Prostaglandins (PG) have been described as mediators in spinal nociceptive processing after peripheral inflammation. Enzymes essential for PG biosynthesis, cyclooxygenase isozymes COX-1 and COX-2, have not yet been investigated in the spinal cord. In two studies on rats with adjuvant-induced peripheral inflammation levels of mRNA expression of both COX isoforms were analyzed in the lumbar section of the spinal curd using reverse transcription-polymerase chain reaction (RT-PCR) technique. We could show that mRNA of both COX isoforms is expressed constitutively in the spinal cord with COX-2 as the predominant isoform. Six hours after induction of peripheral inflammation, levels of COX-2 mRNA expression were raised significantly in respect to untreated control rats and returned to baseline within 3 days after induction of inflammation. COX-2 might therefore be regarded as the COX isozyme responsible for spinal PG release in nociceptive processing under a peripheral inflammatory stimulus.l~ey words: Cyclooxygenase-2; Inflammation; Spinal cord; R F-PCR densa of the kidney [8] the testis or the brain, where COX-2 is not only expressed constitutively but also considered to be the dominating COX isoform [9][10][11]. In the central nervous system (CNS) prostaglandins maintain important functions as neuroregulators [12]. It has been reported that PGs are released from the spinal cord by various processes as stimulation of afferent nerves [13], noxious thermal stimulation [14] and by increased potassium levels [15]. Prostaglandins are also known to be involved in transmission of nociceptive information in the spinal cord after peripheral inflammation [16]. Functional evidence thus indicates a role for cyclooxygenases in the spinal cord, expression of the enzyme itself, however, has not yet been investigated. We conducted two studies to determine the spinal presence and distribution of COX isozymes using the rat model of adjuvant-induced inflammation. Tissue samples of hindpaws and the lumbar section of the spinal cord were taken before and after induction of inflammation and examined for levels of COX mRNA expression by reverse transcription-polymerase chain reaction (RT-PCR).

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This paper reviews recent studies that have aimed to establish the relative bioavailability of a new oral formulation of meloxicam, and to evaluate its safety and efficacy in a clinical setting. For the bioavailability study, 16 healthy volunteers were randomised to receive either an oral or a solid formulation of meloxicam 15 mg. The performance of the oral suspension was tested in 286 patients with osteoarthritis who were randomised to receive either formulation at 7.5 mg daily. It was found that the new oral suspension was bioequivalent to the capsules formulation, and was more rapidly absorbed after a single dose. No clinical differences were observed in both efficacy and tolerability parameters with either type of formulation in patients with osteoarthritis. The oral suspension was well accepted by the patients. Hence, the oral suspension provides a useful alternative to solid formulations in the treatment of inflammatory joint diseases and painful musculoskeletal disorders.

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Clofibrate altered the stereoselective disposition of ibuprofen in healthy volunteers by increased formation of R-ibuprofenoyl-coenzyme A rather than by an effect on oxidative metabolism of ibuprofen. This interaction has potential therapeutic implications.

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