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Books on the topic 'Xanthines'

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Author: Grafiati

Published: 4 June 2021

Last updated: 7 September 2023

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1

Xanthines and cancer: An experimental study of tumour inhibition. Aberdeen: Aberdeen University Press, 1988.

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2

1946-, Barnes Peter J., ed. The Mechanism of action of Xanthines in respiratory disease. London: Royal Society of Medicine Services, 1988.

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3

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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4

Services, IBC Technical, ed. Xanthines: an update on their chemistry, pharmacology and therapeutics: Conference documentation : London, 1988. London: IBC TechnicalServices, 1988.

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5

1944-, Costello J. F., Piper Priscilla J, and Royal Society of Medicine (Great Britain). Respiratory Section., eds. Methylxanthines and phosphodiesterase inhibitors in the treatment of airways disease: The proceedings of a meeting held by the Respiratory Section of the Royal Society of Medicine, London, November 1993. London: Parthenon Pub. Group, 1994.

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6

International Workshop on Adenosine and Xanthine Derivatives (1984 Wiesbaden, Germany). Adenosine: Receptors and modulation of cell function : proceedings of the International Workshop on Adenosine and Xanthine derivatives. Oxford [Oxfordshire]: IRL Press, 1985.

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7

Nilson, G. The mountain vipers of the Middle East: The Vipera xanthina complex (Reptilia, Viperidae). Bonn: Zoologisches Forschungsinstitut und Museum Alexander Koenig, 1986.

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8

Neish, William J. P. Xanthines and cancer. Aberdeen University Press, 1988.

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9

(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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10

Neish, William J. P. Xanthines and Cancer: An Experimental Study of Tumour Inhibition. MacMillan Publishing Company, 1988.

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11

Methylxanthines. Springer, 2011.

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12

Fredholm, Bertil B. Methylxanthines. Springer, 2016.

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13

Fredholm, Bertil B. Methylxanthines. Springer, 2010.

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14

Stevens, Helena Louise. Xanthias New BFF. Austin Macauley Publishers Ltd., 2021.

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15

Stefanovich, V. Pharmacology of Adenosine and Xanthine Derivatives. Irl Pr, 1985.

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16

Hicking, W., P. Leskovar, R. Hartung, A. Hesse, and D. Bach. Harnsäure-, Zystin-, Xanthin-Stein. Springer London, Limited, 2013.

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17

Menard, Cédric. Recettes et menus pour les coliques néphrétiques xanthiques. Books on Demand, 2021.

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18

Gowan, Simon William Mac. Evaluation of the possible role of xanthine oxidase in the pathogenesis of acute pancreatitis. 1992.

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19

Dalbeth, Nicola. Urate-lowering therapy agents. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0009.

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Xanthine oxidase (allopurinol or febuxostat) is considered first-line urate-lowering therapy. Combination therapy with uricosuric agents may be required. The choice of urate-lowering therapy is dictated by co-morbidities, particularly renal and hepatic impairment. Appropriate monitoring for drug adverse effects as well as serum urate to ensure targets are achieved is required.

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20

Rice, Pauline. From The Land Of Glee, Xanthie And Zaybar Make New Friends. Small World Publishing, 2001.

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21

Richette, Pascal. Principles of gout management. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0044.

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The general goals of gout therapy are to manage acute flares and to prevent recurrences and prevent or reverse the complications of urate deposition by lowering urate levels. The choice of drug should be made on the basis of the patient’s co-morbidities, other medications, and side effect profile. Treatment of flares can be achieved with non-steroidal anti-inflammatory drugs, colchicine, or corticosteroids (systemic or intra-articular). Interleukin-1 blockers could become an alternative in patients contraindicated for traditional anti-inflammatory agents. Lowering of urate levels below monosodium urate (MSU) saturation point with both a non-pharmacological and pharmacological approach allows to dissolve MSU crystals and to cure gout. Serum urate (SUA) levels should be maintained below 6 mg/dL (360 μ‎mol/L) or below 5 mg/dL (300 μ‎mol/L) in patients with severe gout to facilitate faster dissolution of crystals. Urate-lowering therapy (ULT) should be initiated close to the first diagnosis of gout. Allopurinol and febuxostat are the most widely used xanthine oxidase inhibitors to lower SUA levels. If the SUA target cannot be reached by these agents, uricosurics are indicated, either alone or in combination with a xanthine oxidase inhibitor. In patients with severe tophaceous gout in whom the SUA target cannot be reached with any other available drug, pegloticase is indicated. Since ULT initiation may trigger acute attacks of gout, prophylaxis with an anti-inflammatory agent is recommended, mostly with low-dose colchicine. Of note, patient education, appropriate lifestyle advice, and treatment of comorbidities are also important parts of the management of patients with gout.

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22

Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.

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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal histologic changes include arteriolosclerosis, glomerulosclerosis, and tubulointerstitial fibrosis. In patients with urate nephropathy, hypertension is common, but usually there is only mild proteinuria and a slight increase in serum creatinine. The reduction of serum uric acid, using xanthine oxidase inhibitors and perhaps low-purine diet, is the mainstay of therapy. There is current research around the question of whether it is beneficial to lower serum uric acid in asymptomatic patients with renal disease or with cardiovascular risk factors.

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23

Dambrova, Maija. Discovery of N-Hydroxyguanidines As Novel Electron Acceptors of Xanthine Oxidase: Potential New Drugs for Treatment of Ischemia and Reperfusion Injury ... from the Faculty of Pharmacy, 217). Uppsala Universitet, 1999.

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24

(Contributor), WHO, ed. Coffee, Tea, Mate, Methylxanthines and Methylglyoxal (IARC Monographs on the Evaluation of Carcinogenic Risks to H). World Health Organisation, 1991.

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