Disease relevance of Tiaprofensaeure

• Liver dysfunction caused by tiaprofenic acid [1].
• Current evidence suggests that nonbacterial cystitis is more likely to be associated with tiaprofenic acid than with other NSAIDs [2].
• Multicentre double-blind comparison of sustained action formulations of tiaprofenic acid and indomethacin in osteoarthritis [3].
• Tiaprofenic acid. A review of its pharmacological properties and therapeutic efficacy in rheumatic diseases and pain states [4].
• Tiaprofenic acid is a new non-steroidal anti-inflammatory agent advocated for use in rheumatoid arthritis, osteoarthritis, musculoskeletal disorders, soft-tissue injuries and inflammatory conditions and acute pain of varying origin [4].

Psychiatry related information on Tiaprofensaeure

• CASE SUMMARY: A woman treated with lithium for bipolar affective disorder was concurrently treated with tiaprofenic acid 200 mg tid for shoulder pain [5].
• How does cystitis affect a comparative risk profile of tiaprofenic acid with other non-steroidal antiinflammatory drugs? An international study based on spontaneous reports and drug usage data. ADR Signals Analysis Project (ASAP) Team [6].

High impact information on Tiaprofensaeure

• Clinical pharmacokinetics of tiaprofenic acid and its enantiomers [7].
• Recent data suggested that possibility of stereoselective distribution of tiaprofenic acid into synovium and cartilage [7].
• The area under the plasma concentration-time curve (AUC) of tiaprofenic acid is proportional to the oral dose administered [7].
• Tiaprofenic acid is eliminated following extensive biotransformation to glucuronide-conjugated metabolites [7].
• The rate of excretion of tiaprofenic acid and its conjugates may be related to renal function; accumulation of conjugates occurs in end-stage renal disease, but not in young individuals or elderly patients [7].

Chemical compound and disease context of Tiaprofensaeure

• Comparative double-blind study of tiaprofenic acid versus piroxicam in the treatment of osteoarthritis of the knee [8].
• Comparative clinical trial of two injectable NSAIDs, tiaprofenic acid and alclofenac, in acute sciatica [9].
• Cyclophosphamide and tiaprofenic acid can cause chemical cystitis, and should be withdrawn if a patient develops irritative symptoms or haematuria [10].
• Based on the composition of the oxygenated photomixtures and the relative toxicity of the different photoproducts, it is possible to account for most of the observed toxicity in the case of tiaprofenic acid but not in the case of naproxen [11].
• The arylpropionic acid derivatives (APADs) ketoprofen and tiaprofenic acid can provoke photoallergic dermatitis [12].

Biological context of Tiaprofensaeure

• Synovial fluid and plasma kinetics of repeat dose sustained action tiaprofenic acid in patients with rheumatoid arthritis [13].
• Drug-photosensitized protein modification: identification of the reactive sites and elucidation of the reaction mechanisms with tiaprofenic acid/albumin as model system [14].
• Nonlinear pharmacokinetics and protein binding of tiaprofenic acid in female Lewis rats [15].
• Mechanism of lipid peroxidation photosensitized by tiaprofenic acid: product studies using linoleic acid and 1,4-cyclohexadienes as model substrates [16].
• M-5011 and tiaprofenic acid prevented this decrease in vertebral bone mineral density [17].

Anatomical context of Tiaprofensaeure

• Effects of tiaprofenic acid and other NSAIDs on proteoglycan metabolism in articular cartilage explants [18].
• These results indicate that with the exception of tiaprofenic acid all the NSAIDs examined produced a general reduction in chondrocyte metabolic activity [18].
• Tiaprofenic acid is a potent non-steroidal anti-inflammatory drug which, in conventional tablet form, has been shown to be rapidly absorbed and eliminated from the plasma, while synovial fluid concentrations remain constant for at least 8 hours [13].
• The results obtained both in vitro and in vivo confirmed the absence of any oxidative action of tiaprofenic acid on the erythrocytes of G6PD-deficient subjects [19].
• Treatment with tiaprofenic acid appreciably reduced the level of plasminogen activators in the medium of 3T3-Balb mouse fibroblasts, as revealed by both a fibrin plate assay and amidolytic determination with chromogenic substrates [20].

Associations of Tiaprofensaeure with other chemical compounds

• Ten patients suffering from rheumatoid arthritis were studied, with 5 patients receiving tiaprofenic acid and 5 indomethacin for a 1-week period [21].
• Relative efficacy and tolerance of tiaprofenic acid and ketoprofen in rheumatoid arthritis [22].
• At the same time, tiaprofenic acid was able to inhibit the production of plasminogen activators induced by phorbol myristate acetate, a powerful inflammation and tumour promoter, added to the cell monolayers [20].
• GSH concentrations were also evaluated in vitro after incubation of G6PD-deficient erythrocytes with increasing doses of tiaprofenic acid (20, 50, 100, 150 and 200 mg/L) and with acetylphenylhydrazine 5 mg [19].
• The aim of this study was to evaluate in vivo if treatment with tiaprofenic acid 600 mg daily for 15 days would reduce erythrocyte GSH (reduced glutathione) concentrations and thus produce erythrocytolysis (assessed by evaluation of 51Cr-labelled erythrocyte survival) in subjects with G6PD deficiency [19].

Gene context of Tiaprofensaeure

• In the absence of LPS and at therapeutic concentration, tiaprofenic acid decreased both the synthesis and release of IL-1 beta [23].
• Tiaprofenic acid induced a dose-dependent decrease in uPA synthesis in both OA and RA, particularly in OA synovium, but had no true effect on tPA [24].
• The results of this study indicate that a decrease in uPA synthesis may be one of the mechanisms by which tiaprofenic acid could exert its effects on the arthritic process [24].
• RESULTS: All tested NSAIDs dose dependently inhibited the IL-1 induced mRNA expression of tPA, whereas only indomethacin and tiaprofenic acid were also able to reduce the expression of uPA [25].
• Comparative studies in patients with rheumatoid arthritis or osteoarthritis receiving tiaprofenic acid 600 mg/day demonstrated improvements in pain intensity, duration of morning stiffness, articular index and other clinical variables which were similar to those achieved with alternative NSAIDs [2].

Analytical, diagnostic and therapeutic context of Tiaprofensaeure

• Benefits from tiaprofenic acid injection were noted within 60 minutes by about 47% of the patients with acute gout and about 85% of the whole group of patients enrolled in the multicentre study [26].
• Clinical experiences with the intramuscular injection of tiaprofenic acid in rheumatic diseases, with particular emphasis on time of onset and duration of the analgesic effect [26].
• Efficacy and tolerability of an injectable formulation of tiaprofenic acid in patients with acute back and neck pain [27].
• Synovial fluid samples from 4 patients before and after treatment with tiaprofenic acid were also assayed for plasminogen activator activity by the fibrin lysis method [20].
• At the end of the parallel-group study, patients receiving tiaprofenic acid or placebo entered a 4-week blinded cross-over study of tiaprofenic acid or placebo, both given for 2 weeks [28].

References