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1
K, Dessain Scott, ed. Human antibody therapeutics for viral disease. Berlin: Springer Verlag, 2008.
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2
1960-, Grossbard Michael L., ed. Monoclonal antibody-based therapy of cancer. New York: Dekker, 1998.
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3
A, Foon Kenneth, and Morgan Alton C, eds. Monoclonal antibody therapy of human cancer. Boston: Nijhoff, 1985.
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4
W, Baldwin R., Byers Vera S, and Mann R. D. 1928-, eds. Monoclonal antibodies and immunoconjugates in cancer treatment. Carnforth: Parthenon Publishing, 1990.
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5
Ceriani, Roberto L., ed. Antigen and Antibody Molecular Engineering in Breast Cancer Diagnosis and Treatment. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2443-4.
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6
L, Ceriani Roberto, and International Workshop on Breast Cancer Research (5th : 1992 : San Francisco, Calif.), eds. Antigen and antibody molecular engineering in breast cancer diagnosis and treatment. New York: Plenum Press, 1994.
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7
E, Frankel Arthur, ed. Immunotoxins. Boston: Kluwer Academic Publishers, 1988.
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8
1927-, Baldwin R. W., Byers Vera S, and Mann Ronald D. 1928-, eds. Monoclonal antibodies and immunoconjugates. Carnforth, Lancs, UK: Parthenon Pub. Group, 1990.
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9
G, Melton Roger, and Knox Richard J, eds. Enzyme-prodrug strategies for cancer therapy. New York: Kluwer Academic/Plenum Publishers, 1999.
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10
Oehlrich, Marcus. Recombinant monoclonal antibody trastuzumab for the treatment of metastatic breast cancer with tumors overexpressing the HER2-neu proto-oncogene: A systematic review. Berlin: dissertation.de, 2003.
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11
Tufton Trust Conference (1994 Royal Society of Medicine). New antibody technology and the emergence of useful cancer therapy: Proceedings of the Tufton Trust Conference held at the Royal Society of Medicine on the 10th and 11th of October 1994. London: Royal Society of Medicine Press, 1995.
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12
Foon, Kenneth A., and Alton C. Morgan. Monoclonal Antibody Therapy of Human Cancer. Springer, 2012.
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13
Foon, Kenneth A., and Alton C. Morgan. Monoclonal Antibody Therapy of Human Cancer. Springer London, Limited, 2012.
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14
Antigen and Antibody Molecular Engineering in Breast Cancer Diagnosis and Treatment. Springer, 2014.
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15
Ceriani, Roberto L. Antigen and Antibody Molecular Engineering in Breast Cancer Diagnosis and Treatment. Springer, 2012.
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16
Ceriani, Roberto L. Antigen and Antibody Molecular Engineering in Breast Cancer Diagnosis and Treatment. Springer London, Limited, 2012.
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17
Frankel, Arthur E. Immunotoxins. Springer, 2012.
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18
Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0120.
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The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
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Khamashta, Munther A., Graham R. V. Hughes, and Guillermo Ruiz-Irastorza. Anti-phospholipid antibody syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0120_update_001.
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The anti-phospholipid syndrome (APS) described almost 30 years ago, is now recognized as a major cause of deep vein thrombosis, stroke, and heart attacks in young people (<45 years of age). It is also the commonest treatable cause of recurrent miscarriages and a major cause of late fetal death. Other clinical manifestations are cardiac valvular disease, livedo reticularis, renal thrombotic microangiopathy, thrombocytopenia, haemolytic anaemia, epilepsy, and cognitive impairment. The presence of anti-phospholipid antibodies (aPL) has been closely related to the development of thrombosis and complications in pregnancy. However, not all patients with aPL will develop the clinical features. Lupus anticoagulant is generally thought to be more strongly associated with the risk of clinical manifestations of APS than anticardiolipin and anti ?2-glycoprotein I antibodies. The exact pathogenic mechanisms leading to thrombosis and/or pregnancy morbidity are poorly understood. Therapy of thrombosis is based on long-term oral anti-coagulation and patients with arterial events should be treated aggressively. Obstetric care is based on combined medical-obstetric high-risk management and treatment with aspirin and heparin.
20
Begent, Richard, and Anne S. Hamblin. New Antibody Technology and the Emergence of Useful Cancer Therapy. Royal Society of Medicine Press Ltd, 1995.
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21
McKinley, Charlotte. The potentials and limitations of monoclonal antibody therapy in the treatment of cancer. 2005.
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22
Wong, Han Hsi, Basma Greef, and Tim Eisen. Treatment of metastatic renal cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0089.
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Metastatic renal cancer is resistant to standard chemotherapy. Although some patients with indolent disease can be initially managed with observation, the majority of patients will require aggressive treatment soon after diagnosis. Options include cytoreductive nephrectomy, resection of a solitary metastasis in highly selected cases, or systemic therapy options. The TKIs sunitinib and pazopanib are currently the first-line treatments of choice. Whilst axitinib and cabozantinib have important roles in the second line the PD-1 checkpoint inhibitor, nivolumab, is now established as standard second line therapy. Inhibitors of the mammalian target of rapamycin (mTOR) pathway, everolimus and temsirolimus, interleukin-2 as well as the anti-angiogenic antibody bevacizumab have also been shown to be effective. The treatment paradigm of metastatic renal cancer is constantly changing as evidence from clinical trials continues to emerge. With the development of agents addressing novel targets such as T-cell regulation, the future certainly looks brighter for patients diagnosed with this disease.
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Josephs, Debra H., Heather J. Bax, Giulia Pellizzari, James F. Spicer, Ana Montes, and Sophia N. Karagiannis. Antibody Therapeutics for Ovarian Carcinoma and Translation to the Clinic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0001.
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Despite improvements over the past decade in the treatment of ovarian cancer, many patients are at risk of recurrent disease and emerging drug resistance. The increased selectivity and reduced toxicity of molecularly targeted anti-cancer agents renders them attractive for development in ovarian cancer, and monoclonal antibodies targeting ovarian cancer-specific tumor antigens represent the largest such group investigated in this clinical setting. This chapter describes examples of monoclonal antibodies clinically evaluated for efficacy in ovarian cancer. These agents recognize molecular targets expressed on tumors or within tumor microenvironments that may be essential for tumor cell survival and proliferation. Recently, antibodies targeting checkpoint molecules on immune cells have shown efficacy in modulating anti-tumor immunity, and applications in ovarian carcinomas are evaluated. The chapter focuses on therapeutic agents’ attributes on targeting key cancer growth and progression pathways, and propensity to engender effector functions by activating immune effector cells in tumors and the circulation.
24
Jayne, David. Treatment of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132.
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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Additional therapy with intravenous methylprednisolone and plasma exchange is employed in severe presentations with failing vital organ function. Drug toxicity contributes to comorbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem, with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn. Disease relapse occurs in 50% and requires early detection at a stage when it will not adversely affect outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator. Outcomes of vasculitis depend heavily on the level of tissue damage at diagnosis, especially renal dysfunction, but are also influenced by patient age, ANCA subtype, disease extent, and response to therapy. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)is treated along similar principles to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis but the persistence of steroid-dependent asthma in over one-third and differences in pathogenesis has suggested alternative treatment approaches. Chronic morbidity results from tissue damage and is especially common in the upper and lower respiratory tract and kidneys. Tracheobronchial disease is a severe late complication of GPA, while deafness, nasal obstruction, and chronic sinusitis are sequelae of nasal and ear vasculitis. Chronic infection of damaged epithelial surfaces acts as a drive for vasculitic activity and adequate infection control is necessary for stable remission. Chronic kidney disease can stabilize for many years but the risks of endstage renal disease (ESRD) are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful, with similar outcomes to other causes of ESRD.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 59-Year-Old Man with Progressive Difficulties with Balance and Weight Loss. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0014.
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Paraneoplastic peripheral neuropathies are rare but important to consider in the evaluation of subacute peripheral neuropathy. The clinical and electrophysiological pattern as well as antibody evaluation is essential order to identify a specific paraneoplastic neuropathy. A positive paraneoplastic antibody in the cerebral spinal fluid is not required to make the diagnosis, but is helpful to consider if the serum antibodies are negative. This chapter emphasizes the importance of differential diagnosis and work up. Treatment options are described. Immunotherapy is also an important consideration.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 46-Year-Old Man with Double Vision and Proximal Leg Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0033.
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Lambert-Eaton myasthenic syndrome (LEMS) can be a difficult condition to diagnose. In this chapter, the clinical picture and characteristics are discussed. The pathophysiology is also reviewed. Features to distinguish LEMS from more common neuromuscular junction conditions such as myasthenia gravis are reviewed. We review features that distinguish between idiopathic and paraneoplastic forms, and we discuss the importance of tumor surveillance. Antibody testing and the correct electrodiagnostic strategy are presented. Treatment of LEMS is outlined.Lambert-Eaton syndrome (LES) is a difficult condition to diagnose. The unique clinical picture and its characteristics are discussed. This is especially true in the patient without a diagnois of cancer. Antibody testing and the correct electrodiagnostic strategy are presented. Treatment of LES is outlined.
27
Foster, Helen, and Paul A. Brogan, eds. Systemic diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199592630.003.0004.
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VasculitisThe classification of paediatric vasculitis 168The epidemiology of paediatric vasculitis 171The investigation of primary systemic vasculitis 172The standard treatment of childhood vasculitis 174Henoch–Schönlein purpura 179Kawasaki disease 183The anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides 188Polyarteritis nodosa (PAN) 192Cutaneous polyarteritis nodosa (cPAN) ...
28
Majid, Adrian, and Bruce L. Gilliam. Future Antiretrovirals, Immune-Based Strategies, and Therapeutic Vaccines. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0023.
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Highly active antiretroviral therapy remains the mainstay of treatment for patients chronically infected with HIV. Novel drugs, both within existing classes and new ones, are in various stages of development and testing. New medications within existing classes of antiretroviral agents are in clinical trials and will likely offer activity against resistant HIV-1 strains and provide alternatives for combination pill therapy. Novel therapeutics including oral attachment inhibitors and monoclonal antibody treatments continue to show efficacy against HIV-1 and progress in clinical trials. Tenofovir alafenamide is a prodrug that produces higher intracellular levels of tenofovir diphosphate with likely less renal and bone toxicity. Among traditional classes of HIV treatment, both doravirine (a non-nucleoside reverse transcriptase inhibitor) and cabotegravir (an integrase strand inhibitor) are newer agents with activity against resistant virus. Maturation inhibitors are a new class of treatment that block protease cleavage, leading to the release of an immature virion.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 35-Year-Old Man with Progressive Left-Hand Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0001.
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Multifocal motor neuropathy (MMN) may be mistaken for common entrapment neuropathies, although absence of significant sensory findings is a helpful clue to the diagnosis. Multifocal motor neuropathy may also mimic motor neuron disease. Electrophysiological evidence of conduction block at a nerve site not typically prone to compression is consistent with MMN. A positive anti-GM1 antibody also supports the diagnosis. First-line treatment of MMN is intravenous immunoglobulin (IVIG), and the majority of patients have rapid improvement of their weakness. The clinical features, differential diagnosis, investigations, and treatment options are described in this chapter.
30
Rush, David N., and Peter W. Nickerson. Rejection. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0283_update_001.
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Rejection of the transplanted kidney is an important cause of graft loss despite modern cross-matching techniques and immunosuppressive agents. The incidence of acute rejection episodes in the first post-transplant year is down to less than 15% in low-risk recipients, but as many as one-third of allograft losses over 10 years result from alloimmunity. Rejection may occur at any time following transplantation, from minutes—hyperacute, to days—acute, or in the longer term—chronic. Rejection can be predominantly through either T-cell-mediated or antibody-mediated mechanisms. It may present clinically as either abrupt or insidious dysfunction of the graft, or it may be subclinical and thus silent, detected only by protocol biopsy or other technology. The prevention and treatment of T-cell-mediated rejection is usually successful with current immunosuppressive agents. Antibody-mediated rejection, on the other hand, is not easily treated and is the principal cause of late renal allograft loss. This chapter presents the concepts and details of this central issue in clinical transplantation.
31
Pickering, Matthew C., and Jyoti Bakshi. Complement. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0064.
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In this chapter we summarize clinically important aspects of complement biology. This information is used to present a comprehensive overview of complement deficiency states and provide a logical basis for understanding complement assays in clinical practice. Hypocomplementaemic urticarial vasculitis syndrome, a condition associated with anti-C1q antibodies and complement consumption, is discussed. We summarize the use of eculizumab, a monoclonal antibody that targets and inhibits complement C5, in the treatment of haemolysis in paroxysmal nocturnal haemoglobinuria and atypical haemolytic uraemic syndrome.
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Pickering, Matthew C., and Jyoti Bakshi. Complement. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0064_update_001.
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In this chapter we summarize clinically important aspects of complement biology. This information is used to present a comprehensive overview of complement deficiency states and provide a logical basis for understanding complement assays in clinical practice. Hypocomplementaemic urticarial vasculitis syndrome, a condition associated with anti-C1q antibodies and complement consumption, is discussed. We summarize the use of eculizumab, a monoclonal antibody that targets and inhibits complement C5, in the treatment of haemolysis in paroxysmal nocturnal haemoglobinuria and atypical haemolytic uraemic syndrome.
33
Volcheck, Gerald W. Allergy. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0018.
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Standard allergy testing relies on identifying the IgE antibody specific for the allergen in question. Two classic methods of doing this are the immediate wheal-and-flare skin prick tests (a small amount of antigen is introduced into the skin and evaluated at 15 minutes for the presence of an immediate wheal-and-flare reaction) and in vitro testing. Allergy testing that does not have a clear scientific basis includes cytotoxic testing, provocation-neutralization testing or treatment, and "yeast allergy" testing. Allergy-related conditions such as asthma, chronic rhinitis, urticaria and angioedema, anaphylaxis, food allergy, stinging insect allergy, and drug allergy are reviewed.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 55-Year-Old Female with Slowly Progressive Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0010.
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Chronic inflammatory demyelinating polyneuropathy (CIPD) typically presents with both proximal and distal weakness, areflexia, and distal sensory findings. Two-thirds of patients have a progressive course over many months to years, however one-third of patients have a relapsing course with partial or complete recovery. It is important to be aware of several systemic disorders which may be associated with CIDP. Immunoglobulin M antibody–producing neuropathies have a monoclonal protein that is usually detected with serum protein electrophoresis, which may mimic CIDP. This chapter emphasizes the importance of differential diagnosis and workup. Treatment options are also described.
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Miller, Aaron E., and Teresa M. DeAngelis. Progressive Multifocal Leukoencephalopathy Syndrome and Immune Reconstitution Inflammatory Syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0007.
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Progressive multifocal leukoencephalopathy (PML), an opportunistic viral infection of the central nervous system caused by the JC virus, typically manifests in severely immunocompromised conditions, ranging from HIV/AIDS to lymphoproliferative malignancies to the consequence of immunosuppressant medications such as natalizumab, a monoclonal antibody approved for the treatment of relapsing forms of MS. In this chapter, we discuss the typical symptomatology and radiographic findings of PML and how to distinguish it from those of MS. In addition, we review the management of PML in natalizumab-treated MS patients as well as the features of immune reconstitution inflammatory syndrome (IRIS), the potentially life-threatening consequence of natalizumab withdrawal in patients with PML.
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Chinoy, Hector, and Robert G. Cooper. Polymyositis and dermatomyositis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0124.
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Polymyositis (PM), dermatomyositis (DM), and inclusion body myositis (IBM) form part of the idiopathic inflammatory myopathies (IIM), a heterogeneous group of rare autoimmune diseases characterized by an acquired proximal muscle weakness, raised muscle enzymes (including creatine kinase), inflammatory cell infiltrates in muscle biopsy tissue, electrophysiological abnormalities, and presence of circulating myositis-specific/myositis-associated autoantibodies. The underlying aetiology of IIM is poorly understood, but likely involves interactions between environmental and genetic risk factors. Myositis may also manifest in association with other connective tissue disorders. The predominant clinical presentation of IIM is skeletal muscle weakness, but many extramuscular features can also occur. Access to good neuropathological support is essential in securing an accurate IIM diagnosis and excluding non-inflammatory myopathies, although IBM is often difficult to distinguish from PM. Antibody testing can help define IIM clinical subtypes, including cancer-associated myositis, predict prognosis, and help in optimizing treatment decisions. MRI can be invaluable for differentiating disease activity from damage, and detecting treatment-induced interval changes. Therapeutic effectiveness of new and existing treatments (where the evidence base remains poor) depends on making a prompt diagnosis and initiating early and appropriately aggressive treatment to prevent establishment of muscle damage. This chapter attempts to summarize the salient features of IIM and update the reader about currently used diagnostics and treatment paradigms in this rare and understudied disease.
37
Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.
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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.
38
Barton, Richard. Serology of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0042.
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Examination of serum and other body fluids for the presence of antibodies to fungi, or the direct detection of the fungal antigens themselves, can play an important role in the diagnosis of fungal disease. Various methods have been applied, though currently the most commonly used is some form of enzyme-linked immunosorbent assay. Antigen detection has become a standard method for diagnosing cryptococcosis and can play a key role in detecting aspergillosis, and to a lesser extent candidiasis, depending on the underlying disease. Antibody testing is routine for many fungal diseases, including coccidioidomycosis, histoplasmosis, and many forms of aspergillosis. Beta-D-glucan is a generic fungal antigen found in the cell walls of many fungi, and detection of BDG is a test which many find useful when screening the sera of at-risk patients. Increasingly, physicians and scientists are looking to serodiagnostic tests not only to diagnose, but also to monitor treatment outcomes.
39
Kuwabara, Satoshi. Neuromuscular junction disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0014.
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Ten seminal papers on disorders of the neuromuscular junction are described, covering historical aspects, recent advances in immunological, biological, and genetic researches, and future perspectives. Early descriptions of myasthenia gravis (MG) date back to the seventeenth century, and MG acquired its name in the nineteenth century. The first symptomatic treatment with cholinesterase inhibitors was reported in 1934, leading to the development of modern immunological therapies. Following the discovery of anti-MuSK (muscle-specific tyrosine kinase) antibody in 2001, MG is currently classified into three categories: AChR-positive, MuSK-positive, and dual-seronegative. Lambert-Eaton myasthenic syndrome was recognized in 1956, followed by the discovery of antibodies to voltage-gated calcium channels in the pre-synaptic membrane, facilitating diagnosis and improving the understanding of the pathophysiological mechanisms. Since the late twentieth century, many types of congenital myasthenic syndromes with pre-synaptic, synaptic, and post-synaptic defects have been identified, and a classification based on molecular genetics is in evolution.
40
Rodriguez-Iturbe, Bernardo, and Mark Haas. Glomerulonephritis associated with endocarditis, deep-seated infections, and shunt nephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0079_update_001.
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Endocarditis is a cause of glomerulonephritis. Healthcare interventions (prosthetic valves, indwelling catheters, pacemaker wires) and intravenous drug abuse are presently the most common causes of endocarditis and Staphylococcus aureus is frequently the infecting bacteria. Shunt nephritis is a form of glomerulonephritis associated with infection of ventriculoatrial shunts implanted to relieve hydrocephalus and, typically, are caused by prolonged infections of low-pathogenicity microorganisms. This complication led to the replacement of the technique by ventriculoperitoneal shunts. Deep-seated infections such as chronic abscesses and osteomyelitis can sometimes cause a similar syndrome. In all cases, treatment of the infection is the key strategy. The nature of the glomerulonephritis tends in subacute infection to be a lobular membranoproliferative glomerulonephritis type I pattern associated with low C3 levels. However, an acute post-infectious pattern may also be seen, and a third pattern is focal necrotizing and crescentic glomerulonephritis, which tends to be pauci-immune as seen in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, but usually without positive fluorescence or solid phase assays for ANCA antigens.
41
Wells, Elizabeth M. Anti-N-Methyl-D-Aspartate Receptor Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0091.
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Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe but treatable recently identified form of immune-mediated encephalitis associated with antibodies in serum and cerebrospinal fluid (CSF) against the GluN1 subunit of the NMDAR. Research has rapidly expanded the understanding of disease mechanisms and how the condition manifests in different populations (e.g., pediatrics vs. adult, cancer vs. noncancer, male vs. female). Immunocytochemical, physiological, and molecular studies of the effects of human CSF on the rodent and murine brain in vitro and in vivo indicate a noncytotoxic antibody-mediated mechanism of disease pathogenesis. Finding positive antibodies prompts a search for occult neoplasm, most likely ovarian teratoma in young women; other age groups and male patients are less likely to have tumor but need to be screened. Fifty percent of patients respond to first line steroids, IVIG, plasma exchange or a combination, and many others improve with addition of rituximab or cyclophosphamide. Cured patients may have cognitive or motor sequelae, and refractory disease and death may occur despite treatment. Knowledge about etiology and biomarkers of refractory disease are lacking. Additional work is needed to further elucidate the origin of the immune-mediated response, to determine optimal clinical management and develop effective therapies for refractory patients.
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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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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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K. Gautam, Rupesh, Lokesh Deb, and Kamal Dua, eds. Natural Products for the Management of Arthritic Disorders. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/97898150507761220101.
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Rheumatoid arthritis (RA) is the most common inflammatory complication and affects approximately 1 % of the global population. It affects three times more women than men. RA is an autoimmune disorder elicited by exposure of genetic factors from the host to unknown antigens causing arthritogenic complaints. It also includes the activation of lymphocytes as well as CD4+ helper T cells along with local release of chronic inflammatory mediators and cytokines like tumor necrosis factor (TNF α) and various cytokines like interleukins (IL) that enormously affect the joints. The available allopathic therapies for RA are not a cure for the complications, and antibody therapy and surgical procedures are expensive. However, in the present era, researchers and healthcare professionals have moved toward natural medicines obtained from plants and other natural sources. Research based on developments in phytomedicine has progressed steadily. Evidence has been collected to show the massive therapeutic potential of medicinal plants used in various traditional systems against many pathological complications. Researchers have focused on the therapeutic potential of natural products used for treatment and counteracting various disorders along with their complications having negligible adverse effects. Natural Products for the Management of Arthritic Disorders compiles current knowledge about the bioactive compounds and herbal formulations useful in the treatment of rheumatoid arthritis. 11 chapters explain the role of natural products in the management of rheumatoid arthritis. Topics have been contributed by experts in medicinal chemistry and rheumatology. The book first introduces the reader to rheumatoid arthritis before delving into conventional and alternative therapies for the disease. The editors have also included special topics such as the biomarkers for RA, cytokines and anti-inflammatory mediators, preclinical and clinical studies. The range of topics should provide a comprehensive overview of natural remedies for arthritis and the role of natural products in anti-arthritic drug development. The information will be useful for many readers including medical and pharmacology students, multidisciplinary research scholars, scientists, pharma / herbal / food industrialists, and policy makers.
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Cohen, Mary Ann, Harold Goforth, Joseph Lux, Sharon Batista, Sami Khalife, Kelly Cozza, and Jocelyn Soffer. Handbook of AIDS Psychiatry. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195372571.001.0001.
Full textAbstract:
The Handbook of AIDS Psychiatry is a practical guide for AIDS psychiatrists and other mental health professionals as well as for other clinicians who work with persons with HIV and AIDS and a companion book to the Comprehensive Textbook of AIDS Psychiatry (Cohen and Gorman, 2008). The Handbook provides insights into the dynamics of adherence to risk reduction and medical care in persons with HIV and AIDS as well as strategies to improve adherence using a biopsychosocial approach. Psychiatric disorders can accelerate the spread of the virus by creating barriers to risk reduction. Risky sexual behaviors and sharing of needles in intravenous drug users account for the majority of new cases each year. Delirium, dementia, depression, substance dependence, PTSD, and other psychiatric disorders complicate the course and add considerably to the pain and suffering of persons with AIDS. HIV infection and AIDS also are risk factors for suicide, and the rate of suicide has been shown to be higher in persons with AIDS. Psychiatric care can help prevent HIV transmission through recognition and treatment of substance-related disorders, dementia, and mood disorders such as mania. Comprehensive, coordinated care by a multidisciplinary AIDS team, including AIDS psychiatrists, can provide a biopsychosocial approach that is supportive to patients, families, and clinicians. Psychiatric interventions are valuable in every phase of infection, from identification of risk behaviors to anticipation about HIV testing; from exposure and initial infection to confirmation with a positive HIV antibody test; from entry into systems of care to managing complex antiretroviral regimen; from healthy seropositive to onset of first AIDS-related illness; from late stage AIDS to end-stage AIDS and death. There is no comprehensive handbook of AIDS psychiatry to guide clinicians in providing much needed care. The Handbook of AIDS Psychiatry is a practical pocket guide that provides protocols for the recognition and treatment of the psychiatric disorders most prevalent in persons with AIDS and most relevant for primary physicians, infectious disease specialists, and other caregivers because of their impact on health, adherence, behavior, and quality of life.
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Reddy, Ugan, and Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.
Full textAbstract:
Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR resulting in a decreased receptor density resulting in a reduced postsynaptic end-plate potential following motor nerve stimulation and leading to muscle weakness. Although all voluntary muscles can be affected, ocular, bulbar, respiratory, and proximal limb weakness predominates. In the majority of seronegative patients, an antibody directed towards a NMJ protein called muscle specific tyrosine kinase (MUSK) is found. Anti-MUSK MG is characterized by severe bulbar and respiratory muscle weakness. Diagnosis of MG requires a high degree of clinical suspicion coupled with pharmacological and electrophysiological testing, and detection of the various causative antibodies. Treatment of MG involves enhancing neuromuscular transmission with long-acting anticholinesterase agents and immunosuppression. Acute exacerbations are treated with either plasma exchange or intravenous immunoglobulin. Myasthenic crisis is associated with severe muscle weakness that necessitates tracheal intubation and mechanical ventilation. LEMS is an autoimmune disease in which IgG antibodies are directed towards the pre-synaptic voltage-gated calcium channels at the NMJ. It is often associated with malignant disease (usually small cell carcinoma of the lung). Autonomic dysfunction is prominent and patients show abnormal responses to neuromuscular blocking drugs.
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Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0057.
Full textAbstract:
Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet's syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
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Thornton, Clare, and Justin Mason. Vascular biology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0057_update_001.
Full textAbstract:
Vascular biology is the study of the physiology of the vasculature and how it may be the target for disease processes. An understanding of vascular biology is central to the study of rheumatic disease for three reasons: it is an integral part of a functioning immune system; it is the primary site of pathology in many conditions; and it is the site of the important secondary complications of chronic inflammation, endothelial dysfunction and atherosclerosis. Vascular biology requires a detailed knowledge of the anatomy and physiology of the vasculature and its constituent vessels. The multistep process by which leucocytes interact with endothelium lining postcapillary venules in order to leave the circulation and migrate towards a site of inflammation is central to the pathology of inflammatory disease. The vasculature is the primary site of injury in several rheumatic diseases, including the vasculitides. It may also be damaged by chronic inflammation, leading to endothelial dysfunction and accelerated atherosclerosis. Thrombosis is also a critical pathological process in several chronic inflammatory diseases, particularly the anti-phospholipid antibody syndrome and Behçet’s syndrome. The vascular endothelium is central to angiogenesis, the process of new capillary outgrowth, upon which synovial proliferation in inflammatory arthritis is dependent. Angiogenesis is inhibited by current anti-rheumatic therapies and may become a target for novel anti-rheumatic drugs. An increasing area of research concerns the direct effects of drugs used in the treatment of atherosclerosis and inflammatory disease on the endothelium, and whether these agents are beneficial or harmful. Of particular interest to rheumatologists are the vascular effects of statins, disease-modifying anti-rheumatic drugs (DMARDs), immunosuppressants, and cyclooxygenase inhibitors.
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Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.
Full textAbstract:
The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes endothelial cell injury fibroblast activation and autoimmunity that lead to skin and internal organ manifestations. The majority of cases exhibit characteristic serum autoantibodies. Some of these antibodies are scleroderma-specific reactivities including anti-centromere (ACA), anti-topoisomerase-1 (ATA or Scl 70) or anti-RNA polymerase III antibodies. These anti-nuclear antibody (ANA) patterns are generally mutually exclusive and serve as useful clinical markers of disease subgroups. Additional subsetting of scleroderma cases, based on the extent of skin sclerosis, permits classification into limited and diffuse subsets. Because of the heterogeneity of the disease patients may suffer from different organ manifestations, such as lung fibrosis, hypertensive renal crisis, severe cardiac disease, gastrointestinal involvement, and pulmonary arterial hypertension. Although outcomes have improved recently, systemic sclerosis still has the highest case-specific mortality of any of the autoimmune rheumatic diseases and requires careful and systematic investigation, management and follow-up. Treatment includes symptomatic strategies with attention to each involved organ system; it is still an area where therapeutic progress and better understanding of pathogenesis is increasingly anticipated.
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Eckert, J., P. Deplazes, and P. Kern. Alveolar echinococcosis (Echinococcus multilocularis). Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0061.
Full textAbstract:
In this chapter three forms of echinococcosis in humans are described that are caused by a larval stage (metacestode) of Echinococcus multilocularis Leuckart, 1863, Echinococcus oligarthrus (Diesing, 1863) or Echinococcus vogeli Rausch and Bernstein, 1972. E. multilocularis is the causative agent of alveolar echinococcosis (AE). In the human host the metacestode of E. multilocularis behaves like a malignant tumour, characterized by infiltrative proliferation and the potential to induce serious disease. The liver is nearly exclusively the primary site of metacestode development, but metastases may by formed in adjacent and distant organs. Typically AE exhibits a chronic progressive clinical course, which finally leads to death in up to 90% of untreated patients within 10 years after diagnosis. An undefined proportion of cases are abortive with inactivation of the parasite. Evidence has accumulated in recent years that anti-parasitic therapy with benzimidazoles (albendazole or mebendazole) over many years or lifelong, if necessary combined with interventional procedures, can inhibit disease progression and improve or stabilse the patient’s clinical condition. Radical surgery in an early stage of the infection combined with anti-parasitic therapy for two years may lead to cure. The introduction of benzimidazole therapy of AE (1977), combined with improved diagnostic and surgical procedures, has resulted in significantly increased life-expectancies of adequately treated AE patients. In highly endemic areas ultrasound population screening (partially combinated with antibody detection) has been successfully used for early detection of AE cases. Countrywide annual AE incidence rates are mostly low at approximately < 0.1 to 2.0 per 100,000 inhabitants, but they can be much higher locally. Furthermore, there are indications of emerging case numbers in some areas of Europe and Asia. In spite of relatively low case numbers, AE is a significant disease due to its severity and high costs of treatment (median costs of approximately 145,800 per case).