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Journal articles on the topic "Glucocorticoids – Therapeutic use"
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Grbovic, Leposava, and Miroslav Radenkovic. "Therapeutic use of glucocorticoids and immunosuppressive agents." Srpski arhiv za celokupno lekarstvo 133, Suppl. 1 (2005): 67–73. http://dx.doi.org/10.2298/sarh05s1067g.
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Pharmacotherapy of autoimmune thyroid disease (AITD) is complex. Apart from the replacement hormone therapy, antithyroid agents, beta adrenoceptor blockers and other drugs, in regard to the present symptoms, it also includes the administration of glucocorticoids and immunosuppressive agents. Physiological actions of glucocorticoids are significant in number, well known and described in details. The most prominent pharmacological properties of glucocorticoids, that are important for their clinical use, are antiinflammatory and immunosuppressive actions. In this article, the most notable clinical pharmacology aspects of glucocorticoids have been presented, including the basic principles of their therapeutic use, as well as the most important indications with the examples of dosing regiments (rheumatic disorders, renal diseases, allergic reactions, bronchial asthma, gastrointestinal inflammatory diseases, thrombocytopenia, organ transplantation, and Graves? ophthalmopathy). In addition, adverse and toxic effects of glucocorticoids as well as their interactions with other drugs have been described. Immunosuppressive agents have important role in treatment of immune disorders, including the reduction of immune response in autoimmune diseases and organ transplantation. Apart from glucocorticoids, immunosuppressive agents consist of calcineurin inhibitors (cyclosporine, tacrolimus), antiproliferative and antimetabolic agents (sirolimus, azathioprine, mycophenolate mofetil, methotrexate, cyclophosphamide), monoclonal antibodies: anti-CD3 antibody (muromonab-CD3), anti- CD25 antibody (daclizumab), anti-TNF-alpha antibody (infliximab). In this part, the most updated facts about mechanism of action, rational therapeutic use, as well as adverse and toxic effects of immunosuppressive agents have been reviewed.
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Ouanes, S. "Glucocorticoid-based therapeutic options for PTSD." European Psychiatry 33, S1 (March 2016): S215. http://dx.doi.org/10.1016/j.eurpsy.2016.01.521.
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IntroductionPTSD has been associated with HPA axis alterations, mainly consisting of reduced cortisol levels, elevated CRH and enhanced glucocorticoid receptor responsiveness. These findings led to the emergence of glucocorticoid-based therapeutic options for PTSD.ObjectiveTo outline the different glucocorticoid-based interventions for PTSD either for prophylactic or for curative treatment.MethodsA systematic review was performed. The Medline database was searched using the following keywords: ‘PTSD’, ‘treatment’, ‘Glucocorticoids’, ‘hydrocortisone’.ResultsGlucocorticoid-based therapeutic for PTSD comprise preventive and curative interventions. Preventive interventions mainly consist of administering one single bolus of hydrocortisone shortly following the exposure to a traumatic event. Evidence comes from six published trials, all positive. Curative interventions include: prescribing hydrocortisone over short periods of time to treat PTSD symptoms, using Glucocorticoids to augment psychotherapy (in particular exposure therapy) for PTSD and using Mifepristone, a glucocorticoid receptor antagonist. Moreover, novel glucocorticoid receptor modulators are currently being developed and tested on animal models as a potential curative treatment for PTSD.ConclusionsUse of hydrocortisone in preventing PTSD might be tempting, as is the use of hydrocortisone or Glucocorticoid receptors antagonists/modulators in treating PTSD. Yet, it should be emphasized that these interventions are not mainstream yet. They rather reflect a revolutionary new direction.Disclosure of interestThe author has not supplied his/her declaration of competing interest.
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Kamada, Alan K. "Therapeutic Controversies in the Treatment of Asthma." Annals of Pharmacotherapy 28, no. 7-8 (July 1994): 904–14. http://dx.doi.org/10.1177/106002809402800716.
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OBJECTIVE: To introduce readers to the current controversial topics in the area of asthma therapy. Background is provided such that clinicians are aware of these issues and can make rational decisions. DATA SOURCES: Pertinent articles were individually identified and reviewed from each journal. STUDY SELECTION: Relevant studies, determined by topic and other specific criteria, e.g., testing methodology, were included. DATA SYNTHESIS: Further investigation is required in the areas discussed. Systemic effects, specifically growth suppression (in children), adrenal suppression, and osteoporosis, have been demonstrated with high-dose inhaled glucocorticoids; however, the clinical relevance of such intravenous glucocorticoid formulations via nebulizer have not been demonstrated. Likewise, data on the equivalence of the inhaled glucocorticoids, with regard to efficacy and potential systemic effects, and the differences between metered-dose inhalers and dry powder inhalers, with regard to aerosol characteristics and drug delivery, are unclear. Theophylline, when used with inhaled β-adrenergic agonists and systemic glucocorticoids for the treatment of acute asthma, as not been shown to provide clear benefit and may result in increased adverse effects. The use of regular (vs. “as needed” or prn) inhaled β-adrenergic agonists, although shown in two studies to be detrimental to the control of asthma and result in an increased risk of death or near death caused by asthma, has not been conclusively demonstrated to be harmful. CONCLUSIONS: Monitoring for adverse effects and the use of techniques to minimize systemic absorption (spacers and mouth rinsing) are recommended when high-dose inhaled glucocorticoid therapy is used. Intranasal and intravenous glucocorticoid products are not recommended for administration via nebulizer because of safety concerns. Until further data are available, inhaled glucocorticoids are thought to be equivalent on a μg-per-μg basis rather than an actuation-per-actuation basis. Theophylline is no longer recommended for treatment of acute exacerbations in nonhospitalized patients not already receiving the medication, and the link between deterioration of asthma control (and the risk for death) and regular inhaled beta-adrenergic agonists appears weak.
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Hughes, David, Nicole Vlahovich, Marijke Welvaert, Nicolin Tee, Peter Harcourt, Susan White, Alan Vernec, Ken Fitch, and Gordon Waddington. "Glucocorticoid prescribing habits of sports medicine physicians working in high-performance sport: a 30-nation survey." British Journal of Sports Medicine 54, no. 7 (February 5, 2020): 402–7. http://dx.doi.org/10.1136/bjsports-2019-101175.
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ObjectivesGlucocorticoids are commonly prescribed in medicine. When administered via certain routes, glucocorticoids are prohibited for incompetition use by WADA. The glucocorticoid prescribing habits of sports medicine doctors have not been reported.MethodsAn online survey was distributed internationally to physicians working in high-performance sports. The survey queried the doctors about their use of glucocorticoids with athletes and their understanding of WADA’s regulations regarding glucocorticoid use in competition.Results603 sports medicine doctors from 30 different countries participated. The majority (>85%) routinely injected glucocorticoids and/or prescribed glucocorticoids by other routes. There were substantial differences in the common routes of injection as well as types of glucocorticoid used among the physicians from various countries. A relatively small percentage of sports doctors (<25%) accurately identified which routes of glucocorticoid administration are prohibited in competition by WADA. There was a great variation in how long before competition the use of glucocorticoids would cause the doctor to consider applying for a therapeutic use exemption (TUE). A better understanding of the clearance rates of glucocorticoids from athletes’ bodies would greatly aid sports medicine doctors’ decisions on how and when to apply for a TUE. A small number of doctors had observed side effects of glucocorticoid administration, with the majority of side effects being minor in nature.ConclusionGlucocorticoids are widely prescribed by sports physicians. There is a need to better educate sports physicians on the current WADA regulations in relation to glucocorticoid administration.
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López, Francisco J., Robert J. Ardecky, Bruce Bebo, Khalid Benbatoul, Louise De Grandpre, Sha Liu, Mark D. Leibowitz, et al. "LGD-5552, an Antiinflammatory Glucocorticoid Receptor Ligand with Reduced Side Effects, in Vivo." Endocrinology 149, no. 5 (January 24, 2008): 2080–89. http://dx.doi.org/10.1210/en.2007-1353.
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Treatment of inflammation is often accomplished through the use of glucocorticoids. However, their use is limited by side effects. We have examined the activity of a novel glucocorticoid receptor ligand that binds the receptor efficiently and strongly represses inflammatory gene expression. This compound has potent antiinflammatory activity in vivo and represses the transcription of the inflammatory cytokine monocyte chemoattractant protein-1 and induces the antiinflammatory cytokine IL-10. The compound demonstrates differential gene regulation, compared with commonly prescribed glucocorticoids, effectively inducing some genes and repressing others in a manner different from the glucocorticoid prednisolone. The separation between the antiinflammatory effects of LGD-5552 and the side effects commonly associated with glucocorticoid treatment suggest that this molecule differs significantly from prednisolone and other steroids and may provide a safer therapeutic window for inflammatory conditions now commonly treated with steroidal glucocorticoids.
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Otlewska, Anna, Grzegorz Szpotowicz, and Agnieszka Otlewska. "Effects of glucocorticoids on the skin." Pediatria i Medycyna Rodzinna 16, no. 3 (October 30, 2020): 257–60. http://dx.doi.org/10.15557/pimr.2020.0047.
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Glucocorticoids are widely used in the treatment of many diseases. They have multiple therapeutic applications mainly because of their anti-inflammatory, immunosuppressive and antiproliferative activity. Glucocorticoids are broadly used in the therapy of dermatological diseases. Various routes of glucocorticoids administration are known. In the treatment of skin disorders, glucocorticoids are often administered topically. It must be noted that glucocorticoid-induced complications may occur not only as a result of systemic treatment, but also topical application of glucocorticoids to the skin. Commonly reported cutaneous adverse effects resulting from glucocorticoid therapy include changes in facial appearance – rounded appearance of the face, redness, development of stretch marks, difficulty in wound healing, and easy bruising. It needs to be highlighted that glucocorticoids also affect metabolism, water and electrolyte balance, and bones. Therefore, in addition to dermatological disorders, they may also cause many other types of complications. As a result, a degree of caution is advised in the use of drugs of this class. In order to reduce the risk of adverse effects, glucocorticoids should be used at the smallest effective dose for the shortest possible time.
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Ponticelli, Claudio, and Francesco Locatelli. "Glucocorticoids in the Treatment of Glomerular Diseases." Clinical Journal of the American Society of Nephrology 13, no. 5 (February 23, 2018): 815–22. http://dx.doi.org/10.2215/cjn.12991117.
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Glucocorticoids exert anti-inflammatory and immunosuppressive activities by genomic and nongenomic effects. The classic genomic effects are mediated by cytosolic glucocorticoid receptors that can upregulate the expression of anti-inflammatory proteins in the nucleus (transactivation) or repress the translocation of proinflammatory transcription factors from the cytosol into the nucleus (transrepression). The nongenomic effects are probably mediated by membrane glucocorticoid receptors. Glucocorticoid receptors are expressed also in podocytes and experimental data suggest that glucocorticoids may protect from podocyte injury. Glucocorticoids have a low therapeutic index and may exert a number of time-dependent and dose-dependent side effects. Measures to prevent or attenuate side effects include single-morning administration of short-acting glucocorticoids, dietetic counseling, increasing physical activity, frequent monitoring, and adapting the doses to the clinical conditions of the patient. Synthetic glucocorticoids, either given alone or in combination with other immunosuppressive drugs, are still the cornerstone therapy in multiple glomerular disorders. However, glucocorticoids are of little benefit in C3 glomerulopathy and may be potentially deleterious in patients with maladaptive focal glomerulosclerosis. Their efficacy depends not only on the type and severity of glomerular disease, but also on the timeliness of administration, the dosage, and the duration of treatment. Whereas an excessive use of glucocorticoids can be responsible for severe toxicity, too low a dosage and too short duration of glucocorticoid treatment can result in false steroid resistance.
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van der Goes, Marlies C., Johannes W. G. Jacobs, and Johannes W. J. Bijlsma. "Rediscovering the therapeutic use of glucocorticoids in rheumatoid arthritis." Current Opinion in Rheumatology 28, no. 3 (May 2016): 289–96. http://dx.doi.org/10.1097/bor.0000000000000278.
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Ruiz-Irastorza, Guillermo, Amaia Ugarte, Ioana Ruiz-Arruza, and Munther Khamashta. "Seventy years after Hench’s Nobel prize: revisiting the use of glucocorticoids in systemic lupus erythematosus." Lupus 29, no. 10 (June 15, 2020): 1155–67. http://dx.doi.org/10.1177/0961203320930099.
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In 1950, Hench, Kendall and Reichstein were awarded with the Nobel Prize in Physiology and Medicine for the isolation and first therapeutic use of glucocorticoids. Since then, they have become one of the main agents in the treatment of systemic lupus erythematosus (SLE). The use of high-dose oral glucocorticoids (usually 1 mg/kg/day of prednisone equivalent) have become the rule for treating moderate to severe lupus activity. In addition, tapering schemes have not been well defined, all this leading to prolonged exposures to potentially damaging amounts of glucocorticoids. Several studies have shown that glucocorticoids are a major cause of toxicity in SLE in a dose-dependent manner, with prolonged doses greater than 7.5 mg/day being associated with damage accrual. Thus, there is an urgent need for different therapeutic schedules that can achieve a rapid and durable control of lupus activity while reducing the many unwanted effects of glucocorticoids. Recent data show that pulses of methyl-prednisolone are an effective first-line therapy to treat lupus flares (not only severe ones) without major short or long-term toxicity and allowing a reduction in oral prednisone doses. Universal use of hydroxychloroquine – always recommended, infrequently accomplished – and early therapy with immunosuppressive drugs also help control SLE and reduce prednisone load. Results from observational studies confirm the more rapid achievement of remission and the reduction of long-term damage using these combination schedules with reduced prednisone doses. Seventy years after their first therapeutic use, we are learning to use glucocorticoids in a more efficient and safe manner.
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Sjögren, Sara E., and Johan Flygare. "Progress towards Mechanism-Based Treatment for Diamond-Blackfan Anemia." Scientific World Journal 2012 (2012): 1–8. http://dx.doi.org/10.1100/2012/184362.
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Diamond-Blackfan anemia (DBA) is a congenital erythroid hypoplastic anemia, characterized by macrocytic anemia, reticulocytopenia, and severely reduced numbers of erythroid precursors in the bone marrow. For more than fifty years, glucocorticoids have remained the main option for pharmacological treatment of DBA. While continuous glucocorticoid administration increases hemoglobin levels in a majority of DBA patients, it also causes severe side effects. There is therefore a great need for more specific and effective treatments to boost or replace the use of glucocorticoids. Over the years, many alternative therapies have been tried out, but most of them have shown to be ineffective. Here we review previous and current attempts to develop such alternative therapies for DBA. We further discuss how emerging knowledge regarding the pathological mechanism in DBA and the therapeutic mechanism of glucocorticoids treatment may reveal novel drug targets for DBA treatment.
Dissertations / Theses on the topic "Glucocorticoids – Therapeutic use"
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Wyrwoll, Caitlin Sarah. "Adverse developmental programming of the adult phenotype by fetal glucocorticoid excess and its prevention by postnatal dietary Omega-3 fatty acids." University of Western Australia. School of Anatomy and Human Biology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0164.
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[Truncated abstract] Increased incidence of hypertension, insulin resistance, obesity and dyslipidemia, collectively referred to as the metabolic syndrome, has been linked to low birth weight, an indicator of a poor fetal environment. This association reflects developmental programming, a process by which organ systems are affected during early development such that disease states are more likely to emerge in adult life. Fetal glucocorticoid overexposure is thought to be a key factor that mediates developmental programming. Accordingly, maternal treatment with the synthetic glucocorticoid dexamethasone retards fetal growth and leads to delayed puberty, hypertension, hyperinsulinemia, and hyperleptinemia, either with or without increased adiposity, in adult offspring. Importantly, the postnatal environment can either amplify or attenuate the long-term outcome of developmental programming. The focus of this thesis was whether adverse developmental programming outcomes can be attenuated by the postnatal environment and thus provide therapeutic potential. Specifically, the effects of a postnatal diet rich in omega-3 fatty acids on glucocorticoid-induced developmental programming outcomes was investigated. ... The adipocyte phenotype was examined in Study 6, with hyperleptinaemia evident in offspring at 6 and 12 months of age in dexamethasone-exposed animals on a standard omega-3 diet, but this effect was prevented by a high omega-3 diet. The pattern of plasma leptin was paralleled by changes in leptin mRNA in retroperitoneal fat. Similarly, plasma levels of the inflammatory markers IL-6 and IL-1β were upregulated by prenatal glucocorticoid exposure and these were attenuated by postnatal dietary omega-3 fatty acids. Overall, omega-3 ingestion reduced adiposity, as indicated by measures of body composition. In conclusion, the studies presented in this thesis demonstrate for the first time that many of the detrimental effects of excess glucocorticoid exposure in utero on the adult phenotype can be attenuated by a postnatal diet rich in omega-3 fatty acids. This beneficial effect of omega-3 fatty acids was associated with a reversal of some (e.g. adiposal leptin) but not all (e.g. renal GR) 'programmed' changes in gene expression. These findings raise the possibility that dietary supplementation with omega-3 fatty acids may provide a viable therapeutic option for preventing and/or reducing adverse programming outcomes in humans.
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Hewitt, Damien Phillip. "Impact of glucocorticoids on placental growth and vascularisation." University of Western Australia. School of Anatomy and Human Biology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0195.
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[Truncated abstract] Glucocorticoids are critical for the maturation of the fetus late in pregnancy. Indeed, clinical administration of glucocorticoids is used to accelerate fetal lung maturation in mothers at risk of pre-term delivery. Increased glucocorticoid exposure, however, can have detrimental effects on fetal and placental growth and increase the risk of disease in later life. Many studies have focused on the effect of an increase in the transplacental passage of glucocorticoids on both fetal growth and subsequent postnatal development. But there is a growing body of evidence to suggest that the impact of glucocorticoids on fetal growth is mediated, in part, via their direct effects on the placenta . . . Overall, these studies quantify the labyrinth zone-specific increases in placental expression of PPARG and VEGF in association with a marked increase in vascularisation observed near term. Furthermore, this study demonstrates for the first time that these increases in gene expression are prevented by maternal dexamethasone treatment which also inhibits growth of the fetal capillary network. Elevated expression of SFRP4 in the regressing basal zone late in gestation and in both placental zones after dexamethasone-induced placental growth restriction is consistent with a role for SFRP4 in glucocorticoid-mediated inhibition of wnt signalling. Collectively, the data presented in this thesis show that glucocorticoid inhibition of fetal growth is mediated in large part via effects on the placenta, specifically through inhibition of signals that promote proliferation and vascularisation.
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Schloms, Lindie. "The inhibition of adrenal steroidogenic enzymes and modulation of glucocorticoid levels in vitro and in vivo by aspalathus linearis (rooibos)." Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97000.
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Thesis (PhD)--Stellenbosch University, 2015.ENGLISH ABSTRACT: This study describes: • the influence of a methanolic extract of unfermented Rooibos and five major Rooibos flavonoids, aspalathin, nothofagin, rutin, orientin and vitexin, on the activities of key adrenal steroidogenic enzymes - cytochrome P450 17β- hydroxylase/17,20-lyase (CYP17A1), 3β-hydroxysteroid dehydrogenase • the development of a novel UPLC-MS/MS method for the separation and quantification of 21 adrenal steroid metabolites; • the influence of Rooibos and aforementioned flavonoids on adrenal steroid hormone production in H295R cells - a human adrenal carcinoma cell line expressing the enzymes catalysing the production of mineralocorticoids, glucocorticoids and adrenal androgens, assayed under both basal (normal) and forskolin-stimulated (stressed) conditions; • the influence of Rooibos on the inter-conversion between cortisol and cortisone by 11βHSD1 and 11βHSD2 expressed in CHO-K1 cells; • the influence of Rooibos consumption on circulating steroid hormone levels and ratios in male Wistar rats; • the influence of Rooibos consumption on circulating steroid hormone levels and ratios in male and female human test subjects at risk for developing cardiovascular disease. (3βHSD2), cytochrome P450 21-hydroxylase (CYP21A2) and cytochrome P450 11β-hydroxylase (CYP11B1), expressed in non-steroidogenic COS-1 cells;
AFRIKAANSE OPSOMMING: Hierdie studie beskryf: • die invloed van metanoliese ekstrakte van ongefermenteerde Rooibos en vyf van die hoof flavonoïedverbindings in Rooibos, aspalatien, notofagien, rutien, oriëntien en viteksien, op die aktiwiteite van ensieme wat steroïedbiosintese in die bynier kataliseer – sitochroom P450 17α-hidroksilase/17,20-liase (CYP17A1), 3β-hidroksisteroïed dehidrogenase (3βHSD2), sitochroom P450 21-hidroksilase (CYP21A2) en sitochroom P450 11β-hidroksilase (CYP11B1), uitgedruk in nie-steroïed produserende COS-1 selle; • die ontwikkeling van ‘n geskikte UPLC-MS/MS metode vir die skeiding en kwantifisering van 21 steroïedmetaboliete in die bynier; • die invloed van Rooibos en die bg. flavonoïede op steroïedproduksie in H295R selle – ‘n menslike bynier kanker sellyn gekenmerk deur die ekspressie van die steroidogeniese ensieme wat die produksie van mineralokortikoïede, glukokortikoïede en bynierandrogene kataliseer, geanaliseer onder beide basale (normale) en forskoliengestimuleerde (gestresde) kondisies; • die invloed van Rooibos op die omeenskakeling tussen kortisol en kortisoon deur 11βHSD1 and 11βHSD2 in CHO-K1 selle; • die invloed van Rooibosinname op vlakke van sirkulerende steroïed hormone en relatiewe verhoudings in die bloed van manlike Wistarrotte; • die invloed van Rooibosinname op sirkulerende steroïed hormoon vlakke en relatiewe verhoudings in die bloed van mans en vrouens met ‘n hoë risiko vir die ontwikkeling van kardiovaskulêre siektes.
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Stubsrud, Elisabeth. "An investigation of the role of phosphorylation at Ser211 of the glucocorticoid receptor in ligand-specific transcriptional regulation." Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/2497.
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Thesis (MSc (Biochemistry))--University of Stellenbosch, 2005.Endogenous glucocorticoids (GCs) modulate many physiological functions in the human body and synthetic GCs are the most effective therapy in the treatment of inflammation, autoimmune and endocrine disorders. However, the long-term usage of synthetic GCs is associated with severe side-effects. GCs mediate their effects through the ligand-dependent transcription factor, the glucocorticoid receptor (GR), either by causing an increase (transactivation) or a decrease (transrepression) in gene transcription. The bioactivity of a ligand in GR-mediated transcriptional regulation is established by a transcriptional doseresponse curve, where the potency (EC50 value) and the efficacy (maximal response) of the ligand are determined. A central question is how different GR ligands elicit their differential physiological responses for the same gene in the same cell. The main aim of this thesis is to investigate if the phosphorylation of GR at serine 211 (Ser211) correlates with the potency and/or efficacy of a particular ligand in transactivation and transrepression of gene expression.
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Ng, Man-ting, and 吳憫婷. "The transcriptional control of aquaporins." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42182219.
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Huynh, Tony. "Selective glucocorticoid receptor modulation as a therapeutic option in dystrophic muscle." Phd thesis, 2014. http://hdl.handle.net/1885/155870.
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Duchenne Muscular Dystrophy is a devastating neuromuscular condition defined by the absence of the integral sarcolemma-associated protein, dystrophin, and characterised by myofibre necrosis, muscle regeneration, inflammatory infiltration, and premature satellite cell senescence. The anti-inflammatory properties of glucocorticoids, mediated predominantly through monomeric glucocorticoid receptor inhibition of transcription factors such as NF-kappaB (transrepression), are postulated to be an important mechanism for their beneficial effects in Duchenne Muscular Dystrophy. The chronic use of supraphysiological doses of glucocorticoids in Duchenne Muscular Dystrophy is associated with well-recognised glucocorticoid-related side effects such as growth suppression, reduced bone mineral density and increased fracture rates, muscle atrophy, and metabolic disturbances such as increased adiposity, impaired glucose tolerance, and insulin resistance. It has been postulated that these detrimental effects are mediated through direct glucocorticoid homodimer interactions with glucocorticoid response elements (transactivation). Compound A is a non-steroidal selective glucocorticoid receptor modulator with the ability to bind the glucocorticoid receptor and induce transrepression, without promoting glucocorticoid receptor dimerization (Section 1.7.3). It has the theoretical potential to attenuate and modulate the inflammatory signature in dystrophic muscle without the associated adverse systemic effects. These properties were tested in the mdx mouse, a model of Duchenne Muscular Dystrophy. The in vitro cell studies performed in Chapter 3 confirm the anti- NF-kappaB activity of Compound A in H-2Kb-tsA58 mdx myoblasts and myotubes and demonstrate the absence of glucocorticoid receptor-mediated transactivation of genes that represent the basis for hypothalamic-pituitary-adrenal axis suppression. The in vivo studies involving the mdx mouse model in Chapters 4 to 7 provide information pertaining to the bioactivity, potential toxicity, as well as the extent and nature of positive benefits of Compound A treatment in dystrophic muscle. Intraperitoneal but not oral Compound A at doses up to 7.5mg/kg/day had significant positive effects on muscle strength and inflammation in mdx mice. When administered via the intraperitoneal route at 7.5mg/kg/day, Compound A caused detrimental effects on muscle mass and voluntary locomotor activity in WT mice. Intraperitoneal Compound A treatment in mdx mice from a postnatal age of 18 days increased the absolute and normalised forelimb and hindlimb grip strength, attenuated cathepsin-B activity in forelimb and hindlimb muscles, decreased serum creatine kinase levels, and reduced Interleukin-6, Chemokine (C-C motif) ligand 2, Interferon-gamma, Tumour Necrosis Factor, and Interleukin-12p70 cytokine levels in gastrocnemii muscles. Compared with Compound A, prednisolone treatment in mdx mice increased osteopontin (Spp1) gene expression and osteopontin protein levels, and had less favourable effects on expression of genes that determine muscle mass including Foxo1, Foxo3, Fbxo32, and Trim63, as well as hepatic Igf1. In conclusion, the results of these studies confirm the integral role of glucocorticoid receptor-mediated transrepression in improving pathological features in the mdx mouse model. Selective glucocorticoid receptor modulation by Compound A may represent a more effective therapeutic strategy in Duchenne Muscular Dystrophy, with advantages over glucocorticoids. However, this therapeutic potential may be limited by its associated toxicity profile.
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Herbert, Cristan Medical Sciences Faculty of Medicine UNSW. "Effects of glucocorticoid and phosphodiesterase-4 inhibitor therapy in a mouse model of chronic asthma." 2007. http://handle.unsw.edu.au/1959.4/40535.
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Asthma is a chronic inflammatory disease of the airways. Using a murine model which replicates many characteristic features of human asthma, this study evaluated the effects of treatment with anti-inflammatory drugs on the lesions of chronic asthma, and investigated potential underlying molecular mechanisms. Treatment with dexamethasone, a glucocorticoid, was compared with roflumilast, a novel phosphodiesterase-4 (PDE4) inhibitor. BALB/c mice sensitised to ovalbumin were challenged with a low mass concentration of aerosolised antigen for 30 min/day, 3 days/week for 6 weeks. In weeks 5 and 6, groups of animals were treated with either dexamethasone or roflumilast. Assessment included changes in acute-on-chronic inflammation, structural remodelling of the airways and airway hyper-responsiveness to a bronchoconstrictor stimulus. These were correlated with the expression of pro-inflammatory cytokines and growth factors. Compared to vehicle-treated control animals, dexamethasone- and roflumilast-treated mice exhibited reduced accumulation of intra-epithelial eosinophils and chronic inflammatory cells, including CD3+ T-lymphocytes in the airways. Similarly, both drugs inhibited subepithelial fibrosis and airway epithelial thickening, although only dexamethasone inhibited goblet cell hyperplasia/metaplasia. Airway hyper-reactivity was not diminished by either drug. Both treatments suppressed production of Th2 cytokines by ovalbumin-restimulated peribronchial lymph node cells. In selectively dissected airway tissue from vehicletreated animals, increased expression of mRNA for several pro-inflammatory cytokines (TNF-α, GM-CSF, IL-6) and cytokines characteristic of Th1 (IFN-γ), Th2 (IL-5, IL-13)and Th17 (IL-17A) cells was demonstrated using real-time PCR. Enhanced expression of growth factors (TGF-β1 and FGF-2) was also demonstrated in airway epithelium isolated by laser capture microdissection. Interestingly, whereas treatment with dexamethasone significantly inhibited expression of mRNA for all of the inflammationrelated cytokines examined, roflumilast inhibited only IL-17A, TNF-α, GM-CSF and IL-6. Both drugs inhibited mRNA expression of growth factors by epithelial cells. Because roflumilast was as effective as dexamethasone in suppressing inflammation and most changes of remodelling, the selective suppression of IL-17A, TNF-α, GM-CSF and IL-6 suggests that these mediators, or the cells that produce them, may have critical roles in pathogenesis. Furthermore, they may be particularly appropriate therapeutic targets in chronic asthma.
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Burt, Morton Garth St Vincent's Clinical School UNSW. "Mechanisms underlying glucocorticoid-induced protein wasting and potential treatment with anabolic hormoness." 2007. http://handle.unsw.edu.au/1959.4/41293.
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Protein wasting is a complication of glucocorticoid (GC) therapy. It causes substantial morbidity and there is no treatment. This thesis investigates the metabolic mechanisms underlying GC-induced protein wasting and the potential for anabolic hormones to reverse protein loss. The models of GC excess were Cushing's syndrome and GC therapy. Whole body protein metabolism was assessed using the leucine turnover technique and body composition by dual-energy X-ray absorptiometry to estimate lean body mass (LBM) and fat mass (FM). As previous studies demonstrated that LBM and FM influenced rates of protein metabolism, the magnitude of body compositional abnormality in Cushing's syndrome was determined. After accounting for the greater FM (30%) and lesser LBM (15%), protein metabolism in Cushing's syndrome was characterised by a significant increase in protein oxidation, an abnormality that leads to irreversible protein loss. Successful treatment of Cushing's syndrome normalised protein oxidation. Studies of the acute and chronic effects of therapeutic GCs revealed a time-dependent effect on protein metabolism. GCs acutely increased protein oxidation. However, the rate of protein oxidation during chronic therapy at a similar dose was not significantly different to untreated control subjects. This time-dependent change suggests that GC-induced stimulation of protein oxidation does not persist and could represent a metabolic adaptation to limit protein loss. This finding contrasts with that in Cushing's syndrome, where protein oxidation is persistently elevated. This difference may represent a dose effect. Studies in GH-deficient subjects revealed that GH induced a fall in protein oxidation that was significantly correlated with a subsequent gain in LBM. This suggests that the anabolic potential of a therapeutic substance can be predicted by its ability to suppress protein oxidation acutely. Finally, the potential for GH and androgens to reverse the metabolic effects of GCs was assessed. A preliminary study in GC users revealed that a GH dose of 0.8 mg/d was effective in reducing protein oxidation. In a subsequent study, the GH-induced reduction in protein oxidation in women on GCs was enhanced by combined treatment with dehydroepiandrosterone, an androgen. In summary, GCs induce protein loss by stimulating protein oxidation. GH reverses this effect and this action is enhanced by coadministration of androgens. GH and androgens may be used therapeutically to prevent protein loss induced by GCs.
Books on the topic "Glucocorticoids – Therapeutic use"
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Pelt, Annemarie C. Glucocorticoids: Effects, action mechanisms, and therapeutic uses. Hauppauge, N.Y: Nova Science, 2011.
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Wolthers, Ole D. Exogenous glucocorticoids in paediatric asthma. Trivandrum: Transworld Research Network, 2007.
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C, Hogg James, Ellul-Micallef R, and Brattsand R, eds. Glucocorticosteroids, inflammation and bronchial hyperreactivity ; symposium at the 3rd Congress of the European Society of Pneumology, Basel, September 19, 1984. Amsterdam: Excerpta Medica, 1985.
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Rudy, Capildeo, ed. Steroids in diseases of the central nervous system. Chichester: Wiley, 1989.
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Ian, Adcock, and Chung K. Fan 1951-, eds. Overcoming steroid insensitivity in respiratory disease. Chichester, West Sussex: J. Wiley, 2008.
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M, Cutolo, and New York Academy of Sciences., eds. Basic and clinical aspects of neuroendocrine immunology in rheumatic diseases. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.
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(Editor), N. J. Goulding, and R. J. Flower (Editor), eds. Glucocorticoids (Milestones in Drug Therapy). Birkhauser, 2001.
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Kuhn, Andrew L. Effects of prednisolone on neuromusclar transmission. 1986.
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Christian, Korting Hans, and Maibach Howard I, eds. Topical glucocorticoids with increased benefit/risk ratio. Basel: Karger, 1993.
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(Editor), Tomoshige Kino, Evangelia Charmandari (Editor), and George P. Chrousos (Editor), eds. Glucocorticoid Action: Basic And Clinical Implications (Annals of the New York Academy of Sciences, V. 1024). New York Academy of Sciences, 2004.
Find full textBook chapters on the topic "Glucocorticoids – Therapeutic use"
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Spruill, William Jerry, and William Elton Wade. "Other Connective Tissue Disorders and The Use of Glucocorticoids." In Applied Therapeutics, 1555–69. London: Palgrave Macmillan UK, 1992. http://dx.doi.org/10.1007/978-1-349-13175-4_76.
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Mazziotti, Gherardo, Andrea Giustina, Ernesto Canalis, and John P. Bilezikian. "Glucocorticoid-induced osteoporosis." In Oxford Textbook of Endocrinology and Diabetes, 754–59. 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 receiving or initiating long-term glucocorticoid therapy are not evaluated for their skeletal health. Furthermore, patients often do not receive specific preventive or therapeutic agents when indicated. New knowledge of the pathophysiological mechanisms underlying GIO has been accompanied by the availability of effective strategies to prevent and treat GIO (1).
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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. "Large-vessel vasculitis." In Oxford Textbook of Rheumatology, 1113–24. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_004.
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Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
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Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. "Large-vessel vasculitis." In Oxford Textbook of Rheumatology, 1113–24. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_005.
Full textAbstract:
Large-vessel vasculitis includes giant cell arteritis (GCA) and Takayasu’s arteritis (TAK). GCA affects patients aged over 50, mainly of white European ethnicity. GCA occurs together with polymyalgia rheumatica (PMR) more frequently than expected by chance. In both conditions, females are affected two to three times more often than males. GCA mainly involves large- and medium-sized arteries, particularly the branches of the proximal aorta including the temporal arteries. Vasculitic involvement results in the typical manifestations of GCA including temporal headache, jaw claudication, and visual loss. A systemic inflammatory response and a marked response to glucocorticoids is characteristic of GCA. GCA usually remits within 6 months to 2 years from disease onset. However, some patients have a chronic-relapsing course and may require longstanding treatment. Mortality is not increased, but there is significant morbidity mainly related to chronic glucocorticoid use and cranial ischaemic events, especially visual loss. The diagnosis of GCA rests on the characteristic clinical features and raised inflammatory markers, but temporal artery biopsy remains the gold standard to support the clinical suspicion. Imaging techniques are also used to demonstrate large-vessel involvement in GCA. Glucocorticoids are the mainstay of treatment for GCA, but other therapeutic approaches have been proposed and novel ones are being developed. TAK mainly involves the aorta and its main branches. Women are particularly affected with a female:male ratio of 9:1. In most patients, age of onset is between 20 and 30 years. Early manifestations of TAK are non-specific and include constitutional and musculoskeletal symptoms. Later on, vascular complications become manifest. Most patients develop vessel stenoses, particularly in the branches of the aortic artery, leading to manifestations of vascular hypoperfusion. Aneurysms occur in a minority of cases. There are no specific laboratory tests to diagnose TAK, although most patients have raised inflammatory markers, therefore, imaging techniques are required to secure the diagnosis. Glucocorticoids are the mainstay of treatment of TAK. However, many patients have an insufficient response to glucocorticoids alone, or relapse when they are tapered or discontinued. Immunosuppressive agents and, in refractory cases, biological drugs can often attain disease control and prevent vascular complications. Revascularization procedures are required in patients with severe established stenoses or occlusions.
Conference papers on the topic "Glucocorticoids – Therapeutic use"
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Marques, Grazielle de Oliveira, Guilherme Rodrigues Fontes Moura, Gabriela Brill Ney, and Pablo Henrique da Costa Silva. "Neuromyelitis optica (NMO): treatment during pregnancy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.284.
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Background: NMO is a demyelinating autoimmune disorder of the CNS which affects the optic nerves and the spinal cord. Method: review based on papers from 2016 to 2020. Platforms used: MEDLINE and Pubmed. The descriptors: “NMO” AND “Treatment”. Objective: to review therapeutic approaches and restrictions for NMO during pregnancy. Case report: G.V.L, 17 years, 23 weeks pregnant, diagnosis of NMO in Dec/2020, with progressive loss of visual acuity and limbs paresthesia. The patient received intravenous methylprednisolone pulses 1g/5 days, followed by 7 sessions of plasmapheresis (PLEX), showing partial symptoms remission, prednisone 60 mg was maintained. March/2021: she presented symptoms reissue, cranial MRI w/o: nerves signal alteration, chiasma and bilateral optical tracts. Spine MRI w/o: slight signal alteration in the dorsal root of the spinal cord, which extends from C1 to C4. Other 5 sessions of PLEX were attempted, without improvement. Results: during pregnancy, intravenous glucocorticoid, Rituximab and Eculizumab proved to be safe in the treatment of NMO. PLEX is indicated in cases of remissions resistant to medications. The therapy with immunosuppressants, such as methotrexate, mycophenolate mofetil and mitoxantrone, isn’t recommended. These immunosuppressants can cause miscarriage or pose a risk to the fetus. However, the immunosuppressant azathioprine has a safety profile in pregnancy; furthermore, it is considered the most appropriate maintenance treatment in combination with prednisone. Conclusion: due to the risk of miscarriage and teratogenicity, NMO treatment during pregnancy is restrict to intravenous glucocorticoids, rituximab and eculizumab, and in specific cases PLEX.
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Freijanes, Loise Maria de Souza, Elisa Yuki Kurosawa Ueda, Paola Restum Antonio Lemaitre, and Isabela Pierotti Prado. "Tuberculous Meningitis: Literature Review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.163.
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Background: Tuberculous meningitis is the most severe form of M.tuberculosis infection, and occurs when there is an invasion of the membranes and cerebrospinal fluid by the bacteria. It develops as a complication of primary infection and reactivation in immunosuppressed. Objectives: This study aims to characterize tuberculous meningitis and bring updates. Design and setting: This is a literature review from the Escola de Medicina Souza Marques‘s students, Brazil. Methods: The used articles were published between 2012 and 2021, from the UpToDate, Scielo, PubMed, and Google Scholar databases. Results: Relevant epidemiological factors, such as HIV, and the absence of the Tuberculosis vaccine could raise the diagnosis hypothesis for the disease. Furthermore, clinical features as headaches, myalgia, fever, emesis, and sudden mood swings are also red flags. Patients should always be tested for HIV infection since mortality in these cases is about 60%. Tuberculous meningitis has a high lethality due to the delay in diagnosis and, in the absence of therapeutics, it worsens the prognosis. The complications are hydrocephalus, cranial nerve paralysis, strabismus, and coma. The diagnostic methods include CSF examination, computed tomography, magnetic resonance imaging, and GeneXpert. The treatment consists of antituberculosis therapy with glucocorticoids. Conclusions: It is essential to identify the disease and start immediate treatment, in addition to emphasizing the BCG vaccine and HIV prevention to reduce cases.
Reports on the topic "Glucocorticoids – Therapeutic use"
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Ma, He, Jifu Zhao, and Zhilei Wang. Efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2022. http://dx.doi.org/10.37766/inplasy2022.9.0114.
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Review question / Objective: This study is the protocol for a systematic review to evaluate the efficacy and safety of HuaYu TongFu Method combined with acupuncture in the treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease. we conducted a systematic review and meta-analysis of published randomized clinical trials (RCTs) of such combined therapy in the treatment of AECOPD, It provides a reliable scientific basis for clinicians to use this approach to treat AECOPD. Condition being studied: Chronic obstructive pulmonary disease is the third leading cause of death worldwide. AECOPD is the most common cause of hospitalization and death in patients with COPD. As lung function deteriorates and the disease progresses, the risk of alveolar hypoxia and consequent hypoxemia increases. Inflammation plays an important role in the progression of AECOPD. Modern medicine mainly treats AECPD by anti-inflammatory, relief of airway spasm, glucocorticoids, inhalants and other methods. Long-term application can easily lead to bacterial flora imbalance and drug resistance in patients. Comparatively, traditional Chinese medicine and acupuncture therapy are safe and effective.To assess the therapeutic efficacy and safety of HuaYu TongFu Method combined with acupuncture in AECOPD, we created a protocol for a systematic review to inform future clinical applications.