Endocrinology and Metabolism

Review Article

Glucocorticoid-Induced Hyperglycemia: A Neglected Problem: Jung-Hwan Cho, Sunghwan Suh; Received February 1, 2024 Accepted February 20, 2024 Published online March 27, 2024; DOI: https://doi.org/10.3803/EnM.2024.1951 [Epub ahead of print]

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Abstract PDF PubReader ePub: Glucocorticoids provide a potent therapeutic response and are widely used to treat a variety of diseases, including coronavirus disease 2019 (COVID-19) infection. However, the issue of glucocorticoid-induced hyperglycemia (GIH), which is observed in over one-third of patients treated with glucocorticoids, is often neglected. To improve the clinical course and prognosis of diseases that necessitate glucocorticoid therapy, proper management of GIH is essential. The key pathophysiology of GIH includes systemic insulin resistance, which exacerbates hepatic steatosis and visceral obesity, as well as proteolysis and lipolysis of muscle and adipose tissue, coupled with β-cell dysfunction. For patients on glucocorticoid therapy, risk stratification should be conducted through a detailed baseline evaluation, and frequent glucose monitoring is recommended to detect the onset of GIH, particularly in high-risk individuals. Patients with confirmed GIH who require treatment should follow an insulin-centered regimen that varies depending on whether they are inpatients or outpatients, as well as the type and dosage of glucocorticoid used. The ideal strategy to maintain normoglycemia while preventing hypoglycemia is to combine basal-bolus insulin and correction doses with a continuous glucose monitoring system. This review focuses on the current understanding and latest evidence concerning GIH, incorporating insights gained from the COVID-19 pandemic.

Original Articles

Diabetes, Obesity and Metabolism
Effect of the Concomitant Use of Subcutaneous Basal Insulin and Intravenous Insulin Infusion in the Treatment of Severe Hyperglycemic Patients: Yejee Lim, Jung Hun Ohn, Joo Jeong, Jiwon Ryu, Sun-wook Kim, Jae Ho Cho, Hee-Sun Park, Hye Won Kim, Jongchan Lee, Eun Sun Kim, Nak-Hyun Kim, You Hwan Jo, Hak Chul Jang; Endocrinol Metab. 2022;37(3):444-454. Published online June 3, 2022; DOI: https://doi.org/10.3803/EnM.2021.1341

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Background
No consensus exists regarding the early use of subcutaneous (SC) basal insulin facilitating the transition from continuous intravenous insulin infusion (CIII) to multiple SC insulin injections in patients with severe hyperglycemia other than diabetic ketoacidosis. This study evaluated the effect of early co-administration of SC basal insulin with CIII on glucose control in patients with severe hyperglycemia.
Methods
Patients who received CIII for the management of severe hyperglycemia were divided into two groups: the early basal insulin group (n=86) if they received the first SC basal insulin 0.25 U/kg body weight within 24 hours of CIII initiation and ≥4 hours before discontinuation, and the delayed basal insulin group (n=79) if they were not classified as the early basal insulin group. Rebound hyperglycemia was defined as blood glucose level of >250 mg/dL in 24 hours following CIII discontinuation. Propensity score matching (PSM) methods were additionally employed for adjusting the confounding factors (n=108).
Results
The rebound hyperglycemia incidence was significantly lower in the early basal insulin group than in the delayed basal insulin group (54.7% vs. 86.1%), despite using PSM methods (51.9%, 85.2%). The length of hospital stay was shorter in the early basal insulin group than in the delayed basal insulin group (8.5 days vs. 9.6 days, P=0.027). The hypoglycemia incidence did not differ between the groups.
Conclusion
Early co-administration of basal insulin with CIII prevents rebound hyperglycemia and shorten hospital stay without increasing the hypoglycemic events in patients with severe hyperglycemia.

Citations

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16. Diabetes Care in the Hospital: Standards of Care in Diabetes—2024
Nuha A. ElSayed, Grazia Aleppo, Raveendhara R. Bannuru, Dennis Bruemmer, Billy S. Collins, Laya Ekhlaspour, Rodolfo J. Galindo, Marisa E. Hilliard, Eric L. Johnson, Kamlesh Khunti, Ildiko Lingvay, Glenn Matfin, Rozalina G. McCoy, Mary Lou Perry, Scott J.
Diabetes Care.2024; 47(Supplement): S295. CrossRef
16. Diabetes Care in the Hospital: Standards of Care in Diabetes—2023
Nuha A. ElSayed, Grazia Aleppo, Vanita R. Aroda, Raveendhara R. Bannuru, Florence M. Brown, Dennis Bruemmer, Billy S. Collins, Marisa E. Hilliard, Diana Isaacs, Eric L. Johnson, Scott Kahan, Kamlesh Khunti, Jose Leon, Sarah K. Lyons, Mary Lou Perry, Priya
Diabetes Care.2023; 46(Supplement): S267. CrossRef
Effectiveness and safety of early insulin glargine administration in combination with continuous intravenous insulin infusion in the management of diabetic ketoacidosis: A randomized controlled trial
Kitti Thammakosol, Chutintorn Sriphrapradang
Diabetes, Obesity and Metabolism.2023; 25(3): 815. CrossRef

Clinical Study
Fasting and Postprandial Hyperglycemia: Their Predictors and Contributions to Overall Hyperglycemia in Korean Patients with Type 2 Diabetes: Jaecheol Moon, Ji Young Kim, Soyeon Yoo, Gwanpyo Koh; Endocrinol Metab. 2020;35(2):290-297. Published online June 24, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.2.290

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Background
This study aimed to identify factors that affect fasting hyperglycemia (FHG) and postprandial hyperglycemia (PPG) and their contributions to overall hyperglycemia in Korean patients with type 2 diabetes mellitus (T2DM).
Methods
This was a retrospective study conducted on 194 Korean T2DM patients with 7-point self-monitoring blood glucose (SMBG) profiles plotted in 4 days in 3 consecutive months. We calculated the areas corresponding to FHG and PPG (area under the curve [AUC]_FHG and AUC_PPG) and contributions (%) in the graph of the 7-point SMBG data. The levels of glycated hemoglobin (HbA1c) were categorized by tertiles, and the contributions of FHG and PPG were compared.
Results
The relative contribution of FHG increased (44.7%±5.6%, 58.0%±4.4%, 66.5%±2.8%; PANOVA=0.002, PTREND <0.001), while that of PPG decreased (55.3%±5.5%, 42.0%±4.4%, 33.5%±2.8%; PANOVA=0.002, PTREND <0.001) with the elevated HbA1c. Multivariate analysis showed that HbA1c (β=0.615, P<0.001), waist circumference (β=0.216, P=0.042), and triglyceride (β=0.121, P=0.048) had a significant association with AUCFHG. Only HbA1c (β=0.231, P=0.002) and age (β=0.196, P=0.009) was significantly associated with AUC_PPG.
Conclusion
The data suggested that in Korean T2DM patients, FHG predominantly contributed to overall hyperglycemia at higher HbA1c levels, whereas it contributed to PPG at lower HbA1c levels. It is recommended that certain factors, namely age, degree of glycemic control, obesity, or triglyceride levels, should be considered when prescribing medications for T2DM patients.

Citations

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Prospective study of the association between chronotype and cardiometabolic risk among Chinese young adults
Tingting Li, Yang Xie, Shuman Tao, Liwei Zou, Yajuan Yang, Fangbiao Tao, Xiaoyan Wu
BMC Public Health.2023;[Epub] CrossRef
Effects of mulberry twig alkaloids(Sangzhi alkaloids) and metformin on blood glucose fluctuations in combination with premixed insulin-treated patients with type 2 diabetes
Ziyu Meng, Chengye Xu, Haoling Liu, Xinyuan Gao, Xinyu Li, Wenjian Lin, Xuefei Ma, Changwei Yang, Ming Hao, Kangqi Zhao, Yuxin Hu, Yi Wang, Hongyu Kuang
Frontiers in Endocrinology.2023;[Epub] CrossRef
Evaluating Triglyceride and Glucose Index as a Simple and Easy-to-Calculate Marker for All-Cause and Cardiovascular Mortality
Kyung-Soo Kim, Sangmo Hong, You-Cheol Hwang, Hong-Yup Ahn, Cheol-Young Park
Journal of General Internal Medicine.2022; 37(16): 4153. CrossRef
A new approach for investigating the relative contribution of basal glucose and postprandial glucose to HbA1C
Jing Ma, Hua He, Xiaojie Yang, Dawei Chen, Cuixia Tan, Li Zhong, Qiling Du, Xiaohua Wu, Yunyi Gao, Guanjian Liu, Chun Wang, Xingwu Ran
Nutrition & Diabetes.2021;[Epub] CrossRef
The Clinical Characteristics of Gestational Diabetes Mellitus in Korea: A National Health Information Database Study
Kyung-Soo Kim, Sangmo Hong, Kyungdo Han, Cheol-Young Park
Endocrinology and Metabolism.2021; 36(3): 628. CrossRef

Clinical Study
Comparison of the Efficacy and Safety of Insulin Detemir Administered Once Daily According to Two Titration Algorithms (3-0-3 and 2-4-6-8) in Patients with Type 2 Diabetes Mellitus: Hea Min Yu, Kang Seo Park, Jun Hwa Hong, Keun Yong Park, Jong Min Lee, Bon Jeong Ku, Yeo Joo Kim, Tae Kun Oh; Endocrinol Metab. 2020;35(1):142-148. Published online March 19, 2020; DOI: https://doi.org/10.3803/EnM.2020.35.1.142

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Background

This study was conducted to compare glycaemic control with insulin detemir administered according to two titration algorithms (3-0-3 and 2-4-6-8) after 20 weeks of treatment in subjects with type 2 diabetes mellitus inadequately controlled on metformin.

Methods

This was a 20-week, randomised, multicentre, open-labelled, treat-to-target trial. Forty-six patients were randomised in a 1:1 manner to either the 3-0-3 (G3, n=23) or 2-4-6-8 (G2, n=23) algorithm. The primary endpoint was change of haemoglobin A1c (HbA1c), and the secondary safety endpoint included hypoglycaemic events.

Results

After 20 weeks, HbA1c decreased similarly in the G3 and G2 groups, with a mean change of −0.9% from baseline. The mean change in fasting plasma glucose was numerically similar in both groups. The hypoglycaemia event rate per 100-patient-years of exposure (r) in the G2 group (r=1,427) was higher than that in the G3 group (r=807).

Conclusion

Both treatment groups had numerically similar HbA1c reductions. A trend towards fewer hypoglycaemia episodes after dose stabilisation was seen with the simpler G3. Clinically, this may be an important observation, as a simpler titration algorithm may support self-management and maintenance of insulin therapy.

Citations

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Time for Using Machine Learning for Dose Guidance in Titration of People With Type 2 Diabetes? A Systematic Review of Basal Insulin Dose Guidance
Camilla Heisel Nyholm Thomsen, Stine Hangaard, Thomas Kronborg, Peter Vestergaard, Ole Hejlesen, Morten Hasselstrøm Jensen
Journal of Diabetes Science and Technology.2022; : 193229682211459. CrossRef
Efficacy and safety of patient-led versus physician-led titration of basal insulin in patients with uncontrolled type 2 diabetes: a meta-analysis of randomized controlled trials
Marco Castellana, Filippo Procino, Rodolfo Sardone, Pierpaolo Trimboli, Gianluigi Giannelli
BMJ Open Diabetes Research & Care.2020; 8(1): e001477. CrossRef

Clinical Study
Favorable Glycemic Control with Once-Daily Insulin Degludec/Insulin Aspart after Changing from Basal Insulin in Adults with Type 2 Diabetes: Han Na Jang, Ye Seul Yang, Seong Ok Lee, Tae Jung Oh, Bo Kyung Koo, Hye Seung Jung; Endocrinol Metab. 2019;34(4):382-389. Published online December 23, 2019; DOI: https://doi.org/10.3803/EnM.2019.34.4.382

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Background

Conflicting results have been reported on the efficacy of insulin degludec/insulin aspart (IDegAsp) compared to basal insulin in type 2 diabetes. We investigated the effects of changing basal insulin to IDegAsp on glycemic control and sought to identify factors related to those effects.

Methods

In this retrospective study of patients from three referral hospitals, patients with type 2 diabetes using basal insulin with hemoglobin A1c (HbA1c) levels less than 11.0% were enrolled. Basal insulin was replaced with IDegAsp, and data were analyzed from 3 months before to 3 months after the replacement.

Results

Eighty patients were recruited (52.5% male; mean age, 67.0±9.8 years; mean duration of diabetes, 18.9±8.5 years; mean HbA1c, 8.7%±1.0%). HbA1c levels increased during 3 months of basal insulin use, but significantly decreased after changing to IDegAsp (8.28%±1.10%, P=0.0001). The reduction was significant at 6 months in 35 patients whose longer-term data were available. Patients with a measured fasting plasma glucose (m-FPG) lower than their predicted FPG (p-FPG) by regression from HbA1c showed a significant HbA1c reduction caused by the change to IDegAsp, even without a significantly increased insulin dose. However, patients whose m-FPG was higher than their p-FPG did not experience a significant HbA1c reduction, despite a significantly increased insulin dose. Furthermore, the HbA1c reduction caused by IDegAsp was significant in patients with low fasting C-peptide levels and high insulin doses.

Conclusion

We observed a significant glucose-lowering effect by replacing basal insulin with IDegAsp, especially in patients with a lower m-FPG than p-FPG.

Citations

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Evaluation of the efficiency of insulin degludec/insulin aspart therapy in controlling hyperglycemia and hypoglycemia in patients with type 2 diabetes mellitus: a real-life experience
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Low fasting glucose‐to‐estimated average glucose ratio was associated with superior response to insulin degludec/aspart compared with basal insulin in patients with type 2 diabetes
Han Na Jang, Ye Seul Yang, Tae Jung Oh, Bo Kyung Koo, Seong Ok Lee, Kyong Soo Park, Hak Chul Jang, Hye Seung Jung
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Efficacy and Safety of Insulin Degludec/Insulin Aspart Compared with a Conventional Premixed Insulin or Basal Insulin: A Meta-Analysis
Shinje Moon, Hye-Soo Chung, Yoon-Jung Kim, Jae-Myung Yu, Woo-Ju Jeong, Jiwon Park, Chang-Myung Oh
Metabolites.2021; 11(9): 639. CrossRef
Fear of Hypoglycemia in Adults with diabetes mellitus switching to Treatment with IDegAsp Co-formulation to Examine real-world setting: an observational study (The HATICE study)
Ulaş Serkan Topaloğlu, Hatice Kayış Topaloğlu, Melih Kızıltepe, Mesut Kılıç, Sami Bahçebaşı, Sibel Ata, Şeyma Yıldız, Yasin Şimşek
Drug Metabolism and Drug Interactions.2021; 36(2): 129. CrossRef
Response: Favorable Glycemic Control with Once-Daily Insulin Degludec/Insulin Aspart after Changing from Basal Insulin in Adults with Type 2 Diabetes (Endocrinol Metab 2019; 34:382-9, Han Na Jang et al.)
Han Na Jang, Hye Seung Jung
Endocrinology and Metabolism.2020; 35(1): 194. CrossRef
Letter: Favorable Glycemic Control with Once-Daily Insulin Degludec/Insulin Aspart after Changing from Basal Insulin in Adults with Type 2 Diabetes (Endocrinol Metab 2019; 34:382-9, Han Na Jang et al.)
Sang Youl Rhee
Endocrinology and Metabolism.2020; 35(1): 192. CrossRef
Fear of hypoglycemia in adults with diabetes mellitus switching to treatment with IDegAsp co-formulation to examine real-world setting: an observational study (The HATICE study)
Ulaş Serkan Topaloğlu, Hatice Kayış Topaloğlu, Melih Kızıltepe, Mesut Kılıç, Sami Bahçebaşı, Sibel Ata, Şeyma Yıldız, Yasin Şimşek
Drug Metabolism and Personalized Therapy.2020;[Epub] CrossRef

Review Articles

Glucocorticoid-Induced Diabetes Mellitus: An Important but Overlooked Problem: Sunghwan Suh, Mi Kyoung Park; Endocrinol Metab. 2017;32(2):180-189. Published online May 29, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.2.180

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Abstract PDF PubReader ePub

Glucocorticoids are widely used as potent anti-inflammatory and immunosuppressive drugs to treat a wide range of diseases. However, they are also associated with a number of side effects, including new-onset hyperglycemia in patients without a history of diabetes mellitus (DM) or severely uncontrolled hyperglycemia in patients with known DM. Glucocorticoid-induced diabetes mellitus (GIDM) is a common and potentially harmful problem in clinical practice, affecting almost all medical specialties, but is often difficult to detect in clinical settings. However, scientific evidence is lacking regarding the effects of GIDM, as well as strategies for prevention and treatment. Similarly to nonsteroid-related DM, the principles of early detection and risk factor modification apply. Screening for GIDM should be considered in all patients treated with medium to high doses of glucocorticoids. Challenges in the management of GIDM stem from wide fluctuations in postprandial hyperglycemia and the lack of clearly defined treatment protocols. Together with lifestyle measures, hypoglycemic drugs with insulin-sensitizing effects are indicated. However, insulin therapy is often unavoidable, to the point that insulin can be considered the drug of choice. The treatment of GIDM should take into account the degree and pattern of hyperglycemia, as well as the type, dose, and schedule of glucocorticoid used. Moreover, it is essential to instruct the patient and/or the patient's family about how to perform the necessary adjustments. Prospective studies are needed to answer the remaining questions regarding GIDM.

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Acute Hyperglycemia Associated with Anti-Cancer Medication: Yul Hwangbo, Eun Kyung Lee; Endocrinol Metab. 2017;32(1):23-29. Published online March 20, 2017; DOI: https://doi.org/10.3803/EnM.2017.32.1.23

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Hyperglycemia during chemotherapy occurs in approximately 10% to 30% of patients. Glucocorticoids and L-asparaginase are well known to cause acute hyperglycemia during chemotherapy. Long-term hyperglycemia is also frequently observed, especially in patients with hematologic malignancies treated with L-asparaginase-based regimens and total body irradiation. Glucocorticoid-induced hyperglycemia often develops because of increased insulin resistance, diminished insulin secretion, and exaggerated hepatic glucose output. Screening strategies for this condition include random glucose testing, hemoglobin A1c testing, oral glucose loading, and fasting plasma glucose screens. The management of hyperglycemia starts with insulin or sulfonylurea, depending on the type, dose, and delivery of the glucocorticoid formulation. Mammalian target of rapamycin (mTOR) inhibitors are associated with a high incidence of hyperglycemia, ranging from 13% to 50%. Immunotherapy, such as anti-programmed death 1 (PD-1) antibody treatment, induces hyperglycemia with a prevalence of 0.1%. The proposed mechanism of immunotherapy-induced hyperglycemia is an autoimmune process (insulitis). Withdrawal of the PD-1 inhibitor is the primary treatment for severe hyperglycemia. The efficacy of glucocorticoid therapy is not fully established and the decision to resume PD-1 inhibitor therapy depends on the severity of the hyperglycemia. Diabetic patients should achieve optimized glycemic control before initiating treatment, and glucose levels should be monitored periodically in patients initiating mTOR inhibitor or PD-1 inhibitor therapy. With regard to hyperglycemia caused by anti-cancer therapy, frequent monitoring and proper management are important for promoting the efficacy of anti-cancer therapy and improving patients' quality of life.

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Original Articles

Clinical Study
Obesity and Hyperglycemia in Korean Men with Klinefelter Syndrome: The Korean Endocrine Society Registry: Seung Jin Han, Kyung-Soo Kim, Wonjin Kim, Jung Hee Kim, Yong-ho Lee, Ji Sun Nam, Ji A Seo, Bu Kyung Kim, Jihyun Lee, Jin Ook Chung, Min-Hee Kim, Tae-Seo Sohn, Han Seok Choi, Seong Bin Hong, Yoon-Sok Chung; Endocrinol Metab. 2016;31(4):598-603. Published online December 20, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.4.598

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Background

The aim of this study was to investigate the prevalence of obesity in Korean men with Klinefelter syndrome (KS) and the associated risk factors for obesity and hyperglycemia.

Methods

Data were collected retrospectively from medical records from 11 university hospitals in Korea between 1994 and 2014. Subjects aged ≥18 years with newly diagnosed KS were enrolled. The following parameters were recorded at baseline before treatment: chief complaint, height, weight, fasting glucose level, lipid panel, blood pressure, testosterone, luteinizing hormone, follicle-stimulating hormone, karyotyping patterns, and history of hypertension, diabetes, and dyslipidemia.

Results

Data were analyzed from 376 of 544 initially enrolled patients. The rate of the 47 XXY chromosomal pattern was 94.1%. The prevalence of obesity (body mass index ≥25 kg/m²) in Korean men with KS was 42.6%. The testosterone level was an independent risk factor for obesity and hyperglycemia.

Conclusion

Obesity is common in Korean men with KS. Hypogonadism in patients with KS was associated with obesity and hyperglycemia.

Citations

Citations to this article as recorded by

A dual-center study of predictive factors for sperm retrieval through microdissection testicular sperm extraction and intracytoplasmic sperm injection outcomes in men with non-mosaic Klinefelter syndrome
Jong Hyeun Baeck, Tae Jin Kim, Tae Heon Kim, Seung-Ryeol Lee, Dong Soo Park, Hwang Kwon, Ji Eun Shin, Dong Hyeon Lee, Young Dong Yu
Investigative and Clinical Urology.2023; 64(1): 41. CrossRef
Cardiorespiratory fitness in adolescents and young adults with Klinefelter syndrome – a pilot study
Julia Spiekermann, Kathrin Sinningen, Beatrice Hanusch, Michaela Kleber, Michael M. Schündeln, Cordula Kiewert, Heide Siggelkow, Jakob Höppner, Corinna Grasemann
Frontiers in Endocrinology.2023;[Epub] CrossRef
Metabolic Profile in a Cohort of Young Sicilian Patients with Klinefelter’s Syndrome: The Role of Irisin
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International Journal of Endocrinology.2022; 2022: 1. CrossRef
Metabolic and Nutritional Aspects in Paediatric Patients with Klinefelter Syndrome: A Narrative Review
Chiara Mameli, Giulia Fiore, Arianna Sangiorgio, Marta Agostinelli, Giulia Zichichi, Gianvincenzo Zuccotti, Elvira Verduci
Nutrients.2022; 14(10): 2107. CrossRef
Klinefelter syndrome in an adolescent with severe obesity, insulin resistance, and hyperlipidemia, successfully treated with testosterone replacement therapy
Shota Fukuhara, Jun Mori, Hisakazu Nakajima
Clinical Pediatric Endocrinology.2021; 30(3): 127. CrossRef
Glucose metabolic disorder in Klinefelter syndrome: a retrospective analysis in a single Chinese hospital and literature review
Shixuan Liu, Tao Yuan, Shuoning Song, Shi Chen, Linjie Wang, Yong Fu, Yingyue Dong, Yan Tang, Weigang Zhao
BMC Endocrine Disorders.2021;[Epub] CrossRef
What Every Internist-Endocrinologist Should Know about Rare Genetic Syndromes in Order to Prevent Needless Diagnostics, Missed Diagnoses and Medical Complications: Five Years of ‘Internal Medicine for Rare Genetic Syndromes’
Anna G. W. Rosenberg, Minke R. A. Pater, Karlijn Pellikaan, Kirsten Davidse, Anja A. Kattentidt-Mouravieva, Rogier Kersseboom, Anja G. Bos-Roubos, Agnies van Eeghen, José M. C. Veen, Jiske J. van der Meulen, Nina van Aalst-van Wieringen, Franciska M. E. H
Journal of Clinical Medicine.2021; 10(22): 5457. CrossRef
Klinefelter Syndrome and Diabetes
Mark J. O’Connor, Emma A. Snyder, Frances J. Hayes
Current Diabetes Reports.2019;[Epub] CrossRef
Endocrine aspects of Klinefelter syndrome
Adriana Herrera Lizarazo, Michelle McLoughlin, Maria G. Vogiatzi
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Karthickeyan Chella Krishnan, Margarete Mehrabian, Aldons J. Lusis
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Klinefelter Syndrome: Integrating Genetics, Neuropsychology, and Endocrinology
Claus H Gravholt, Simon Chang, Mikkel Wallentin, Jens Fedder, Philip Moore, Anne Skakkebæk
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Temeka Zore, Maria Palafox, Karen Reue
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Andrea Salzano, Roberta D’Assante, Liam M. Heaney, Federica Monaco, Giuseppe Rengo, Pietro Valente, Daniela Pasquali, Eduardo Bossone, Daniele Gianfrilli, Andrea Lenzi, Antonio Cittadini, Alberto M. Marra, Raffaele Napoli
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A. Yamaguchi, P. Knoblovits
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Articles inEndocrinology and Metabolismin 2016
Won-Young Lee
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Sex differences in obesity: X chromosome dosage as a risk factor for increased food intake, adiposity and co-morbidities
Karen Reue
Physiology & Behavior.2017; 176: 174. CrossRef
Klinefelter Syndrome with Morbid Obesity Before Bariatric Surgery: A Case Report
Parisa Janmohammadi, Gholamreza Mohammadi-Farsani, Hana Arghavani, Mahmoud Arshad, Tayebeh Mokhber
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Clinical Study
Prognostic Factors in Patients Hospitalized with Diabetic Ketoacidosis: Avinash Agarwal, Ambuj Yadav, Manish Gutch, Shuchi Consul, Sukriti Kumar, Ved Prakash, Anil Kumar Gupta, Annesh Bhattacharjee; Endocrinol Metab. 2016;31(3):424-432. Published online September 1, 2016; DOI: https://doi.org/10.3803/EnM.2016.31.3.424

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Background

Diabetic ketoacidosis (DKA) is characterized by a biochemical triad of hyperglycemia, acidosis, and ketonemia. This condition is life-threatening despite improvements in diabetic care. The purpose of this study was to evaluate the clinical and biochemical prognostic markers of DKA. We assessed correlations in prognostic markers with DKA-associated morbidity and mortality.

Methods

Two hundred and seventy patients that were hospitalized with DKA over a period of 2 years were evaluated clinically and by laboratory tests. Serial assays of serum electrolytes, glucose, and blood pH were performed, and clinical outcome was noted as either discharged to home or death.

Results

The analysis indicated that significant predictors included sex, history of type 1 diabetes mellitus or type 2 diabetes mellitus, systolic blood pressure, diastolic blood pressure, total leukocyte count, Acute Physiology and Chronic Health Evaluation II (APACHE II) score, blood urea nitrogen, serum creatinine, serum magnesium, serum phosphate, serum osmolality, serum glutamic oxaloacetic transaminases, serum glutamic pyruvic transaminases, serum albumin, which were further regressed and subjected to multivariate logistic regression (MLR) analysis. The MLR analysis indicated that males were 7.93 times more likely to have favorable outcome compared with female patients (odds ratio, 7.93; 95% confidence interval, 3.99 to 13.51), while decreases in mean APACHE II score (14.83) and serum phosphate (4.38) at presentation may lead to 2.86- and 2.71-fold better outcomes, respectively, compared with higher levels (APACHE II score, 25.00; serum phosphate, 6.04).

Conclusion

Sex, baseline biochemical parameters such as APACHE II score, and phosphate level were important predictors of the DKA-associated mortality.

Citations

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Diabetes & Metabolic Syndrome: Clinical Research & Reviews.2019; 13(4): 2357. CrossRef
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Review Article

Obesity and Metabolism
Neurocognitive Changes and Their Neural Correlates in Patients with Type 2 Diabetes Mellitus: Junghyun H Lee, Yera Choi, Chansoo Jun, Young Sun Hong, Han Byul Cho, Jieun E Kim, In Kyoon Lyoo; Endocrinol Metab. 2014;29(2):112-121. Published online June 26, 2014; DOI: https://doi.org/10.3803/EnM.2014.29.2.112

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As the prevalence and life expectancy of type 2 diabetes mellitus (T2DM) continue to increase, the importance of effective detection and intervention for the complications of T2DM, especially neurocognitive complications including cognitive dysfunction and dementia, is receiving greater attention. T2DM is thought to influence cognitive function through an as yet unclear mechanism that involves multiple factors such as hyperglycemia, hypoglycemia, and vascular disease. Recent developments in neuroimaging methods have led to the identification of potential neural correlates of T2DM-related neurocognitive changes, which extend from structural to functional and metabolite alterations in the brain. The evidence indicates various changes in the T2DM brain, including global and regional atrophy, white matter hyperintensity, altered functional connectivity, and changes in neurometabolite levels. Continued neuroimaging research is expected to further elucidate the underpinnings of cognitive decline in T2DM and allow better diagnosis and treatment of the condition.

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Case Reports

Visual Seizure: A Reversible Complication of Non-Ketotic Hyperglycemia.: Na Young Kim, Min Su Park; Endocrinol Metab. 2012;27(2):155-158. Published online June 20, 2012; DOI: https://doi.org/10.3803/EnM.2012.27.2.155

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Abstract PDF: A 65-year-old man with diabetes mellitus was presented with left visual aura, followed by a versive seizure, each lasting approximately 3 minutes. Neurological examination showed an intermittent left homonymous hemianopsia. Brain magnetic resonance imaging (MRI) showed right occipital lobe lesion, with cytotoxic edema. Blood glucose was 593 mg/dL and serum osmolarity was 309 mOsm/kg. The seizures were controlled by normalization of blood sugar and short-term anticonvulsant, and the lesions were resolved in a follow-up MRI. We report a case of visual seizures associated with non-ketotic hyperglycemia.

A Case of Retroperitoneal Paraganglioma Manifested as Intractable Constipation with Paralytic Ileus and Aggravated Hyperglycemia.: Seung Joon Hwang, Mi kwang Kwon, Suk Chon; J Korean Endocr Soc. 2008;23(6):450-455. Published online December 1, 2008; DOI: https://doi.org/10.3803/jkes.2008.23.6.450

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Abstract PDF: Paragangliomas are extra-adrenal pheochromocytomas that arise from specialized neural crest cells. They are distributed anywhere from the upper neck to the pelvic floor, and they are classified on the basis of their anatomic origin. Functioning paragangliomas can cause the same clinical manifestations as pheochromocytoma, such as hypertension, diabetes mellitus, hyperadrenergic spells and so on. We experienced a retroperitoneal paraganglioma that was found in 66 year-old male who suffered from intractable constipation, and his constipation was caused by paralytic ileus and uncontrolled hyperglycemia. After he was diagnosed, removal of the paraganglioma was done and his clinical symptoms and sustained hyperglycemia were successfully resolved.

Original Articles

The Abundance and Nuclear Distribution of TonEBP in Response to Changes of Tonicity in Hyperglycemic Cells .: Won Kun Park; J Korean Endocr Soc. 2004;19(5):501-510. Published online October 1, 2004

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Abstract PDF: BACKGROUND
TonEBP (Tonicity-responsive enhancer binding protein) regulates the transcription of tonicity responsive genes, such as sodium-myo-inositol and the sodium- chloride-betaine co- transporters (SMIT & BGT1), heat shock protein 70 (HSP70) and aldose reductase (AR). To characterize the signals that activate TonEBP in hyperglycemic human retinal pigment epithelial (hRPE) cells, the abundance and nuclear distribution of TonEBP were studied in response to changes of tonicity in culture media. METHODS: After the cultures reached confluence, the hRPE cells were exposed for 3 days to 25 mM glucose and 100 mM NaCl, both with and without 20 M tolrestat. The expressions of AR, SMIT and HSP 70 were determined by northern blot, and the abundances of TonEBP by western blot. The nuclear distributions of TonEBP were observed by fluorescence microscopy, after immuno staining. RESULTS: The AR and SMIT mRNA levels in hyperglycemic and hypertonic media were decreased compared to those in hypertonic media alone. These decreased AR and SMIT mRNA expressions were also observed to be significantly prevented in those cells incubated with tolrestat. Stimulation of TonEBP in hypertonic medium occurs due to a combination of an increased abundance of TonEBP and an increased distribution into the nucleus from the cytoplasm. However, the expressions and nuclear distributions of TonEBP in hyperglycemic and hypertonic media were not different from those in hypertonic media alone. CONCLUSION: The expressions of AR and SMIT genes that may influence the development of diabetic complication were down-regulated by the intracellular accumulation of sorbitol in sustained hyperglycemia. TonEBP does not play a key role in the hypertonicity-induced transcriptional regulation of AR and SMIT in hyperglycemic cells, due to the intracellular accumulation of sorbitol and depletion of myo-inositol

Effect of Acute Hyperglycemia - and Isoproterenol - induced Hypothalamic Somatostatin Release on the Thyroid Hormone Releasing Hormone - induced Thyroid Stimulating Hormone Secretion.: Cheol Young Park, In Myung Yang, Seung Joon Oh, Deog Yoon Kim, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi; J Korean Endocr Soc. 2000;15(4-5):486-492. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Acute hyperglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion and thyroid stimulating hormone (TSH) from the anterior pituitary gland. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. Recently, We demonstrated that isoproterenol, a beta-adrenergic agonist, had an additional suppressive effect on the suppression by glucose of GHRH-stimulated GH response. Therefore, the present study aimed to determine whether isoproterenol has an additional suppressive effect on the suppression by glucose of TRH-stimulated TSH response. METHODS: Seven healthy young men, aged 24 to 27 years, were studied. Four different TRH stimulation tests were carried out. (Test 1) TRH (Hoechst AG, Germany), 200 microgram bolus, was given intravenously at 0 minute. (Test 2) Glucose, 100 g, was given orally 30 min before TRH administration. (Test 3) Isoproterenol(Isuprel, Sanofi Winthrop, USA), 0.012 pg/kg, was infused continuously for 120 min after TRH administration. (Test 4) After pretreatment with glucose as Test 2, isoproterenol and TRH were administered as Test 3. RESULTS: Oral glucose ingestion significantly suppressed the TRH-stimulated TSH secretion. Isoproterenol infusion significantly suppressed the TRH-stimulated TSH secretion. Glucose-induced suppression of the TSH response was significantly greater than that by isoproterenol. 1soproterenol infusion after glucose pretreatment did not show any additional suppressive effect on the glucose-induced suppression of TSH response to TRH. CONCLUSION: The results suggest that isoproterenol infusion in addition to glucose pretreatment before the TRH stimulation test is not necessary for the development of stronger stimulation test for the hypothalamic somatostatin secretion.

Effect of Isoproterenol on the Glucose-induced Hypothalamin Somatostatin Release.: Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, In Myoung Yang, Jung Taek Woo, Chul Young Park, Sun Woo Kim, Jung Hyun Ro, Sang Hwa Kim, Seung Joon Oh, Duk Yoon Kim; J Korean Endocr Soc. 1999;14(2):255-264. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Acute hypoglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion from the anterior pituitary gland. However, the exact mechanism of glucose increases the hypothalamic SRIH secretion is not well known. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. We, therefore, hypothesized that the glucose-induced SRIH release may be mediated by the stimulation of the central beta-adrenergic system, and investigated to determine whether a beta-adrermgic aganist, isoproterenol, contribute the suppressive effect of glucose on the GHRH-induced GH secretian. METHODS: Ten healthy young men, aged 23 to 26 years, were studied. Four endocrinological tests were carried out. (Test 1) GHRH (Bachem, CA, U.S.A.), 100pg bolus, was given intravenously at 0 minute. (Test 2) Glucose 100 gm dissolved in water, was given orally at -30 minute and GHRH was administered as Test 1. (Test 3) Isoproterenol (Isuprel, Sanofi Winthrop, USA), 0.012 mg/kg, wasinfused continuously between 0 minute and 120 minute, and GHRH was administered as Test 1. (Test 4) Isoproterenol, 0.012 mg kg was infused continuously between 0 minute and 120 minute, and glucose and GHRH were administered as Test 2. RESULTS: Oral glucose ingestion significantly suppressed the GHRH-induced GH secretion. The acute hyperglycemia significantly suppressed GHRH-induced GH secretion. The pretreatments with isoproterenol significantly suppressed the GHRH-induced GH levels. The pretreatment with glucose and isoproterenol suppressed the GHRH-induced GH levels more compared to those induced by glucose in Test 2. The GH levels in Test 4 did not significantly differ from those in Test 3. CONCLUSION: The results of this study suggests that the hypothalamic somatostatinergic activity induced by the oral glucose administeration is not mediated by the beta-adrenergic pathway in normal men. (J Kor Soc Endocrinool 14:255-264, 1999)

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