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Books on the topic 'Immunosuppressive agents Mechanism of action'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

B, Strom T., ed. The mode of action of immunosuppressive agents. 2nd ed. Amsterdam: Elsevier Science Publishers, 1985.

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2

Bach, J. F. The mode of action of immunosuppressive agents. 2nd ed. Amsterdam: Elsevier, 1985.

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3

1937-, Toyama Junji, and Hondeghem Luc, eds. Current topics in antiarrhythmic agents: Mode of action and clinical usage : International Satellite Symposium of the 53rd Annual Meeting of the Japanese Circulation Society, Nagoya, Japan, March 27-28, 1989. Amsterdam: Excerpta Medica, 1989.

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4

Hiroshi, Takagi, ed. Regulatory roles of neuropeptides: Proceedings of the Sixth Workshop on Neurotransmitters and Diseases, Kobe, June 17, 1989. Amsterdam, The Netherlands: Excerpta Medica, 1989.

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5

M, Pinedo H., and Schornagel J. H, eds. Platinum and other metal coordination compounds in cancer chemotherapy 2. New York: Plenum Press, 1996.

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6

International Symposium on Platinum and Other Metal Coordination Compounds in Cancer Chemotherapy (6th 1991 San Diego, Calif.). Platinum and other metal coordination compounds in cancer chemotherapy. New York: Plenum Press, 1991.

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7

S, Abraham, and Amitai G, eds. Calcium channel modulators in heart and smooth muscle: Basic mechanisms and pharmacological aspects : proceedings of the 33rd [i.e. 34th] Oholo Conference, Eilat, Israel, 1989. Rehovot, Israel: Balaban Publishers, 1990.

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8

Fever and antipyresis: The role of the nervous system. Cambridge: Cambridge University Press, 1995.

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9

Misbah, Siraj. Immunosuppressive therapy and therapeutic monoclonal antibodies. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0302.

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The term immunosuppressive therapy encompasses all forms of treatment that dampens function of the recipient’s immune system, with a view to controlling severe autoimmune, inflammatory, or allergic disease. The predominant targets of these agents are T-lymphocytes with multiple downstream effects, including containment of T-cell activation, inhibition of cytokine production, restriction of clonal expansion, and varying degrees of suppression of B-cell function. This chapter reviews the clinical use of monoclonal antibodies and other immunosuppressive agents, and their mechanisms of action.
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10

McCulloh, Russell J., and Steven M. Opal. Drug-induced depression of immunity in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0290.

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Immunosuppressive drugs are among the fastest-growing category of drugs in medicine today, both in terms of new medication development and in terms of use. Glucocorticoids, calcineurin inhibitors, and biological agents, among others, are used in a variety of diseases. . Although often of great benefit to patients, immunosuppressive agents also pose significant long-term risks for opportunistic infection. These drugs can also blunt normal host responses to infection, and patients receiving immunosuppressive medications are at high risk for severe illness, sepsis, and death from opportunistic infections. Knowledge of immunosuppressive agents, their mechanisms of action, effects on the immune system, and commonly-associated infectious complications plays an instrumental role in guiding appropriate diagnostic and treatment plans for immunosuppressed patients. This chapter reviews the most commonly-used immunosuppressive agents today, and provides the reader with the specific effects these medications can have on a patient’s immune system and the potential infectious agents of concern associated with their prolonged use.
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11

W, Thomson Angus, ed. The Molecular biology of immunosuppression. Chichester: Wiley, 1992.

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12

Hahn, Fred E. Mechanism of Action of Antibacterial Agents. Springer, 2012.

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13

Patrick, Graham. Antimalarial Agents: Design and Mechanism of Action. Elsevier, 2020.

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14

Hahn, Fred E. Mechanism of Action of Antieukaryotic and Antiviral Compounds. Springer, 2012.

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15

(Editor), Junji Toyama, and Luc M. Hondeghem (Editor), eds. Current Topics in Antiarrhythmic Agents (Current clinical practice series). Elsevier, 1989.

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16

(Editor), K. F. Tipton, and Federico, M.D. Dajas (Editor), eds. Neurotoxins in Neurobiology: Their Actions and Applications (Ellis Horwood Books in the Biological Sciences). Ellis Horwood, 1994.

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17

F, Tipton Keith, and Dajas Federico, eds. Neurotoxins in neurobiology: Their actions and applications. New York: Ellis Horwood, 1994.

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18

Neurotoxins in Neurobiology: Their Actions and Applications (Ellis Horwood Books in the Biological Sciences). Ellis Horwood, 1994.

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19

V, Trach, ed. Specific heart rate reducing effect of UL-FS 49 Cl: Electrophysiological mechanism of action. Ulm: Universitätsverlag Ulm, 1991.

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20

A, Hickman John, and Tritton Thomas R, eds. Cancer chemotherapy. Oxford: Blackwell Scientific Publications, 1993.

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21

Kameyama, Kuriyama, Nagatsu, and Yoshida. Regulatory Roles of Neuropeptides (International Congress Series). Excerpta Medica, 1990.

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22

Cognitive Enhancing Drugs (Milestones in Drug Therapy). Birkhäuser Basel, 2004.

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23

Platinum and Other Metal Coordination Compounds in Cancer Chemotherapy 2. Springer, 1996.

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24

Kay, Brune, Santoso B. 1950-, and International Symposium on Antipyretic Analgesics (1990 : Yogyakarta, Indonesia), eds. Antipyretic analgesics: New insights : Yogyakarta, March 30th, 1990. Basel: Birkhäuser Verlag, 1992.

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25

BRUNE and SANTOSO. Antipyretic Analgesics : New Insights. Birkhauser, 1992.

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26

Yogyakarta, Indonesia) International Symposium on Antipyretic Analgesics (1990 :. Antipyretic Analgesics: New Insights : Yogjakarta, March 30, 1990. Birkhauser, 1999.

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27

(Editor), Randy J. Read, and Joel L. Sussman (Editor), eds. Evolving Methods for Macromolecular Crystallography: The Structural Path to the Understanding of the Mechanism of Action of CBRN Agents (NATO Science Series II: Mathematics, Physics and Chemistry). Springer, 2008.

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28

(Editor), Randy J. Read, and Joel L. Sussman (Editor), eds. Evolving Methods for Macromolecular Crystallography: The Structural Path to the Understanding of the Mechanism of Action of CBRN Agents (NATO Science Series II: Mathematics, Physics and Chemistry). Springer, 2007.

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29

1949-, Dangman Kenneth H., and Miura Dennis Senji 1943-, eds. Electrophysiology and pharmacology of the heart: A clinical guide. New York: M. Dekker, 1991.

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30

A, Montgomery S., and Corn Timothy H, eds. Psychopharmacology of depression. Oxford: Oxford University Press, 1994.

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31

Suri, Ajay, and Jean R. McEwan. Anti-anginal agents in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0037.

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Angina is chest pain resulting from the lack of blood supply to heart muscle most commonly due to obstructive atherosclerotic. Intensive care unit patients are subject to various stresses that will increase the demand on the heart and are in a pro-thrombotic state. Patients in an intensive treatment unit may be sedated and so cardiac ischaemia may be detected by electrocardiogram, haemodynamic monitoring, and echocardiographic imaging of function. These signs may indicate critical coronary perfusion heralding a myocardial infarction and are alleviated by anti-anginal drugs. Beta-blockers and calcium channel blockers are the usual first-line treatments for angina, but may not be ideal in the critically-ill patient. Nitrates reduce blood pressure without typically affecting heart rate. Nicorandil is a similar mechanism of action and tends to be given orally, while ivabridine, an If channel blocker, is a newer anti-anginal, which acts by reducing heart rate, while not affecting blood pressure. Ranolazine is the one of the newest anti-anginal agents and is believed to alter the transcellular late sodium current thereby decreasing sodium entry into ischaemic myocardial cells.
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32

McCracken, Lindsay M., Mandy L. McCracken, and R. Adron Harris. Mechanisms of Action of Different Drugs of Abuse. Edited by Kenneth J. Sher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199381678.013.010.

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Drugs of abuse represent a spectrum of chemically diverse compounds that are used via various routes of drug administration depending on the drug and its preparation. Although the exact molecular mechanisms by which these agents act to produce their intoxicating effects are not completely understood, many drugs of abuse are known to bind to specific neuronal membrane proteins that produce effects on cellular signaling and ultimately on behavior. With repeated administration of a drug, individuals often develop tolerance, and discontinuation of drug use following chronic administration typically results in withdrawal symptoms. This chapter describes the mechanism of action for the following classes of drugs of abuse: alcohol, cannabinoids, hallucinogens, inhalants, nicotine, opioids, sedative hypnotics, and stimulants. In addition, mechanisms of tolerance and withdrawal are discussed.
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33

Ch, Kessler, Medizinische Universität zu Lübeck. Klinik für Neurologie., and Symposium on Platelet-Vessel Wall Interaction (1989 : Lübeck, Germany), eds. Platelets and atherosclerosis. Berlin: Springer-Verlag, 1990.

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34

1925-, Papirmeister Bruno, ed. Medical defense against mustard gas: Toxic mechanisms and pharmacological implications. Boca Raton: CRC Press, 1991.

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35

Abraham, Shlomo, and Gabriel Amitai. Calcium Channel Modulators in Heart and Smooth Muscle: Basic Mechanisms and Pharmacological Aspects: Proceedings of the 33rd Oholo Conference, eilat. VCH Publishing, 1991.

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36

1960-, Ozawa H., Saito Toshikazu, Takahata Naohiko 1932-, Nihon Seishin Shinkei Gakkai, and Symposium on Affective Disorders and Neuronal Signal Transduction (1996 : Sapporo-shi, Japan), eds. Signal transduction in affective disorders. Tokyo: Springer, 1998.

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37

Immunopharmacology. Springer Verlag, 1990.

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38

Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). Urinalysis may be normal or show low-grade proteinuria (< 1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
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39

1946-, Stephens David N., ed. Anxiolytic [Beta]-carbolines: From molecular biology to the clinic. Berlin: Springer-Verlag, 1993.

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40

Stephens, David N. Anxiolytic B-Carbolines: From Molecular Biology to the Clinic (Psychopharmacology Series). Springer-Verlag Telos, 1993.

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41

Török, M. Estée, Fiona J. Cooke, and Ed Moran. Antiparasitic therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0005.

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This chapter provides a systematic summary of antiparasitic agents, grouped by class and mechanism of action. Each summary provides information on the mode of action, resistance mechanisms, pharmacology, and clinical use.
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42

Török, M. Estée, Fiona J. Cooke, and Ed Moran. Antifungals. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0003.

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This chapter provides a systematic summary of antifungal agents, grouped by class and mechanism of action. Each summary provides information on the mode of action, mechanisms of resistance, pharmacology, and clinical use.
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43

Török, M. Estée, Fiona J. Cooke, and Ed Moran. Antivirals. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199671328.003.0004.

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This chapter provides a systematic summary of antiviral agents, grouped by class and mechanism of action. Each summary provides information on the mode of action, mechanisms of resistance, pharmacology, and clinical use.
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44

J, Garland C., and Angus James A, eds. The pharmacology of vascular smooth muscle. Oxford: Oxford University Press, 1996.

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45

Foo, Joanne, Benazir Saleem, and Philip G. Conaghan. Analgesics. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0078.

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Pain is one of the commonest presenting symptoms of musculoskeletal disorders and may be one the hardest to treat successfully. The available analgesic options provide different modes of action and their ranks continue to expand with new agents, some with multiple target action. This chapter reviews currently available analgesics (paracetamol and opioids) used for managing musculoskeletal pain and the agents used for neuropathic pain, including their mechanism of action, pharmacokinetics and side effects. The role of neuroleptic agents is reviewed, and a brief outline of some newer therapies for the treatment of pain such as tapentadol, and a potential therapy, anti-nerve growth factor monoclonal antibodies.
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46

Iversen, Leslie. The Pharmacology of Delta-9-Tetrahydrocannabinol (THC). Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190846848.003.0002.

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The 19th century was a great era for plant chemistry. Many complex drug molecules, known as alkaloids, were isolated and identified from plants. This chapter discusses the history of the discovery of delta-9-tetrahyrocannabinol (THC) as the psychoactive substance in cannabis products and also the discovery of the cannabinoid receptors CB-1 and CB-2 in the body and brain. The mechanism of action of cannabinoids on such receptors to inhibit neurotransmitter release or other actions is also discussed. In addition, various methods for the ingestion of cannabis, such as smoking and vaping, are reviewed. Synthetic agonists and antagonists at cannabinoid receptors and the proliferation of synthetic agonists as novel psychoactive agents are also discussed.
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47

Ross, Lisa. Electroconvulsive Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190495756.003.0029.

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The anesthetic management of patients who receive electroconvulsive therapy (ECT) for various psychiatric conditions in both the inpatient and the outpatient settings must take into account a number factors, such as its associated physiologic responses, existing comorbidities, medication management, monitoring, complications, and contraindications in order for it to remain a safe procedure. This chapter reviews the indications for ECT, the preprocedure anesthetic evaluation; theories regarding the therapeutic mechanism of action leading to the efficacy of ECT; cerebrovascular, cardiovascular, and neuroendocrine responses and monitoring standards. Furthermore, it discusses the selection of medications for induction, inhalational agents, and muscle relaxants as well as common drug interactions and premedication practices. The chapter culminates with an assessment of the morbidity and mortality associated with ECT both anesthetic and nonanesthetic related.
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48

Cromey, Catherine, and Susan Catling. Adjuvant drugs in neuraxial anaesthesia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0017.

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The addition of adjuvants to local anaesthetics for use in labour epidurals or for intrathecal administration is common practice in obstetric anaesthesia. This chapter provides an overview of the pharmacology of receptors within the epidural and intrathecal spaces and discusses the options available. Adjuncts are classified as opioid and non-opioid and each agent is explored in detail. The mechanism of action, clinical uses, effective dose ranges, speeds of onset and duration, side effects, disadvantages, and special circumstances associated with each agent are explored. Where formal guidelines exist, these are discussed in detail. Although large randomized controlled trial data is lacking, information regarding current knowledge of the behaviour of these agents in obstetric and non-obstetric practice is presented to assist clinicians when deciding about the appropriateness of each agent for their individual practice.
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49

Mease, Philip. Biologic treatments for psoriatic arthritis apart from TNF inhibition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0030.

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Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressive structural damage of joints. However, not all patients responded to these agents and many patients displayed initial response which waned over time, partly due to immunogenicity (development of antibodies which blocked full therapeutic effect of the biologic protein), or because of tolerability and side effect issues. Thus, it has been important to develop new medicines which target other key cytokines and immunologic pathways. Several medicines with a different mechanism of action have been approved or are in development for the treatment of PsA. Ustekinumab inhibits both IL12 and IL23 and thus is felt to work in both the TH1 and TH7 pathways of inflammation. The oral medicine apremilast inhibits phosphodiesterase 4, thus modulating the cyclic AMP pathway in immunologic cells, yielding an anti-inflammatory effect. Both of these medicines have been approved for the treatment of PsA as well as psoriasis. An emerging group of therapies, the IL17 inhibitors, has demonstrated significant effectiveness in psoriasis and PsA and one of these, Secukinumab, has been approved for psoriasis, PsA, and AS. Other medicines in development include the co-stimulatory blockade agent, abatacept, oral Janus Kinase (JAK) inhibitors, and an emerging group of therapies which inhibit IL23. As modulators of immune cell function, these agents have the potential to increase risk for infection, as well as other side effects. These must be discussed with the patient and considered when determining overall risk benefit analysis regarding their use. The emergence of medicines with a different mechanism of action than TNF inhibition has broadened and strengthened our ability to effectively treat PsA.
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50

Zuddas, Alessandro, Tobias Banaschewski, David Coghill, and Mark A. Stein. ADHD treatment. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198739258.003.0041.

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Stimulants are effective medications and should be used as one of the main pharmacological options for the management of ADHD in children, adolescents, and adults. They all inhibit catecholamine uptake, but they differ for specific aspects of the mechanism of action, pharmacokinetics, as well as on efficacy for specific patients. Short-term efficacy in reducing ADHD symptoms is well established, as is the safety profile for these agents. There is increasing evidence that ADHD symptom improvement generally translates or corresponds to improved functioning and quality of life. Stimulant treatment should be based on a comprehensive assessment and diagnosis, including full medical history and physical examination, and it should always be part of a comprehensive treatment plan that includes psychological, behavioural, and educational advice and interventions. Medication treatment should be closely monitored for both common and unusual (but potentially serious) adverse events.
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