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Books on the topic 'Glucocorticoids – Therapeutic use'

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Published: 4 June 2021

Last updated: 25 January 2023

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1

Pelt, Annemarie C. Glucocorticoids: Effects, action mechanisms, and therapeutic uses. Hauppauge, N.Y: Nova Science, 2011.

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2

Wolthers, Ole D. Exogenous glucocorticoids in paediatric asthma. Trivandrum: Transworld Research Network, 2007.

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3

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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4

Rudy, Capildeo, ed. Steroids in diseases of the central nervous system. Chichester: Wiley, 1989.

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5

Ian, Adcock, and Chung K. Fan 1951-, eds. Overcoming steroid insensitivity in respiratory disease. Chichester, West Sussex: J. Wiley, 2008.

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6

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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7

(Editor), N. J. Goulding, and R. J. Flower (Editor), eds. Glucocorticoids (Milestones in Drug Therapy). Birkhauser, 2001.

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8

Kuhn, Andrew L. Effects of prednisolone on neuromusclar transmission. 1986.

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9

Christian, Korting Hans, and Maibach Howard I, eds. Topical glucocorticoids with increased benefit/risk ratio. Basel: Karger, 1993.

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10

(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.

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11

Inhaled glucocorticoids in asthma: Mechanisms and clinical actions. New York: Dekker, 1997.

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12

Hodgkiss, Andrew. Therapeutic strategies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0013.

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A wide range of therapeutic strategies to manage cancer-related psychopathology are described. Evidence-based interventions include: surgery (e.g. oophorectomy for anti-NMDAR limbic encephalitis), radiotherapy, immunotherapy, anti-glucocorticoids, correction of electrolyte abnormalities, correction of vitamin or endocrine deficiencies, and the use of carefully selected antidepressant or antipsychotic medication. Particular attention is paid to the management of cancer-related delirium and mania, and to the depressive phenomena provoked by systemic cancer treatments. The quality of the evidence-base for these treatments is critically reviewed.

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13

(Editor), Robert P. Schleimer, William W. Busse (Editor), and Paul O'Byrne (Editor), eds. Inhaled Glucocorticoids in Asthma: Mechanisms and Clinical Actions (Lung Biology in Health and Disease). Informa Healthcare, 1997.

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14

Schleimer/Obyrn. Inhaled Steroids in Asthma: Optimizing Effects in the Airways (Lung Biology in Health and Disease). Informa Healthcare, 2001.

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15

Glucocorticoids and mechanisms of asthma: Clinical and experimental aspects : proceedings of a symposium in Toronto, 18-19, November 1988. Amsterdam: Excerpta Medica, 1989.

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16

Glucocorticoids and Mechanisms of Asthma: Clinical and Experimental Aspects: Proceedings of a Symposium in Toronto, 18-19 November 1988 (Current cli. Excerpta Medica, 1989.

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17

Bahiru, Gametchu, ed. Glucocorticoid receptor structure and leukemic cell responses. New York: Springer-Verlag, 1995.

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18

Schleimer, Robert P., and Henry N. Claman. Anti-Inflammatory Steroid Action: Basic and Clinical Aspects. Academic Pr, 1989.

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19

P, Schleimer Robert, Claman Henry N. 1930-, and Oronsky Arnold L, eds. Anti-inflammatory steroid action: Basic and clinical aspects. San Diego: Academic Press, 1989.

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20

Schleimer, Robert P., and Henry N. Claman. Anti-Inflammatory Steroid Action: Basic and Clinical Aspects. Academic Pr, 1989.

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21

I, Maibach Howard, and Surber Christian 1955-, eds. Topical corticosteroids. Basel: Karger, 1992.

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22

Enno, Christophers, ed. Topical corticosteroid therapy: A novel approach to safer drugs. New York: Raven Press, 1988.

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23

(Editor), H. W. Mollmann, and B. May (Editor), eds. Glucocorticoid Therapy in Chronic Inflammatory Bowel Disease: From Basic Principles to Rational Therapy (Falk Symposium). Springer, 1996.

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24

Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0133.

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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 long-standing 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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25

Pipitone, Nicolò, Annibale Versari, and Carlo Salvarani. Large-vessel vasculitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0133_update_003.

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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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26

P, Schleimer Robert, ed. Inhaled steroids in asthma: Optimizing effects in the airways. New York: Marcel Dekker, 2002.

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27

Schleimer, Robert P. Inhaled Steroids in Asthma: Optimizing Effects in the Airways. Taylor & Francis Group, 2001.

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28

Schleimer, Robert P. Inhaled Steroids in Asthma: Optimizing Effects in the Airways. Taylor & Francis Group, 2001.

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29

Schleimer, Robert P. Inhaled Steroids in Asthma: Optimizing Effects in the Airways. Taylor & Francis Group, 2001.

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30

Schleimer, Robert P. Inhaled Steroids in Asthma: Optimizing Effects in the Airways. Taylor & Francis Group, 2001.

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31

Schleimer, Robert P. Inhaled Steroids in Asthma: Optimizing Effects in the Airways. Taylor & Francis Group, 2001.

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32

Sauvage, Alexandre, and Maxime Levy. Dexamethasone: Therapeutic Uses, Mechanism of Action and Potential Side Effects. Nova Science Publishers, Incorporated, 2013.

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33

Adcock, Ian, and Kian Fan Chung. Overcoming Steroid Insensitivity in Respiratory Disease. Wiley & Sons, Limited, John, 2008.

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34

Sahetya, Sarina. Acute Uncomplicated Bronchitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0029.

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Acute bronchitis is a respiratory illness characterized predominantly by cough with or without sputum production that lasts for up to 3 weeks in the presence of normal chest radiography. Additional presenting symptoms include rhinorrhea, congestion, sneeze, sore throat, wheezing, low-grade fever, myalgia, and fatigue. Causative organisms include viral and bacterial pathogens. The disease course is characterized by self-limited inflammation of the airways. Chest radiographs should be utilized to distinguish acute bronchitis from pneumonia or interstitial disease. Therapeutic recommendations are typically supportive; however, studies reveal that between 60% and 80% of patients receive unwarranted antibiotic therapy. Only those patients at high risk for serious complications (including patients over 65 with a history of hospitalization, diabetes mellitus, congestive heart failure, or current use of oral glucocorticoids) usually require routine antibiotic therapy directed toward both typical and atypical bacterial pathogens.

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35

Lahita, Robert, J. W. J. Bijlsma, Alfonse Masi, and Rainer Straub. Basic and Clinical Aspects of Neuroendocrine Immunology in Rheumatic Diseases (Annals of the New York Academy of Sciences). Blackwell Publishing Limited, 2006.

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36

Henter, Ioline D., and Rodrigo Machado-Vieira. Novel therapeutic targets for bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0030.

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The long-term course of bipolar disorder (BD) comprises recurrent depressive episodes and persistent residual symptoms for which standard therapeutic options are scarce and often ineffective. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors have consistently been implicated in the pathophysiology of mood disorders and in the development of novel therapeutics for these disorders. Since the rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000, other NMDA receptor antagonists have been studied in major depressive disorder (MDD) and BD. This chapter reviews the clinical evidence supporting the use of novel glutamate receptor modulators for treating BD—particularly bipolar depression. We also discuss other promising, non-glutamatergic targets for potential rapid antidepressant effects in mood disorders, including the cholinergic system, the melatonergic system, the glucocorticoid system, the arachidonic acid (AA) cascade, and oxidative stress and bioenergetics.

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