Książki: „Non-steroidal anti-inflammatory Drug (NSAID)”

1

H, Stewart J., red. Analgesic and NSAID-induced kidney disease. Oxford: Oxford University Press, 1993.

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2

Jørgen, Rask Madsen, i Lauritsen Karsten, red. Aspects of non-steroidal anti-inflammatory drug therapy. London: Baillière Tindall, 2001.

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T, Borda Ivan, i Koff Raymond S. 1939-, red. NSAIDs: A profile of adverse effects. Philadelphia, Pa: Hanley & Belfus, 1992.

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1941-, Rainsford K. D., i Powanda M. C, red. Safety and efficacy of non-prescription (OTC) analgesics and NSAIDs: Proceedings of the international conference held at the South San Francisco Conference Center, San Francisco, CA, USA on Monday 17th March 1997. Dordrecht: Kluwer, 1998.

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5

J, Lowe N., i Hensby C. N, red. Nonsteroidal anti-inflammatory drugs. Basel: Karger, 1989.

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6

Clinch, David. Peptic ulcer and its drug causation: The role of non-steroidal anti-inflammatory drugs. London: Croom Helm, 1986.

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7

Robinson, Dwight R., i Fred E. Silverstein. Nonsteroidal anti-inflammatory drug-induced gastrointestinal damage: Current insights into patient management. Newton, MA: Cahners Pub. Co., 1988.

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8

Ekberg, EwaCarin. Treatment of temporomandibular disorders of arthrogeneous origin: Controlled double-blind studies of non-steroidal anti-inflammatory drug and a stabilisation appliance. Malmo, Sweden: Department of Stomatognathic Physiology Centre for Oral Health Sciences, Lund University, 1998.

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9

F, Willkens Robert, i Dahl Stephen L, red. Therapeutic controversies in the rheumatic diseases. Orlando: Grune & Stratton, 1987.

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10

Kay, Brune, red. Dipyrone: Recent investigations on its mode of action, pharmacokinetics, and clinical use : Berlin, October 24th, 1991. Basel: Birkhäuser Verlag, 1992.

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E, Paulus H., Furst Daniel E. 1942- i Dromgoole Sydney H, red. Drugs for rheumatic disease. New York: Churchill Livingstone, 1987.

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12

SA, Helsinn, red. Prostaglandins, oxidants and histamine in inflammation: A role for nimesulide? : augmented proceedings of a symposium held in Lugano, Switzerland, 30 November 1990. Auckland, New Zealand: Adis International Ltd., 1991.

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13

The Cox-2 connection: Natural breakthrough treatment for arthritis, Alzheimer's, and cancer. Rochester, Vt: Healing Arts Press, 2001.

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14

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

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15

D, Catto Graeme R., red. Drugs and the kidney. Dordrecht: Kluwer Academic Publishers, 1990.

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16

Choosing NSAID therapy: An international reappraisal. ADIS Press, 1985.

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17

Simon, Lee S., i Marc C. Hochberg. Non-steroidal anti-inflammatory drugs. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0030.

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Non-steroidal anti-inflammatory drugs (NSAIDs) are a chemically diverse group of compounds that share three cardinal characteristics: they are anti-inflammatory, analgesic, and antipyretic. They are approved by regulatory authorities for the treatment of patients with osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute gout, and some forms of juvenile idiopathic arthritis. There are at least 20 chemically different NSAIDs currently available in Europe and the United States. These include not only the ‘traditional’ non-selective cyclooxygenase (COX) inhibitors that inhibit both the COX-1 and COX-2 enzymes but also the COX-2 selective inhibitors. This chapter gives a background of NSAIDs, including the mechanism of action, pharmacology and adverse effects (including hypersensitivity and gastrointestinal, cardiovascular thrombotic, and renal adverse effects), before summarizing the use of NSAIDs in patients with osteoarthritis.

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18

Chan, Jonathan, i Nigil Haroon. Treatment: NSAIDs. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0020.

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Non-steroidal anti-inflammatory drugs (NSAIDs) constitute a diverse group of medications that inhibit prostaglandin synthesis. NSAIDs form the first-line pharmacological therapy in ankylosing spondylitis (AS). A number of randomized controlled trials (RCTs) support the efficacy of NSAIDs in reducing pain and improving patient function. Head-to-head comparisons have demonstrated equivalent effect of different NSAIDs in symptom control. The proposed disease-modifying potential of regular NSAID therapy is debatable and recent literature provides evidence to the contrary. Several safety concerns have been raised regarding long-term use of NSAIDs, especially an increase in cardiovascular risk. This chapter discusses the pharmacology, efficacy in treatment of AS, disease-modifying potential, and safety concerns of NSAIDs.

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19

Cheng, Jerry, i David Madigan. Bayesian approaches to aspects of the Vioxx trials: Non-ignorable dropout and sequential meta-analysis. Redaktorzy Anthony O'Hagan i Mike West. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780198703174.013.3.

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This article discusses Bayesian approaches to aspects of the Vioxx trials study, with a focus on non-ignorable dropout and sequential meta-analysis. It first provides a background on Vioxx, a COX-2 selective, non-steroidal anti-inflammatory drug (NSAID) approved by the FDA in May 1999 for the relief of the signs and symptoms of osteoarthritis, the management of acute pain in adults, and for the treatment of menstrual symptoms. However, Vioxx was found to cause an array of cardiovascular side-effects such as myocardial infarction, stroke, and unstable angina. As a result, Vioxx was withdrawn from the market. The article describes an approach to sequential meta-analysis in the context of Vioxx before considering dropouts in the key APPROVe study. It also presents a Bayesian approach to handling dropout and showcases the utility of Bayesian analysis in addressing multiple, challenging statistical issues and questions arising from clinical trials.

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20

Siebert, Stefan, Sengupta Raj i Alexander Tsoukas. Drug treatment for axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0015.

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The pharmacological therapy for patients with axial spondyloarthritis (axSpA), especially those with severe disease, has been transformed by the introduction of the biologic therapies, and anti-TNF therapy in particular. Until approximately 2005, treatment options for ankylosing spondylitis (AS) were limited to exercise therapy and non-steroidal anti-inflammatory drugs (NSAIDs). The TNF inhibitors appear to have a good safety profile in axSpA, with no new safety signals. The high cost of innovator biologics remains an issue and it will be interesting to observe the effect of the introduction of multiple biosimilar TNF inhibitors in clinical practice. New therapeutics targeting different cytokine and signalling pathways should also become available over the next few years, so it remains to be seen what their role will be in the management of axSpA. This chapter reviews some of the key drug therapies and advances in the management of axSpA.

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21

Roddy, Edward, i Michael Doherty. Calcium pyrophosphate crystal deposition (CPPD). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0142.

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Calcium pyrophosphate crystal deposition (CPPD) in articular cartilage is a common age-related phenomenon. Recent important advances in our understanding of the pathophysiology of pyrophosphate metabolism include the identification of a mutation within the ANK gene which associates with familial CPPD, and elucidation of the interleukin-1β‎ (IL-1β‎)-dependent mechanisms by which crystals invoke an inflammatory response. Risk factors for CPPD include age, prior joint damage and osteoarthritis, genetic factors, and occasionally metabolic diseases (hyperparathyroidism, haemochromatosis, hypomagnesaemia, and hypophosphatasia). CPPD is commonly asymptomatic or may present as osteoarthritis with CPPD, acute calcium pyrophosphate (CPP) crystal arthritis, or chronic CPP crystal inflammatory arthritis. Although radiographic chondrocalcinosis is often taken to be synonymous with CPPD, other calcium crystals can also have this appearance and definitive diagnosis requires identification of CPP crystals by compensated polarized light microscopy of aspirated synovial fluid. Recently, the ultrasonographic appearances of CPPD have been described. Treatment of CPPD is targeted to the clinical presentation. Acute CPP crystal arthritis is treated by aspiration and injection of glucocorticosteroid, local ice packs, non-steroidal anti-inflammatory drugs (NSAIDS), low-dose colchicine, oral or parenteral glucocorticosteroids, or adrenocorticotrophic hormone (ACTH). Treatment of osteoarthritis with CPPD is very similar to the treatment of osteoarthritis alone. There is no specific therapy for chronic CPP crystal inflammatory arthritis: options include NSAID, low-dose colchicine, low-dose glucocorticosteroid, methotrexate, and hydroxychloroquine. Recommendations for the management of CPPD are derived from a small evidence base and largely based on clinical experience and extrapolation from gout. Further research into diagnosis and management including novel treatment strategies such as IL-1β‎ blockade is much needed.

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22

Borda, Ivan T. NSAIDs. Hanley & Belfus, 1992.

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23

Foster, Helen, i Paul A. Brogan, red. British Society of Paediatric and Adolescent Rheumatology clinical guidelines and protocols. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199592630.003.0009.

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BSPAR Standards of Care for children and young people with JIA 410BSPAR drug information leaflets for parents and families 412BSPAR guidelines for treatments used in paediatric rheumatology 415Non-steroidal anti-inflammatory drugs (NSAIDs) 416Disease-modifying anti-rheumatic drugs (DMARDs) 418Azathioprine 423Ciclosporin 425Intravenous cyclophosphamide ...

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Abhishek, Abhishek, i Michael Doherty. Treatment of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0052.

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The treatment of calcium pyrophosphate crystal deposition (CPPD) is mainly symptomatic. Acute calcium pyrophosphate (CPP) crystal synovitis should be treated with rest, local application of ice packs, joint aspiration, and/or intra-articular corticosteroid injection (once joint sepsis has been excluded). Oral colchicine or prednisolone may be used if joint aspiration and/or injection are not feasible. Anti-inflammatory agents (with proton pump inhibitors) may be used but in general these should be avoided as most patients with acute CPP crystal arthritis are elderly, and at a high risk of gastrointestinal and renal complication of non-steroidal anti-inflammatory drug (NSAIDs). Principles of management of CPPD with osteoarthritis (OA) are identical to those for isolated OA. However, patients may have more inflammatory signs and symptoms and periodic joint aspiration and corticosteroid injection may be required more often than in isolated OA. Oral NSAIDs (with gastro-protection), colchicine, low-dose corticosteroids, hydroxychloroquine, and radiosynovectomy have been suggested as options for the treatment of chronic CPP crystal arthritis. There is growing interest in use of anti-interleukin-1 agents for acute or chronic CPP crystal arthritis but the efficacy of these agents has not been formally studied, and their use should be considered on an individual basis.

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25

(Editor), K. D. Rainsford, i M. C. Powanda (Editor), red. Safety and Efficacy of Non-Prescription (OTC) Analgesics and NSAIDs. Springer, 1997.

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Abhishek, Abhishek, Adrian Jones i Michael Doherty. Topical pharmacological treatments. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0028.

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Topical pharmacological agents such as non-steroidal anti-inflammatory drugs (NSAIDs) and capsaicin are widely recommended as first-line analgesics in the treatment of osteoarthritis (OA) of the knee, hand, and potentially other peripheral joints in view of their safety and efficacy. Although initial studies were short in duration (2–4 weeks), recent randomized controlled trials have confirmed the efficacy of topical NSAIDs over longer (12-week) study periods. Systematic reviews demonstrate that their efficacy can be equivalent to oral NSAIDs for OA pain, but they have a significantly better systemic toxicity profile than the corresponding oral formulations. Topical capsaicin is less well studied than topical NSAIDs but has been demonstrated to be effective in several placebo-controlled clinical trials. Local warming and an uncomfortable burning sensation is a common problem with initial applications, but this subsides with continued treatment and can be minimized by using a low-strength preparation (e.g. 0.025%) initially. Several other topical treatments such as drug-free transfersome gel and local lignocaine patches have been shown to be effective in controlling pain due to OA. However, they have been studied in relatively few studies and currently are not recommended for general use.

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27

Sjøgren, Per, Frank Elsner i Stein Kaasa. Non-opioid analgesics. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0096.

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Non-opioid analgesics encompass the non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol (acetaminophen). The NSAIDs include acetylsalicylic acid (ASA, aspirin), dipyrone (metamizole), and numerous other drugs in diverse classes. The NSAIDs have potent anti-inflammatory, analgesic and antipyretic activity, and are among the most widely used drugs worldwide. In palliative medicine, they represent the first step of the World Health Organization’s analgesic ladder used for mild pain and they are an important supplement to opioids and adjuvant drugs at higher steps of the ladder. The disadvantages of non-opioid analgesics include a ceiling effect for pain relief and the risk of side effects. NSAIDs are also associated with an increased risk of adverse gastrointestinal, renal, and cardiovascular effects and hepatotoxicity can result from overdosing with paracetamol. This chapter describes the clinical pharmacology of NSAIDs, their classification, molecular mechanisms of action and adverse effects, as well as some recent developments aimed at designing effective anti-inflammatory agents with improved safety and tolerability profiles.

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Borda, Ivan T., i Raymond S., M.D. Koff. Nsaids: A Profile of Adverse Effects. Lippincott Williams & Wilkins, 1992.

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Tsagareli, Merab G., i Nana Tisklauri. Behavioral Study of 'Non-Opioid' Tolerance'. Nova Biomedical, 2011.

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30

Peptic Ulcer & Its Drug Causation: The Role of Non-Steroidal Anti-Inflammatory Drugs. Routledge & Kegan Paul Books Ltd, 1986.

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31

Zhang, Weiya, i Michael Doherty. Guidelines. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0037.

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A number of treatment guidelines have been developed to optimize the treatment of osteoarthritis, some of which were recently updated. Fifty-one non-pharmacological, pharmacological, and surgical treatments are addressed in these guidelines but only two (oral opioid and intra-articular steroid injection) reach the minimal clinically important difference above placebo. Recommendations for these treatments vary depending on joint sites, risk:benefit ratio, and population. Exercise, self-management, and weight reduction if obese are universally recommended. While topical non-steroidal anti-inflammatory drugs (NSAIDs) remain a safe first-line drug option, the safety of paracetamol, the universally recommended first-line oral analgesic is increasingly questioned. Other analgesics such as oral NSAIDs (including selective cyclooxygenase 2 inhibitors), opioids, and antidepressants should be used according to patient characteristics and comorbidities. Nutraceuticals and complementary medicines remain controversial. While lavage is not recommended, total joint replacement is still considered as an effective treatment for the later stage of the disease irrespective of lack of placebo (sham) controlled trials. Stratified care has been attempted for recommendation according to joint affected and comorbidities but there is no evidence to support whether this can improve treatment outcomes. Guideline development groups differ in their composition and methodology. While the overall quality of guidelines has been improved, their applicability remains poor. Of the various factors that may influence implementation, suboptimal publishing and the efficacy paradox need to be recognized as important barriers.

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32

Side-Effects of Anti-Inflammatory Drugs: Volume 3 (Inflammation and Drug Therapy Series). Springer, 1992.

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(Editor), Michel Pairet, i Joanne van Ryn (Editor), red. COX-2 Inhibitors (Milestones in Drug Therapy). Birkhäuser Basel, 2004.

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34

Braun, Juergen, i Irene E. van der Horst-Bruinsma. Treatment: biologics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0022.

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According to classification criteria, the spectrum of spondyloarthritis (SpA) covers axial SpA (axSpA), which includes non-radiographic axSpA and ankylosing spondylitis, and peripheral SpA, which overlaps with psoriatic arthritis. Management recommendations for many forms of SpA have been recently published. Treatment of patients with axSpA with active disease starts with a sufficient dose of non-steroidal anti-inflammatory drugs (NSAIDs) for at least 4 weeks and preferably longer, in combination with exercise. In case of peripheral SpA, several disease-modifying antirheumatic drugs can be given, but these are not efficacious in axial disease. In case of insufficient response to NSAIDs for axSpA, biologic treatment can be added. The biologics most commonly used are TNF-blocking agents, but some other biologic agents seem to be beneficial in axial diseases as well, such as secukinumab (an IL-17 blocker). However, these new drugs have not yet been approved for axSpA at the time of writing this chapter.

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35

Rainsford, K. D., i M. C. Powanda. Safety and Efficacy of Non-Prescription Analgesics and NSAIDs: Proceedings of the International Conference held at The South San Francisco . . . Francisco, CA, USA on Monday 17th March 1997. Springer, 2012.

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Otis, James A. D. Non-Opioid Pharmacotherapies for Chronic Pain (DRAFT). Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190265366.003.0015.

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The objective of chapter 15 is to describe analgesic approaches to chronic pain, excluding opioids. As such, it emphasizes, first, the available pharmacotherapies; and then procedures. The pharmacotherapies divide into analgesics, such as non-steroidal anti-inflammatory drugs (NSAIDs); adjuvant analgesics, such as tricyclic antidepressants and anticonvulsants; oral anesthetic agents (cardiotropics); adrenergic agonists; topical agents such as capsaicin and local anesthetic solutions and ointments; and muscle relaxants such as cyclobenzaprine, tizanidine, and baclofen. Interventions include many best administered by anesthesiologists such as infusions of anesthetic agents; trigger point injections; local and regional blockade, spinal injections including corticosteroids; and electrical spinal cord stimulation. A text box is provided with additional resources.

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Drug Treatment of the Rheumatic Diseases. Wyd. 3. MacLennan & Petty Pty.Ltd ,Australia, 1986.

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Effect of a non-steroidal, anti-inflammatory drug (Indocin) on selected parameters of muscular function following concentric and eccentric work. 1987.

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Effect of a non-steroidal, anti-inflammatory drug (Indocin) on selected parameters of muscular function: Following concentric and eccentric work. 1987.

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Effect of a non-steroidal, anti-inflammatory drug (Indocin) on selected parameters of muscular function: Following concentric and eccentric work. 1987.

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Effect of a non-steroidal, anti-inflammatory drug (Indocin) on selected parameters of muscular function following concentric and eccentric work. 1987.

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42

Effect of a non-steroidal, anti-inflammatory drug (Indocin) on selected parameters of muscular function: Following concentric and eccentric work. 1985.

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Effect of a non-steroidal, anti-inflammatory drug (Indocin) on selected parameters of muscular function following concentric and eccentric work. 1987.

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44

Sirois, Pierre, i Pedro D’Orléans-Juste. The mechanism of aspirin. Redaktorzy Paul Farquhar-Smith, Pierre Beaulieu i Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0015.

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Aspirin has been used for the treatment of pain and inflammation for more than a hundred years; however, the medical use of what we now called aspirin dates back to antiquity, since willow-tree extracts containing salicylates were described in the Egyptian pharmacopoeia around 1543 bc. In 1971, Sir John Vane and his collaborators discovered its mechanism of action. This discovery has generated tremendous interest into the beneficial effect of this drug for the treatment of pain, inflammation, many inflammatory diseases, and even cancers. Vane and his collaborators also tested a number of other well-known aspirin-like drugs, or NSAIDs (for non-steroid anti-inflammatory drugs), and found that they all inhibited to a different extent the release of prostaglandins from organs as well as from tissue homogenates.

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45

Rudwaleit, Martin. Enthesitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0054.

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Enthesitis is one of the key manifestations of spondyloarthritides (SpA) including ankylosing spondylitis (AS) and psoriatic arthritis. Enthesitis can occur alone or in combination with peripheral arthritis, sacroiliitis, or spondylitis. The inflammatory process is typically located at the insertion of the enthesis or ligament to bone, often resulting in osteitis as well. Because of its anatomical and functional complexity the term 'enthesis organ' has been coined. Biomechanical stress applied to the enthesis seems to play an important role for the occurrence of enthesitis in genetically predisposed individuals. Ultrasound imaging of peripheral entheses reveals enthesis abnormalities including entheseal calcification, bony erosion, or bony proliferation. Power Doppler signals demonstrating increased vascularization of inflamed entheses at the insertional site appear to be the most characteristic finding for enthesitis, yet study results are conflicting. Enthesitis-related osteitis and enthesitis at the spine is best visualized by MRI. Enthesitis may resolve spontaneously or may run a chronic course. Standard treatment includes local steroid injections, non-steroidal anti-inflammatory drugs (NSAIDs), and physical therapy. There is little evidence for the efficacy of disease-modifying anti-rheumatic drugs (DMARDs) in enthesitis. In contrast, anti-TNF agents have proven efficacy, and their use in treatment-resistant enthesitis is recommended in the Assessment of SpondyloArthritis international Society (ASAS)/European League Against Rheumatism (EULAR) recommendations for the management of AS and axial SpA and in the EULAR recommendations for psoriatic arthritis.

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46

Gastro-duodenal ulcers associated with the use of non-steroidal anti-inflammatory drugs: A systematic review of preventive pharmacological interventions. Ottawa: Canadian Coordinating Office for Health Technology Assessment, 2003.

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Rudwaleit, Martin. Enthesitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0054_update_002.

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Enthesitis is one of the key manifestations of spondyloarthritis (SpA) including ankylosing spondylitis (AS) and psoriatic arthritis. Enthesitis can occur alone or in combination with peripheral arthritis, sacroiliitis, or spondylitis. The inflammatory process is typically located at the insertion of the enthesis or ligament to bone, often resulting in osteitis as well. Because of its anatomical and functional complexity the term ’enthesis organ’ has been coined. Biomechanical stress applied to the enthesis seems to play an important role for the occurrence of enthesitis in genetically predisposed individuals. Ultrasound imaging of peripheral entheses reveals enthesis abnormalities including entheseal calcification, bony erosion, or bony proliferation. Power Doppler signals demonstrating increased vascularization of inflamed entheses at the insertional site appear to be the most characteristic finding for enthesitis, yet study results are conflicting. Enthesitis-related osteitis and enthesitis at the spine is best visualized by MRI. Enthesitis may resolve spontaneously or may run a chronic course. Standard treatment includes local steroid injections, non-steroidal anti-inflammatory drugs (NSAIDs), and physical therapy. There is little evidence for the efficacy of disease-modifying antirheumatic drugs (DMARDs) in enthesitis. In contrast, anti-TNF agents have proven efficacy, and their use in treatment-resistant enthesitis is recommended in the Assessment of SpondyloArthritis international Society (ASAS)/European League Against Rheumatism (EULAR) recommendations for the management of AS and axial SpA and in the EULAR recommendations for psoriatic arthritis.

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Dalbeth, Nicola. Gout. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0141.

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Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.

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Dalbeth, Nicola. Gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0141_update_003.

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Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.

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Sieper, Joachim. Ankylosing spondylitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0113.

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Ankylosing spondylitis (AS) is a chronic inflammatory disease predominantly of the sacroiliac joint (SIJ) and the spine. It starts normally in the second decade of life and has a slight male predominance. The prevalence is between 0.2 and 0.8% and is strongly dependent on the prevalence of HLA B27 in a given population. For the diagnosis of AS, the presence of radiographic sacroiliitis is mandatory. However, radiographs do not detect active inflammation but only structural bony damage. Most recently new classification criteria for axial spondyloarthritis (SpA) have been developed by the Assessement of Spondylo-Arthritis international Society (ASAS) which cover AS but also the earlier form of non-radiographic axial SpA. MRI has become an important new tool for the detection of subchondral bone marrow inflammation in SIJ and spine and has become increasingly important for an early diagnosis. HLA B27 plays a central role in the pathogenesis but its exact interaction with the immune system has not yet been clarified. Besides pain and stiffness in the axial skeleton patients suffer also from periods of peripheral arthritis, enthesitis, and uveitis. New bone formation as a reaction to inflammation and subsequent ankylosis of the spine determine long-term outcome in a subgroup of patients. Currently only non-steroidal anti-inflammatory drugs (NSAIDs) and tumour necrosis factor (TNF) blockers have been proven to be effective in the medical treatment of axial SpA, and international ASAS recommendations for the structured management of axial SpA have been published based on these two types of drugs. Conventional disease-modifying anti-rheumatic drugs (DMARDs) such as methotrexate are not effective.

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