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1

Holgate, S. T., and Riccardo Polosa. Asthma: Current treatments. Oxford: Clinical Pub., 2007.

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2

Sampson, Anthony P., and Martin K. Church, eds. Anti-Inflammatory Drugs in Asthma. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8751-9.

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3

O’Donnell, Stella R., and Carl G. A. Persson, eds. Directions for New Anti-Asthma Drugs. Basel: Birkhäuser Basel, 1988. http://dx.doi.org/10.1007/978-3-0348-9156-1.

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4

R, O'Donnell Stella, Persson C. G. A, and International Congress of Pharmacology, (10th : 1987 : Sydney, N.S.W.), eds. Directions for anti-asthma drugs. Boston: Birkhauser, 1988.

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5

1962-, Sampson Anthony P., and Church Martin 1942-, eds. Anti-inflammatory drugs in asthma. Basel: Birkhäuser, 1999.

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6

Directions for new anti-asthma drugs. Basel: Birkhauser, 1988.

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7

(Editor), Anthony P. Sampson, and Martin Church (Editor), eds. Anti-Inflammatory Drugs in Asthma (Pir (Series).). Birkhauser, 1999.

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8

(Editor), Riccardo Polosa, and Stephen T. Holgate (Editor), eds. Therapeutic Strategies in Asthma: Current Treatments. Clinical Publishing, 2007.

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9

Barnes, Peter. Asthma Therapy. Taylor & Francis, 1998.

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10

(Editor), K. E. Andersson, and C.G.A. Persson (Editor), eds. Anti-asthma Xanthines and Adenosine (Current clinical practice series). Elsevier, 1986.

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11

New Drugs for Asthma, Allergy and COPD. Muenchen: Karger, 2004.

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12

Karl-Erik, Andersson, Persson C. G. A, and AB Draco, eds. Anti-asthma xanthines and adenosine: Proceedings of a symposium in Copenhagen, February 22-23, 1985. Amsterdam: Excerpta Medica, 1985.

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13

P, Page C., and Barnes Peter J. 1946-, eds. Pharmacology and therapeutics of asthma and COPD. Berlin: Springer, 2004.

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14

Zuzana, Diamant, and Yeadon Michael, eds. New and exploratory therapeutic agents for asthma. New York: Marcel Dekker, 2000.

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15

(Editor), T. T. Hansel, and Peter J. Barnes (Editor), eds. New Drugs for Asthma, Allergy and Copd (Progress in Respiratory Research). S. Karger Publishers (USA), 2001.

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16

O'donnell, S. R. Directions for New Anti-Asthma Drugs. Springer, 2011.

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17

1938-, O'Donnell Stella R., Persson C. G. A, and International Congress of Pharmacology (10th : 1987 : Sydney, N.S.W.), eds. Directions for new anti-asthma drugs. Basel: Birkhäuser, 1988.

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18

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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