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Published: 10 December 2022
Last updated: 28 January 2023

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1

D, Wu Hao Ph, ed. TNF receptor associated factors (TRAFs). New York: Springer Science+Business Media, 2007.

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2

Tumor necrosis factor. New York: Nova Biomedical Books, 2009.

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3

Gregory, Bock, Marsh Joan, and Symposium on Tumour Necrosis Factor and Related Cytotoxins (1987 : London, England), eds. Tumour necrosis factor and related cytotoxins. Chichester: Wiley, 1987.

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4

Zurita, Maria Trinidad. Tumour necrosis factor inhibitory drugs in meningitis. Birmingham: University of Birmingham, 1994.

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5

S, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.

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6

Bock, Gregory, and Joan Marsh, eds. Ciba Foundation Symposium 131 - Tumour Necrosis Factor and Related Cytotoxins. Chichester, UK: John Wiley & Sons, Ltd., 1987. http://dx.doi.org/10.1002/9780470513521.

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7

Mahony, Susan Maria. Weight loss and metabolic alterations induced by recombinant tumour necrosis FACTOR-ALPHA (TNF). Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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8

service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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9

Ennis, Maurice. Tumour necrosis factor alpha and ultraviolet light activation of programmed cell death by apoptosis in D. melanogaster. Ottawa: National Library of Canada, 2001.

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10

Aerts, Joeri. Progesterone Induces Apoptosis in Eosinophilic Granulocytes & Induces Tumour Necrosis Factor-Alpha / Tumour Necrosis Factor Receptor. Leuven Univ Pr, 2002.

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11

Wu, Hao. TNF Receptor Associated Factors (TRAFs). Springer New York, 2010.

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12

Wu, Hao. TNF Receptor Associated Factors (TRAFs). Springer London, Limited, 2007.

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13

Wu, Hao. TNF Receptor Associated Factors (Advances in Experimental Medicine and Biology,). Springer, 2007.

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14

Tumor necrosis factor. Hauppauge, NY: Nova Science, 2009.

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15

Angelo, Corti, and Ghezzi P, eds. Tumor necrosis factor: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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16

Tumor necrosis factor: Methods and protocols. Totowa, N.J: Humana Press, 2004.

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17

(Editor), Angelo Corti, and Pietro Ghezzi (Editor), eds. Tumor Necrosis Factor: Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2004.

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18

Symposium, CIBA Foundation. Tumour Necrosis Factor and Related Cytotoxins. John Wiley & Sons, 1989.

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19

Marsh, Joan, and Gregory R. Bock. Tumour Necrosis Factor and Related Cytotoxins. Wiley & Sons, Incorporated, John, 2008.

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20

Symposium, CIBA Foundation, Joan Marsh, and Gregory R. Bock. Tumour Necrosis Factor and Related Cytotoxins. Wiley & Sons, Limited, John, 2007.

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21

Symposium, Ciba Foundation. Tumour Necrosis Factor and Related Cytotoxins. Wiley & Sons, Incorporated, John, 2008.

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22

Ghezzi, Pietro, and Angelo Corti. Tumor Necrosis Factor: Methods and Protocols. Humana Press, 2010.

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23

Grewal, Iqbal S. Therapeutic Targets of the TNF Superfamily. Springer London, Limited, 2009.

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24

Grewal, Iqbal S. Therapeutic Targets of the TNF Superfamily: Volume 647. Springer, 2010.

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25

S, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.

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26

Dickstein, Jodi B. The effects of sleep and tumour necrosis factor-[alpha] on the lymphatic system. 1999.

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27

TNF -inhibition in the treatment of rheumatoid arthritis. London: Martin Dunitz, 2003.

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28

(Editor), Larry W. Moreland, and Paul Emery (Editor), eds. TNF-Inhibition in the Treatment of Rheumatoid Arthritis. Informa Healthcare, 2002.

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29

Kalthoff, Holger. Death Receptors and Cognate Ligands in Cancer. Springer, 2012.

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30

Hui-Yuen, Joyce Siu-Wah. The role of tumour necrosis factor-alpha in an animal model of Kawasaki disease. 2005.

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31

Hui-Yuen, Joyce Siu-Wah. The role of tumour necrosis factor-[alpha] in an animal model of Kawasaki disease. 2005.

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32

Myocardial dysfunction following ruptured abdominal aortic aneurysm repair: The role of tumour necrosis factor-[alpha]. Ottawa: National Library of Canada, 1999.

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33

Okoye, Remi. The production and contribution of tumour necrosis factor-[alpah] in the progrssion of experimental collagen-induced arthritis in mice. 1994.

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34

Death Receptors in Cancer Therapy (Cancer Drug Discovery and Development). Humana Press, 2004.

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35

Tumour Necrosis Factor Alpha and Atherogenic Index as Predictors of Insulin Resistance and Risks of Cardiovascular Disease Among Obese Subjects in Calabar, Nigeria. Grin Publishing, 2017.

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36

Bawa, Sandeep, Paul Wordsworth, and Inoshi Atukorala. Spondyloarthropathies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.010004.

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♦ Spondyloarthropathies are related conditions typically associated with axial skeletal involvement, absence of rheumatoid factor, familial clustering, and a variable positive association with HLA-B27♦ Ankylosing spondylitis is the prototype with sacroiliac joint involvement being a prerequisite for diagnosis♦ Diagnosis is frequently delayed for several years but the use of magnetic resonance imaging to detect sacroiliitis greatly facilitates the establishment of an early diagnosis♦ Psoriatic arthritis, reactive arthritis, and enteropathic arthritis have prominent peripheral joint involvement with variable degrees of spinal involvement♦ Non-steroidal anti-inflammatory drugs and physical therapy are the cornerstones of management but slow-acting disease-modifying antirheumatic drugs only have a role in peripheral arthritis♦ Anti-tumour necrosis factor biologic agents have revolutionized the treatment of the spondyloarthropathies.
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37

Müller-Quernheim, Joachim, Gernot Zissel, and Antje Prasse. Sarcoidosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0167.

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Sarcoidosis is a systemic disease characterized by non-necrotizing granulomata and manifestations in almost any organ. Diagnosis relies on the exclusion of other granulomatous disorders and a compatible pattern of symptoms and clinical findings. Inflammatory lesions and granulomata may undergo spontaneous resolution or persist in chronic disease with eventual fibrosis and permanent organ damage. Immunological disease mechanisms are linked to severe derangements of the cytokine network. In systemic resolution or under prednisolone therapy of symptomatic disease proinflammatory cytokines are downregulated and histological lesions may completely vanish. Corticosteroid-resistant disease, however, requires treatment with an immunosuppressive regimen consisting of prednisolone and an immunosuppressive agent or anti-tumour necrosis factor (TNF) monoclonal antibodies.
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38

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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39

Lie, Elisabeth, Tore Kristian Kvien, and Mikkel Østergaard. Patient registries. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0024.

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Patient registries can be either disease-based or medication-based, and have a wide range of objectives, such as describing the natural history of disease, determining clinical effectiveness or cost-effectiveness of treatments, safety monitoring, and measuring quality of care. This chapter describes some of the major disease-based and medication-based registries in axial spondyloarthritis, including several so-called biologics registries, which were established in many European countries as well as in other parts of the world following the introduction of the first tumour necrosis factor (TNF) inhibitors in 1999. The main results from registry-based research in axial spondyloarthritis are reviewed, covering areas such as epidemiology, genetics, effectiveness of TNF inhibitor treatment and switching, predictors of TNF inhibitor response and retention, and safety of TNF inhibitors. The current and future role of patient registries within epidemiology, effectiveness research, and surveillance of new therapies in axial spondyloarthritis are discussed.
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40

Figueiredo, Camille, and Georg Schett. Assessment of joint and bone structure in PsA patients: Using high-resolution computed tomography. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0019.

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Psoriatic arthritis (PsA) is associated with a distinct pattern of bone pathology, which influences the clinical picture of the disease. High-resolution computed tomography (CT) has contributed to understanding structural bone changes in PsA. Periarticular bone erosions in PsA are characterized by periosteal responses around the cortical break, distinguishing them from bone erosions in rheumatoid arthritis. Furthermore, a large number of enthesophytes can be found in CT studies of joints of PsA patients and in psoriasis patients without clinical arthritis. This latter observation supports the idea that articular changes start in psoriasis before joint disease commences. Moreover, enthesophytes are not influenced by methotrexate treatment and tumour necrosis factor inhibition. Finally, studies of systemic bone loss by high-resolution CT revealed significant alterations of the bone architecture in PsA but not in patients with skin disease only. In summary, CT has made valuable contributions in understanding the structural bone changes in PsA.
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41

Isaacs, John D., and Philip M. Brown. Rituximab and abatacept. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept's licence permits it use as a first-line biologic. In the United Kingdom, however, the National Institute for Health and Clinical Excellence (NICE) restricts the use of abatacept to patients who develop adverse effects with rituximab or in whom rituximab is contraindicated. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.
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42

Rahimi, Kazem. Chronic heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0092.

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The European Society of Cardiology defines heart failure as a clinical syndrome in which patients have the following features: symptoms typical of heart failure (breathlessness, fatigue, ankle swelling); signs typical of heart failure (tachycardia, tachypnoea, pulmonary crackles, pleural effusion, raised jugular venous pressure, peripheral oedema, hepatomegaly); and objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heat sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration). Heart failure results in activation of the sympathetic nervous system and the renin–aldosterone–angiotensin system, and release of a number of hormones such as natriuretic peptides, and cytokines, including tumour necrosis factor amongst others. While neurohormone activation is initially compensatory and helps in the short term to maintain circulatory needs, ultimately it has detrimental effects on the myocardium and compromises its function further. These mechanisms are therefore therapeutic targets to improve symptoms and lessen the risk of death.
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43

Poddubnyy, Denis, and Hildrun Haibel. Treatment: DMARDs. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0021.

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In axial spondyloarthritis (axSpA) there is little evidence to support use of classical synthetic disease-modifying antirheumatic drugs (DMARDs), with the majority of studies performed in advanced ankylosing spondylitis. Sulfasalazine is the best investigated DMARD in axSpA. Its positive clinical effect, if any, seems to be more prominent in the presence of peripheral arthritis, although a certain proportion of patients with axial disease might benefit from sulfasalazine therapy. Available data indicate that there is no evidence that methotrexate might be effective in axial disease, and only marginal evidence exists in support of methotrexate use in case of peripheral involvement. No true disease-modifying properties (e.g. retardation of structural damage progression in the spine) have been demonstrated for DMARDs in axSpA to date. Efficacy of a combination therapy (e.g. methotrexate plus sulfasalazine) as well as benefits of methotrexate (or other DMARDs) in addition to tumour necrosis factor α‎ inhibitors in axSpA remain uncertain.
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44

Klingenberg, Roland, and Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.

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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α‎ and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
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45

Todd, Stacy, and Nick Beeching. Fungal infection. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0315.

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Fungi, comprising yeasts, moulds, and higher fungi, have a worldwide distribution and are uncommon causes of disease in healthy individuals. However, over the last 20 years, invasive fungal disease (IFD) has become an increasing cause of morbidity and mortality. This is probably due to the increasing numbers of patients with underlying host conditions, which predispose to opportunistic IFD (e.g. transplant and anti-tumour necrosis factor immunosuppression, HIV, or chronic lung disease), and to increased recognition of endemic IFD (e.g. histoplasmosis), which cause disease in both immunocompetent and immunocompromised hosts in selected geographic locations. Diagnosis of IFD remains a challenge. Symptoms are often non-specific, and a definite diagnosis requires invasive sampling with appropriate laboratory testing of these samples. Non-invasive tests are being developed, but their positive and negative predictive values still need validation. Diagnostic criteria (‘proven, probable, and possible’) established primarily for use in research and clinical trials can also prove useful in clinical environments. However, the most important step in identifying patients with IFD is to consider the diagnosis in those at risk. This chapter will focus on the commonest causes of IFD (Candida spp., Aspergillus spp., Cryptococcus spp., and histoplasmosis).
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46

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Amen Sibtain. Colorectal cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0015_update_001.

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Breast cancer reviews the epidemiology and aetiology of this malignancy, with particular attention to the genetics underlying familial breast cancer, its pathology along with its receptors, oestrogen receptor (ER), the growth factor receptor HER2, and epidermal growth factor receptor (EGFR), and the bearing these have on treatment and prognosis. The benefits of breast cancer screening in the population and families at higher risk are discussed. Presenting symptoms and signs are followed by investigation including examination, bilateral mammography, and core biopsy of suspicious lesions. Management of non-invasive in situ disease is considered. Invasive breast cancer is staged according to TNM guidelines. Early breast cancer is defined, managed frequently by breast conserving surgery and sentinel node biopsy from the axilla. A positive sentinel node biopsy requires clearance of the axilla. Larger lesions may require mastectomy. Breast radiotherapy is indicated after breast conserving surgery. Following surgery, the risk of systemic micrometastatic disease is estimated from the primary size, lymph node spread, and tumour grade. Adjuvant chemotherapy improves treatment outcome in all but very good prognosis premenopausal breast cancer, and intermediate or poor prognosis postmenopausal breast cancer. This is combined with trastuzumab in HER2 positive disease. Adjuvant endocrine therapy is recommended for all ER positive breast cancer, tamoxifen in premenopausal, aromatase inhibitors in postmenopausal women. Neoadjuvant chemotherapy may be used in large operable breast cancers to facilitate breast conserving surgery. Locally advanced breast cancer is defined, its high risk of metastatic disease requiring full staging before treatment. Systemic therapy is often best first treatment, according to receptor profile. Metastatic breast cancer although incurable can be controlled for years using endocrine therapy, chemotherapy, trastuzumab, palliative radiotherapy, and bisphosphonates as appropriate. Male breast cancer is uncommon, but management similar.
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47

Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.

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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.
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48

Heijstek, Marloes, Mario Abinun, and Nico Wulffraat. Vaccination in immunocompromised children. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0095.

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Can immunocompromised children be safely and effectively vaccinated? This chapter discusses the recommendations from the European League Against Rheumatism (EULAR) for the immunization of immunocompromised patients. Patients with rheumatic or autoinflammatory diseases treated with high-dose glucocorticoids, high-dose disease-modifying anti-rheumatic drugs (DMARDs), or biologicals are considered immunocompromised. Safe and effective vaccination is crucial in these patients, given their increased risk of infection. Safe vaccination implies that vaccination has no effect on disease activity and has only mild adverse effects. Effective vaccination denotes that patients are protected against infections after immunization. Particularly in severely immunosuppressed patients, concerns arise on the safety of (live-attenuated) vaccines and on the detrimental effect of immunosuppressive treatment on the immunogenicity of vaccines. Overall, vaccinations do not increase disease activity and do not cause severe adverse events. Although non-live vaccines are safe, it is recommended to withhold live-attenuated vaccines in patients on high-dose immunosuppressive drugs and biologicals. However, booster vaccinations can be considered when essential. Generally, immunogenicity of vaccines is good with some exceptions: responses are reduced in patients on high-dose glucocorticoids and rituximab; methotrexate reduces responses to (pneumococcal) polysaccharide vaccines; and anti-tumour necrosis factor alpha (TNFα‎) may lower vaccine-induced antibody concentrations. Offering vaccination before immunosuppressive drugs and/or measuring antibodies after immunization is recommended.
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49

Heijstek, Marloes, Mario Abinun, and Nico Wulffraat. Vaccination in immunocompromised children. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0095_update_003.

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Can immunocompromised children be safely and effectively vaccinated? This chapter discusses the recommendations from the European League Against Rheumatism (EULAR) for the immunization of immunocompromised patients. Patients with rheumatic or autoinflammatory diseases treated with high-dose glucocorticoids, high-dose disease-modifying antirheumatic drugs (DMARDs), or biologicals are considered immunocompromised. Safe and effective vaccination is crucial in these patients, given their increased risk of infection. Safe vaccination implies that vaccination has no effect on disease activity and has only mild adverse effects. Effective vaccination denotes that patients are protected against infections after immunization. Particularly in severely immunosuppressed patients, concerns arise on the safety of (live-attenuated) vaccines and on the detrimental effect of immunosuppressive treatment on the immunogenicity of vaccines. Overall, vaccinations do not increase disease activity and do not cause severe adverse events. It is recommended to withhold live-attenuated vaccines in patients on high-dose immunosuppressive drugs and biologicals, but booster vaccinations can be considered when essential. Generally, immunogenicity of vaccines is good with some exceptions: responses are reduced in patients on high-dose glucocorticoids and rituximab; methotrexate reduces responses to (pneumococcal) polysaccharide vaccines; and tumour necrosis factor alpha (TNFα‎) may lower vaccine-induced antibody concentrations and may cause accelerated waning of immunity. Offering vaccination before immunosuppressive drugs and/or measuring antibodies after immunization is recommended.
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50

McGregor, Laura, Monica N. Gupta, and Max Field. Septic arthritis in adults. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0098.

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Septic arthritis (SA) is a medical emergency with mortality of around 15%. Presentation is usually monoarticular but in more than 10% SA affects two or more joints. Symptoms include rapid-onset joint inflammation with systemic inflammatory responses but fever and leucocytosis may be absent at presentation. Treatment according to British Society of Rheumatology/British Orthopaedic Association (BSR/BOA) guidelines should be commenced if there is a suspicion of SA. At-risk patients include those with primary joint disease, previous SA, recent intra-articular surgery, exogenous sources of infection (leg ulceration, respiratory and urinary tract), and immunosupression because of medical disorders, intravenous drug use or therapy including tumour necrosis factor (TNF) inhibitors. Synovial fluid should be examined for organisms and crystals with repeat aspiration as required. Most SA results from haematogenous spread-sources of infection should be sought and blood and appropriate cultures taken prior to antibiotic treatment. Causative organisms include staphylococcus (including meticillin-resistant Staphylococcus aureus, MRSA), streptococcus, and Gram-negative organisms (in elderly patients), but no organism is identified in 43%, often after antibiotic use before diagnosis. Antibiotics should be prescribed according to local protocols, but BSR/BOA guidelines suggest initial intravenous and subsequent oral therapy. Medical treatment may be as effective as surgical in uncomplicated native SA, and can be cost-effective, but orthopaedic advice should be sought if necessary and always in cases of infected joint prostheses. In addition to high mortality, around 40% of survivors following SA develop limitation of joint function. Guidelines provide physicians with treatment advice aiming to limit mortality and morbidity and assist future research.
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