, Volume 51, Issue 4, pp 639–657 | Cite as


A Review of its Pharmacology and Therapeutic Potential in the Management of Painful and Inflammatory Conditions
  • Julia A. Balfour
  • Andrew Fitton
  • Lee B. Barradell
Drug Evaluation



Lornoxicam (chlortenoxicam), a new nonsteroidal anti-inflammatory drug (NSAID) of the oxicam class with analgesic, anti-inflammatory and antipyretic properties, is available in oral and parenteral formulations. It is distinguished from established oxicams by a relatively short elimination half-life (3 to 5 hours), which may be advantageous from a tolerability standpoint.

Data from preliminary clinical trials suggest that lornoxicam is as effective as the opioid analgesics morphine, pethidine (meperidine) and tramadol in relieving postoperative pain following gynaecological or orthopaedic surgery, and as effective as other NSAIDs after oral surgery. Lornoxicam was also as effective as other NSAIDs in relieving symptoms of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute sciatica and low back pain. Lornoxicam has a tolerability profile characteristic of an NSAID, with gastrointestinal disturbances being the most common adverse events.

Limited clinical experience to date suggests that, as with a number of other NSAIDs, lornoxicam may provide a better-tolerated alternative or adjuvant to opioid analgesics for the management of moderate to severe pain. It has also demonstrated potential as an alternative to other NSAIDs for the management of arthritis and other painful and inflammatory conditions. These preliminary findings require confirmation in further comparative and long term studies.

Pharmacodynamic Properties

As with other nonsteroidal anti-inflammatory agents (NSAIDs), lornoxicam (chlortenoxicam) inhibits prostaglandin (PG) synthesis via inhibition of cyclo-oxygenase, but it does not inhibit 5-lipoxygenase. Lornoxicam was reported to be 100-fold more potent (on a molar basis) than tenoxicam in inhibiting PGD2formation in rat polymorphonuclear leucocytes in vitro and more active than indomethacin or piroxicam in preventing arachidonic acid-induced lethality in mice in vivo.

Lornoxicam has demonstrated analgesic and anti-inflammatory activity in both animal and human models. It produced dose-related analgesia in the human dental extraction model and showed approximately 10-fold greater analgesic activity than tenoxicam in the acetylcholine-induced writhing test in mice. It was also 10-fold more active than tenoxicam in inhibiting carrageenin-induced oedema in the rat and paw swelling in the adjuvant-induced polyarthritic rat.

In comparative studies in healthy volunteers, lornoxicam 16 mg/day induced significantly less endoscopically verified gastroduodenal injury than naproxen 1000 mg/day, and lornoxicam 8 mg/day tended to cause less faecal blood loss than indomethacin 100 mg/day. Moreover, lornoxicam did not increase serum pepsinogen I levels (an index of gastric mucosal status), when given at a dosage of 4mg twice daily for 2 weeks.

Studies in healthy volunteers and patients with renal impairment did not reveal any evidence of nephrotoxicity following administration of lornoxicam (≤16 mg/day for ≤3 weeks).

Pharmacokinetic Properties

Lornoxicam is completely absorbed after oral administration, reaching peak plasma concentrations of 270 μg/L within 2.5 hours after a 4mg dose. It exhibits dose-related kinetics over a dosage range of 2 to 6mg twice daily. The absorption of lornoxicam is delayed and marginally reduced (≈20%) in the presence of food. Instances of excessively high plasma concentrations associated with delayed drug elimination in healthy volunteers suggest that lornoxicam metabolism may be impaired in certain individuals.

As with other oxicam NSAIDs, lornoxicam is highly bound (99%) to plasma proteins with a low apparent volume of distribution (0.2 L/kg). However, it readily penetrates into perivascular interstitial spaces, including synovial fluid.

Lornoxicam is extensively metabolised in the liver, to the inactive metabolite 5′-hydroxy-lornoxicam. Excretion is shared between the renal (42%) and faecal (51%) routes. Lornoxicam has a relatively short terminal plasma elimination half-life (mean 3 to 5 hours in healthy young volunteers), with considerable interindividual variability.

The pharmacokinetics of lornoxicam do not appear to be appreciably modified by advanced age or renal impairment, but accumulation of the inactive major metabolite occurred in patients with impaired hepatic function. Enhanced enterohepatic elimination of the drug may compensate for reduced renal elimination in those with severe renal dysfunction.

Therapeutic Potential

Acute Pain. A small number of preliminary placebo-controlled and other comparative clinical studies have shown that lornoxicam provides effective analgesia following oral or other surgery. Intravenous lornoxicam 8mg was reported to be as effective as pethidine (meperidine) 50mg and at least as effective as tramadol 50mg in providing intravenous analgesia following gynaecological or orthopaedic surgery. Lornoxicam was also comparable to morphine for patient-controlled analgesia in an orthopaedic setting. When used after oral surgery, oral lornoxicam 8mg was as effective as oral ketorolac 10mg, ibuprofen 400mg and aspirin (acetylsalicylic acid) 650mg.

In patients with acute sciatic or lumbosciatic pain, lornoxicam 8mg twice daily was superior to placebo and comparable to oral diclofenac 50mg 3 times daily.

Chronic Pain. In short term (up to 3 months) randomised, double-blind studies, lornoxicam (orally administered in dosages ranging from 4mg twice daily to 8mg twice daily) exhibited efficacy similar to diclofenac in osteoarthritis; diclofenac, naproxen or piroxicam in rheumatoid arthritis; indomethacin in ankylosing spondylitis, and diclofenac or naproxen in low back pain. Although some slight differences in efficacy parameters were noted, none of these were statistically significant. The efficacy of lornoxicam was maintained during long term studies of up to 1 year’s duration in patients with osteoarthritis or rheumatoid arthritis. Lornoxicam 4mg 3 times daily was also reported to be superior to placebo for prophylaxis against migraine.

Tolerability and Drug Interactions

Lornoxicam has a tolerability profile characteristic of NSAIDs, with gastrointestinal disturbances (pain, dyspepsia, nausea, vomiting) being the most prominent events. In comparative clinical trials, the tolerability of oral lornoxicam appeared to be similar to that of diclofenac and better than that of indomethacin in patients with arthritic conditions or chronic low back pain. As would be expected, parenterally administered lornoxicam tended to be better tolerated than parenteral opioid analgesics in patients with postoperative pain.

The pharmacokinetics of lornoxicam are not significantly modified by coadministered antacids or ranitidine. Lornoxicam appears to share with other NSAIDs pharmacokinetic and/or pharmacodynamic interactions with Cimetidine, warfarin, sulphonylureas, lithium, furosemide (frusemide) and methotrexate. Lornoxicam did not alter phenazone (antipyrine) clearance in healthy volunteers, indicating a lack of effect on hepatic drug metabolising enzymes.

Dosage and Administration

The most common dosages of lornoxicam used in clinical trials were 4mg twice or 3 times daily or 8mg twice daily (orally) for management of arthritic conditions, low back pain and ankylosing spondylitis, and single or repeated doses of 4 or 8mg (orally or intravenously) for management of postoperative pain.

Caution is recommended when using lornoxicam in patients with impaired renal function (although dosage adjustment does not appear to be necessary) and in those receiving warfarin, oral sulphonylureas, loop or thiazide diuretics, or digoxin.


Adis International Limited Ankylose Spondylitis Naproxen Tramadol Piroxicam 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Pruss TP, Stroissnig H, Radhofer-Weite S, et al. Overview of the pharmacological properties, pharmacokinetics and animal safety assessment of lornoxicam. Postgrad Med J 1990; 66 Suppl. 4: S18–21PubMedGoogle Scholar
  2. 2.
    Vane JR, Botting RM. New insights into the mode of action of anti-inflammatory drugs. Inflammation Res 1995; 44: 1–10CrossRefGoogle Scholar
  3. 3.
    Brooks PM, Day RO. Nonsteroidal anti-inflammatory drugs — differences and similarities. N Engl J Med 1991; 324(24): 1716–25PubMedCrossRefGoogle Scholar
  4. 4.
    McCormack K. Non-steroidal anti-inflammatory drugs and spinal nociceptive processing. Pain 1994 Oct; 59: 9–43PubMedCrossRefGoogle Scholar
  5. 5.
    Hayllar J, Bjarnason I. NSAIDs, Cox-2 inhibitors, and the gut. Lancet 1995; 346: 521–2PubMedCrossRefGoogle Scholar
  6. 6.
    Wallace JL, Cirino G. The development of gastrointestinal-sparing nonsteroidal anti-inflammatory drugs. TiPS 1994; 15: 405–6PubMedGoogle Scholar
  7. 7.
    Ferber HP, Maleschitz P, Binder D. Chlortenoxicam, a new NSAID, prevents the arachidonic acid-induced toxicity [abstract A387]. 2nd World Conference on Inflammation, Antirheumatics, Analgesics, Immunomodulators; 1986 Mar 19–22; Monte Carlo.Google Scholar
  8. 8.
    McCormack K. The spinal actions of nonsteroidal anti-inflammatory drugs and the dissociation between their anti-inflammatory and analgesic effects. Drugs 1994; 47 Suppl. 5: 28–45PubMedCrossRefGoogle Scholar
  9. 9.
    Kullich W, Klein G. Influence of the nonsteroidal antiinflammatory drug lornoxicam i.v. on the secretion of the endogenous opiate peptides dynorphin and β-endorphin [in German]. Aktuel Rheumatol 1992 Jul; 17: 128–32CrossRefGoogle Scholar
  10. 10.
    Nhrholt SE, Sindet-Pedersen S, Bugge C, et al. A randomized, double-blind, placebo-controlled, dose-response study of the analgesic effect of lornoxicam after surgical removal of mandibular third molars. J Clin Pharmacol 1995 Jun; 35: 606–14Google Scholar
  11. 11.
    Cooper SA, Beaver WT. A model to evaluate mild analgesics in oral surgery. Clin Pharmacol Ther 1976; 20: 241–50PubMedGoogle Scholar
  12. 12.
    Forbes JA. Oral surgery. In: Max M, Portenoy R, Laska E, editors. Advances in pain research and therapy. New York: Raven Press Ltd, 1991: 347–74Google Scholar
  13. 13.
    Schoen RT, Vender RJ. Mechanisms of nonsteroidal anti-inflammatory drug-induced gastric damage. Am J Med 1989; 86: 449–58PubMedCrossRefGoogle Scholar
  14. 14.
    Lichtenstein DR, Syngal S, Wolfe MM. Nonsteroidal antiinflammatory drugs and the gastrointestinal tract. The double-edged sword. Arthritis Rheum 1995; 36: 5–18CrossRefGoogle Scholar
  15. 15.
    Weinstein M. Differentiation of nonsteroidal anti-inflammatory drug-associated and ‘ordinary’ peptic ulcers. In: Soll AH, moderator. Nonsteroidal anti-inflammatory drugs and peptic ulcer disease. Ann Intern Med 1991: 114: 307-19Google Scholar
  16. 16.
    Aabakken L. Gastrointestinal tolerability of lornoxicam compared to that of naproxen in healthy male volunteers. Aliment Pharmacol Ther. In pressGoogle Scholar
  17. 17.
    Warrington SJ, Debbas NMG, Farthing M, et al. Lornoxicam, indomethacin and placebo: comparison of effects on faecal blood loss and upper gastrointestinal endoscopic appearances in healthy men. Postgrad Med J 1990 Aug; 66: 622–6PubMedCrossRefGoogle Scholar
  18. 18.
    Kullich W, Klein G, Pollmann G. Influence of lornoxicam on serum pepsinogen levels. Postgrad Med J 1990; 66 Suppl. 4: S46–48PubMedGoogle Scholar
  19. 19.
    Girgis L, Brooks P. Nonsteroidal anti-inflammatory drugs: differential use in older patients. Drugs Aging 1994; 4: 101–12PubMedCrossRefGoogle Scholar
  20. 20.
    Kenny GNC. Potential renal, haematological and allergic adverse effects associated with nonsteroidal anti-inflammatory drugs. Drugs 1992; 44 Suppl. 5: 31–7PubMedCrossRefGoogle Scholar
  21. 21.
    Adams DH, Michael J, Bacon PA, et al. Non-steroidal anti-inflammatory drugs and renal failure. Lancet 1986; 1: 57–60PubMedCrossRefGoogle Scholar
  22. 22.
    Warrington SJ, Lewis Y, Dawnay A, et al. Renal and gastrointestinal tolerability of lornoxicam, and effects on haemostasis and hepatic microsomal oxidation. Postgrad Med J 1990; 66 Suppl. 4: S35–40PubMedGoogle Scholar
  23. 23.
    Warrington SJ, Dawnay A, Johnston A, et al. Chlortenoxicam and renal function of normal human volunteers [letter]. Hum Toxicol 1989 Jan; 8: 53–4PubMedCrossRefGoogle Scholar
  24. 24.
    Cunningham J, Wilkie M, Beer J, et al. The effect of renal dysfunction on the pharmacokinetic profile of lornoxicam. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  25. 25.
    Merry P, Winyard PG, Morris CJ, et al. Oxygen free radicals, inflammation and synovitis: the current status. Ann Rheum Dis 1989; 48: 864–70PubMedCrossRefGoogle Scholar
  26. 26.
    Ross R, Raines EW, Bowen-Pope DF. The biology of platelet derived growth factor. Cell 1986; 46: 155–69PubMedCrossRefGoogle Scholar
  27. 27.
    Dittrich P, Ferber HP, Kukovetz WR. Determination of chlortenoxicam, a novel nonsteroidal anti-inflammatory drug in human plasma [abstract P573]. 10th International Congress of Pharmacology; 1987 Aug 23–28; SydneyGoogle Scholar
  28. 28.
    Suwa T, Urano H, Shinohara Y, et al. Simultaneous high-performance liquid chromatographic determination of lornoxicam and its 5′-hydroxy metabolite in human plasma using electrochemical detection. J Chromatogr B Biomed Appl 1993 Jul; 617: 105–10CrossRefGoogle Scholar
  29. 29.
    Dittrich P, Radhofer-Welte S, Magometschnigg D, et al. The effect of concomitantly administered antacids on the bioavailability of lornoxicam, a novel highly potent NSAID. Drugs Exp Clin Res 1990; 16(2): 57–62PubMedGoogle Scholar
  30. 30.
    Ankier SI, Brimelow AE, Crome P, et al. Chlortenoxicam pharmacokinetics in young and elderly human volunteers. Postgrad Med J 1988 Oct; 64: 752–4PubMedCrossRefGoogle Scholar
  31. 31.
    Mayerhofer S, Weite S, Magometschnigg D, et al. The effect of food on pharmacokinetic parameters of the new NSAID lornoxicam in healthy volunteers [abstract]. 3rd Interscience World Conference on Inflammation, Antirheumatics, Analgesics and Immunomodulators; 1989 Mar 15-18; Montc Carlo: 223Google Scholar
  32. 32.
    Dittrich P, Radhofer-Welte S, Mayerhofer S, et al. Comparative pharmacokinetics of parenteral lornoxicam [abstract]. Eur J Pharmacol 1990 Jul 6; 183: 2265–6CrossRefGoogle Scholar
  33. 33.
    Olkkola KT, Brunetto AV, Mattila MJ. Pharmacokinetics of oxicam nonsteroidal anti-inflammatory agents. Clin Pharmacokinet 1994 Feb; 26: 107–20PubMedCrossRefGoogle Scholar
  34. 34.
    Hitzenberger G, Radhofer-Welte S, Takacs F, et al. Pharmacokinetics of lornoxicam in man. Postgrad Med J 1990; 66 Suppl. 4: S2–6Google Scholar
  35. 35.
    Albengres E, Urien S, Barre J, et al. Clinical pharmacology of oxicams: new insights into the mechanisms of their dose-dependent toxicity. Int J Tissue React 1993; 15(3): 125–34PubMedGoogle Scholar
  36. 36.
    Leemann TD, Transon C, Bonnabry P, et al. A major role for cytochrome P450tb(CYP2C subfamily) in the actions of nonsteroidal antiinflammatory drugs. Drugs Exp Clin Res 1993; 19: 189–95PubMedGoogle Scholar
  37. 37.
    Bonnabry P, Leemann T, Dayer P. Role of human liver cytochrome P450tb (CYP2C9) in the biotransformation of lornoxicam. Clin Pharmacol Ther 1995 Feb; 57: 152Google Scholar
  38. 38.
    Ravic M, Johnston A, Turner P, et al. The effect of repeated oral doses of lornoxicam on antipyrine elimination in normal human volunteers. Hum Exp Toxicol 1991 Oct; 10: 375–7PubMedCrossRefGoogle Scholar
  39. 39.
    Turner P, Johnston A. Clinical pharmacokinetic studies with lornoxicam. Postgrad Med J 1990; 66 Suppl. 4: S28–29PubMedGoogle Scholar
  40. 40.
    Ravic M, Salas-Herrera I, Johnston A, et al. A pharmacokinetic interaction between Cimetidine or ranitidine and lornoxicam. Postgrad Med J 1993 Nov; 69: 865–6PubMedCrossRefGoogle Scholar
  41. 41.
    Ravic M, Salas-Herrera I, Johnston A, et al. Influence of lornoxicam a new non-steroidal anti-inflammatory drug on lithium pharmacokinetics. Hum Psychopharm 1993 Jul–Aug; 8: 289–92CrossRefGoogle Scholar
  42. 42.
    Boobis SW. Alteration of plasma albumin in relation to decreased drug binding in uraemia. Clin Pharmacol Ther 1977; 22: 147–53PubMedGoogle Scholar
  43. 43.
    Reidenberg MM, Affrime M. Influence of disease on binding of drugs to plasma proteins. Ann N Y Acad Sci 1973; 226: 115–26PubMedCrossRefGoogle Scholar
  44. 44.
    Wanwimolruk S, Birkett DJ, Brooks M. Protein binding of some non-steroidal anti-inflammatory drugs in rheumatoid arthritis. Clin Pharmacokinet 1982; 7: 85–92PubMedCrossRefGoogle Scholar
  45. 45.
    Woodford-Williams E, Alvares AS, Webster D, et al. Serum protein patterns in normal and pathological aging. Gerontologia 1964; 10: 86–99CrossRefGoogle Scholar
  46. 46.
    Wallace S, Whiting B, Runcie J. Factors affecting drug binding in plasma of elderly patients. Br J Clin Pharmacol 1976; 3: 327–30PubMedCrossRefGoogle Scholar
  47. 47.
    Ilias W. Pain control after hysterectomy: an observer-blind, randomised trial of lornoxicam versus tramadol. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  48. 48.
    Rosenow DE, van Krieken F, Stolke D, et al. Intravenous administration of lornoxicam, a new NSAID, and pethidine for postoperative pain. A placebo-controlled pilot study. Clin Drug Invest 1996; 11(1): 11–9CrossRefGoogle Scholar
  49. 49.
    Patel A, Skelly AM, Kohn H, et al. Double-blind placebo-controlled comparison of the analgesic effects of single doses of lornoxicam and aspirin in patients with post-operative dental pain. Br Dent J 1991 Apr 20; 170: 295–9PubMedCrossRefGoogle Scholar
  50. 50.
    Hafslund Nycomed Pharma AG. A prospective single-centre, randomised, double-blinded, controlled phase III study with parallel groups in patients suffering from acute post-operative pain (discectomy/laminectomy) using morphine as the active control drug (2n = 96). Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  51. 51.
    Cooper SA, Hersh EV, Quinn PD, et al. Analgesie efficacy and safety of lornoxicam, a new oxicam derivative. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  52. 52.
    Cooper SA, Lucyk D, Smith B, et al. An analgesic evaluation of lornoxicam [abstract]. 95th Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics; 1994 Mar 31-Apr 1; New Orleans: 126.Google Scholar
  53. 53.
    Hafslund Nycomed Pharma AG. A multicentre study using a randomised, bi-phase (double-blind/open-labelled) parallel group design in patients suffering from acute sciatica (3n = 90 for the confirmatory analysis). Hafslund Nycomed Pharma AG (Data on file)Google Scholar
  54. 54.
    Hafslund Nycomed Pharma AG. Multiple-dose study comparing the efficacy and safety of lornoxicam with placebo and diclofenac in patients with acute sciatica or lumbo-sciatica. Hafslund Nycomed Pharma AG (Data on file)Google Scholar
  55. 55.
    Rainer F, Klein G, Mayrhofer F, et al. A prospective, multicentre, open-label, uncontrolled Phase II study of the local tolerability, safety and efficacy of intramuscular chlortenoxicam in patients with acute low back pain. Eur J Clin Res 1996; 8: 1–13Google Scholar
  56. 56.
    Chariot J. Long term efficacy and tolerability of lornoxicam in elderly patients with rheumatoid arthritis or osteoarthritis: a multicenter, open study. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  57. 57.
    Fernandez I. A multicentre, randomised, double-blind study comparing lornoxicam, a new NSAID, with naproxen in patients with chronic lower back pain. Hafslund Nycomed Pharma AG (Data on file)Google Scholar
  58. 58.
    Leeb B. Lornoxicam in the management of rheumatoid arthritis: a comparative study with piroxicam followed by long-term open-label treatment with lornoxicam. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  59. 59.
    Hafslund Nycomed Pharma AG. Comparison of the efficacy and safety of lornoxicam and diclofenac in rheumatoid arthritis: a multicentre double-blind study followed by treatment with lornoxicam. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  60. 60.
    Bernstein RM, Frenzel W. A comparative study of two dosage regimens of lornoxicam and a standard dosage of naproxen in patients with rheumatoid arthritis. Eur J Clin Res 1995; 7: 259–73Google Scholar
  61. 61.
    Berry H, Bird HA, Black C, et al. A double blind, multicentre, placebo controlled trial of lornoxicam in patients with osteoarthritis of the hip and knee. Ann Rheum Dis 1992 Feb; 51: 238–42PubMedCrossRefGoogle Scholar
  62. 62.
    Hafslund Nycomed Pharma AG. Efficacy and safety of lornoxicam (8mg b.i.d) in comparison with placebo in patients with osteoarthritis of the knee — a four-week, randomized, prospective multicentre, double-blind, placebo-controlled, parallel group phase IIb study. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  63. 63.
    Kidd B. A multicentre, randomised, double-blind study comparing lornoxicam with diclofenac in osteoarthritis. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  64. 64.
    Caruso I, Montrone F, Boari L, et al. Lornoxicam versus diclofenac in rheumatoid arthritis: a double-blind, multicenter study. Adv Ther 1994 May–Jun; 11: 132–8Google Scholar
  65. 65.
    Bernstein RM, Calin HJ, Calin A. A comparison of the efficacy and tolerability of lornoxicam and indomethacin in ankylosing spondylitis. Eur J Rheumatol Inflamm 1992; 12(3): 6–13Google Scholar
  66. 66.
    Mayrhofer F, Siegmeth W, Kolarz G, et al. A multicentre, randomised, double-blind study comparing lornoxicam with diclofenac in patients with chronic lower back pain. Hafslund Nycomed Pharma AG. (Data on file)Google Scholar
  67. 67.
    Sternieri E, Bussone G, Manzoni GC, et al. Lornoxicam, a new non-steroidal anti-inflammatory drug, in migraine prophylaxis: a double-blind multicenter study. Cephalalgia 1991 Jun; 11 Suppl. 11: 154–5Google Scholar
  68. 68.
    Ravic M, Johnston A, Turner P, et al. Does bismuth chelate influence lornoxicam absorption? [letter]. Hum Exp Toxicol 1992 Jan; 11: 59–60PubMedCrossRefGoogle Scholar
  69. 69.
    Ravic M, Johnston A, Turner P. Clinical pharmacological studies of some possible interactions of lornoxicam with other drugs. Postgrad Med J 1990; 66 Suppl. 4: S30–34PubMedGoogle Scholar
  70. 70.
    Ravic M, Johnston A, Turner P, et al. A study of the interaction between lornoxicam and warfarin in healthy volunteers. Hum Exp Toxicol 1990 Nov; 9: 413–4PubMedCrossRefGoogle Scholar
  71. 71.
    Kramer HJ, Dusing R, Stinnesbeck B, et al. Interaction of conventional and antikaliuretic diuretics with the renal prostaglandin system. Clin Sci 1980; 59: 67–70PubMedGoogle Scholar
  72. 72.
    Hitoglou-Makedou A, Lawson M, Turner P, et al. Comparison of chlortenoxicam and indomethacin on furosemide-induced diuresis. Postgrad Med J 1989 Nov; 65: 821–3PubMedCrossRefGoogle Scholar
  73. 73.
    Moote C. Efficacy of nonsteroidal anti-inflammatory drugs in the management of postoperative pain. Drugs 1992; 44 Suppl. 5: 14–30PubMedCrossRefGoogle Scholar
  74. 74.
    Kehlet H, Dahl JB. Are perioperative nonsteroidal anti-inflammatory drugs ulcerogenic in the short term?. Drugs 1992; 44 Suppl. 5: 38–41PubMedCrossRefGoogle Scholar
  75. 75.
    Levy MH. Pharmacologic management of cancer pain. Semin Oncol 1994; 21: 718–39PubMedGoogle Scholar
  76. 76.
    Garcia-Rodriguez LA, Jick H. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet 1994; 343: 769–72PubMedCrossRefGoogle Scholar

Copyright information

© Adis International Limited 1996

Authors and Affiliations

  • Julia A. Balfour
    • 1
  • Andrew Fitton
    • 1
  • Lee B. Barradell
    • 1
  1. 1.Adis International LimitedMairangi Bay, Auckland 10New Zealand

Personalised recommendations