Bibliografías temáticas / Glucocorticoids-Induced diabetes

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Literatura académica sobre el tema "Glucocorticoids-Induced diabetes"

Autor: Grafiati

Publicado: 15 de febrero de 2025

Última modificación: 31 de julio de 2025

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Artículos de revistas sobre el tema "Glucocorticoids-Induced diabetes"

Nurullina, G. I. "Glucocorticoid pulse therapy аnd carbohydrate metabolism in rheumatic diseases". Kazan medical journal 94, № 6 (2013): 920–23. http://dx.doi.org/10.17816/kmj1820.

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Glucocorticoids are used in clinical practice for more than 50 years and are a great advance in the treatment of systemic inflammatory diseases. High doses of intravenous glucocorticoids (pulse therapy) are effective in conditions requiring rapid immunosuppression and antiinflammatory effect, such as systemic lupus erythematosus, rheumatoid arthritis, glomerulonephritis and systemic vasculitides. The advantage of this method are increased efficacy and lower rate of complications associated with prolonged administration of glucocorticoids. At the same time, glucocorticoid pulse therapy is assoc

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Wardani, Indah Sapta. "Steroid Induced Diabetes Mellitus: An Overview." JURNAL SAINS TEKNOLOGI & LINGKUNGAN 9, no. 1 (2023): 206–13. http://dx.doi.org/10.29303/jstl.v9i1.441.

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Glucocorticoids are often used as immunosuppressant and anti-inflammatory therapy in various medical conditions. In addition to providing clinical benefits, glucocorticoids have various side effects, one of which is related to steroid-induced diabetes mellitus (SIDM). Steroid-induced diabetes mellitus can be a new onset or an exacerbation of hyperglycemia in patients who have previously been diagnosed with DM. Acute and chronic hyperglycemia due to steroids can have an impact on lengthening hospitalization, infectious complications, decreased response to therapy and increased mortality. The ch

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Nykytiuk, L. A. "Diabetes Mellitus Induced by Exogenous Administration of Glucocorticoids." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY, no. 8.80 (January 12, 2017): 17–19. http://dx.doi.org/10.22141/2224-0721.8.80.2016.89532.

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Rana, M. Asim, Mujtaba H. Siddiqui, Sitara Raza, et al. "Incidence of Steroid-induced Diabetes in COVID-19 patients." Pakistan Journal of Medical and Health Sciences 15, no. 10 (2021): 2595–96. http://dx.doi.org/10.53350/pjmhs2115102595.

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Background: Since the COVID-19 pandemic has started, glucocorticoids have been proved to be one of the most effective lifesaving treatments for respiratory complications associated with SARS CoV-2. Aim: To review the incidence of steroid induced diabetes and the associated risk factors in COVID-19 patients. Study Design: Retrospective cohort study Place and duration of the study: Bahria International Hospital Lahore from 15th April 2020 to 31st December 2020 Methodology: Two hundred and thirty patients of COVID-19 cases treated with glucocorticoids (Dexamethasone 4mg BID) were enrolled. All kn

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Oğuz, Seda Hanife. "Management of glucocorticoid-induced diabetes." Acta Medica 55 (December 3, 2024): 17–21. https://doi.org/10.32552/2024.actamedica.1097.

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Glucocorticoid-induced diabetes (GID) is a frequent metabolic complication of glucocorticoid therapy. It results from both insulin resistance and impaired insulin secretion, exacerbated by glucocorticoid use. Despite its prevalence, consensus guidelines on screening and management remain limited. GID affects approximately one in five patients receiving long-term glucocorticoid therapy. Risk factors include older age, high BMI, prediabetes, ethnicity, and high-dose systemic glucocorticoids. All patients initiated on moderate to high doses of glucocorticoids should be assessed for GID risk facto

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Schakman, O., H. Gilson, and J. P. Thissen. "Mechanisms of glucocorticoid-induced myopathy." Journal of Endocrinology 197, no. 1 (2008): 1–10. http://dx.doi.org/10.1677/joe-07-0606.

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Glucocorticoid-induced muscle atrophy is characterized by fast-twitch or type II muscle fiber atrophy illustrated by decreased fiber cross-sectional area and reduced myofibrillar protein content. Muscle proteolysis, in particular through the ubiquitin– proteasome system (UPS), is considered to play a major role in the catabolic action of glucocorticoids. The stimulation by glucocorticoids of the UPS is mediated through the increased expression of several atrogenes (‘genes involved in atrophy’), such as atrogin-1 and MuRF-1, two ubiquitin ligases involved in the targeting of protein to be degra

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Schultz, Helga, Birthe Krogh Rasmussen, Peter Lommer Kristensen, Andreas Kryger Jensen, and Ulrik Pedersen-Bjergaard. "Early incidence of glucocorticoid-induced diabetes in patients with brain tumors: a retrospective study of the first 7 days of treatment." Neuro-Oncology Practice 5, no. 3 (2017): 170–75. http://dx.doi.org/10.1093/nop/npx027.

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Abstract Background Hyperglycemia or diabetes is a well-known side effect of treatment with glucocorticoids. In patients with brain tumors, glucocorticoids are widely used to treat symptoms of peritumoral edema. We conducted a retrospective study of patients with suspected brain tumor to determine the incidence of and risk factors for glucocorticoid-induced diabetes. Methods This was a retrospective study of patients referred with suspected brain tumor to a neurological department, using data from a clinical database, electronic medical records, the laboratory system, and the pathology informa

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Aberer, Felix, Daniel A. Hochfellner, Harald Sourij, and Julia K. Mader. "A Practical Guide for the Management of Steroid Induced Hyperglycaemia in the Hospital." Journal of Clinical Medicine 10, no. 10 (2021): 2154. http://dx.doi.org/10.3390/jcm10102154.

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Glucocorticoids represent frequently recommended and often indispensable immunosuppressant and anti-inflammatory agents prescribed in various medical conditions. Despite their proven efficacy, glucocorticoids bear a wide variety of side effects among which steroid induced hyperglycaemia (SIHG) is among the most important ones. SIHG, potentially causes new-onset hyperglycaemia or exacerbation of glucose control in patients with previously known diabetes. Retrospective data showed that similar to general hyperglycaemia in diabetes, SIHG in the hospital and in outpatient settings detrimentally im

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Nangalama, A. W., and G. P. Moberg. "Interaction between cortisol and arachidonic acid on the secretion of LH from ovine pituitary tissue." Journal of Endocrinology 131, no. 1 (1991): 87–94. http://dx.doi.org/10.1677/joe.0.1310087.

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ABSTRACT In several species, glucocorticoids act directly on the pituitary gonadotroph to suppress the gonadotrophin-releasing hormone (GnRH)-induced secretion of the gonadotrophins, especially LH. A mechanism for this action of these adrenal steroids has not been established, but it appears that the glucocorticoids influence LH release by acting on one or more post-receptor sites. This study investigated whether glucocorticoids disrupt GnRH-induced LH release by altering the liberation of arachidonic acid from plasma membrane phospholipids, a component of GnRH-induced LH release. Using perifu

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Thompson, E. Brad. "Mechanisms of T-cell Apoptosis Induced by Glucocorticoids." Trends in Endocrinology & Metabolism 10, no. 9 (1999): 353–58. http://dx.doi.org/10.1016/s1043-2760(99)00187-3.

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Tesis sobre el tema "Glucocorticoids-Induced diabetes"

Tijani, Omolara Khadijat. "Glucocorticoids and Intracrine Cortisol Metabolism in human Islets : Impact on Glucose Stimulated Insulin secretion." Electronic Thesis or Diss., Université de Lille (2022-....), 2024. http://www.theses.fr/2024ULILS061.

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Une exposition excessive aux glucocorticoïdes (GC), comme observée chez les patients recevant une corticothérapie, peut entraîner un dysfonctionnement des cellules β et un diabète chez jusqu'à 40% des patients. Dans l'obésité, une surexposition locale au cortisol secondaire à une altération du métabolisme du cortisol contribue à l'apparition du diabète. Des doses élevées de GC comme la dexaméthasone (DEX) inhibent la sécrétion d'insuline stimulée par le glucose (SISG), mais les effets de doses plus faibles et des autres GC, tels que l'hydrocortisone (HC) et la prednisone (PRED), restent peu ét

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Capítulos de libros sobre el tema "Glucocorticoids-Induced diabetes"

Mazziotti, Gherardo, Andrea Giustina, Ernesto Canalis, and John P. Bilezikian. "Glucocorticoid-induced osteoporosis." In Oxford Textbook of Endocrinology and Diabetes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0497.

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Synthetic glucocorticoids are used in a wide variety of disorders including autoimmune, pulmonary, and gastrointestinal diseases, as well as in patients following organ transplantation and with malignancies. Although the indications for glucocorticoids in these various conditions are clear, their use is fraught with a host of potential side effects. In particular, glucocorticoids are detrimental to bone and glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis (1). Despite the fact that glucocorticoids can cause bone loss and fractures, many patients recei

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Mazziotti, Gherardo, Ernesto Canalis, and John P. Bilezikian. "Glucocorticoid-Induced Osteoporosis." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0092.

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Glucocorticoid-induced osteoporosis (GIO), the most frequent form of secondary osteoporosis, is caused by chronic exposure to glucocorticoid excess. Glucocorticoids have several direct and indirect effects on the skeleton making multifactorial the pathogenesis of GIO. Fragility fractures occur early in GIO and antiosteoporotic drugs along with calcium and vitamin D should be started soon after exposure to glucocorticoid excess. Despite several guidelines and consensus recommendations stating that patients are at a remarkably increased fracture risk, little attention is paid to this risk and gu

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Kaan Akturk, Halis, and Aaron Michels. "Case 19: Immune Checkpoint Inhibitor–Induced Type 1 Diabetes." In Diabetes In Practice: Case Studies with Commentary. American Diabetes Association, 2021. http://dx.doi.org/10.2337/9781580407663.19.

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A 64-year-old Caucasian male with no previous history of diabetes presented with nausea, vomiting, fatigue, increased urination, and thirst over the 3 days before presentation, along with worsening of his mental status. He was being treated with pembrolizumab (monoclonal antibody targeting programmed cell death receptor-1 [PD-1]) infusions for advanced lung cancer. His most recent dose was 3 days before presentation, and his first dose was 24 days prior. He had a normal BMI (24.8 kg/m2), and the only pertinent past medical history was hypertension before the diagnosis of lung cancer. He has a

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