                10.1530/EC-18-0088
                5952240
                29669805
                6f7222dc-e2c0-4a12-ae1b-1ea175401423
                © 2018 The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 04 April 2018
                : 18 April 2018
                Categories
                Research

                glucocorticoid,diabetes,metastatic spinal cord compression (mscc)

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