Steroid anti-inflammatory effectiveness

Schwaiger J, Ferling H, Mallow U, Wintermayr H, Negele R (2004) Toxic effects of non-steroideal anti-inflammatory drug diclofenac. Part I. Histopathological alterations and bioaccumulation in rainbow trout. Aquat Toxicol 68 141-150... 

However, it is important to note that the addition of nephrotoxic agents, such as amphotericin B, aminoglysides (e.g., gentamicin, tobramidn, or amikacin), and non-steroidal anti-inflammatory drugs (NSAIDs e.g., naproxen, ibuprofen, or ketorolac) may potentiate the nephrotoxic effects of the calcineurin inhibitors. 

Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, were utilized primarily to protect from inflammation. Other biological effects were also found gradually, for example, induction of apoptosis [94, 95], stimulation of immune activity... 

These refinements in our knowledge of brain penetration and CNS activity of drugs feature prominently in a major medicinal review of the blood-brain barrier [14]. In vivo perfusion studies on the rate of brain uptake of several non-steroidal anti-inflammatory drugs in rats with increasing concentration of albumin in the perfusate clearly demonstrate the effect of plasma protein binding on the rate (in addition to the extent at steady-state) of brain uptake [15]. 

Khawaja, A.M., Liu, Y.C., and Rogers, D.F., Effect of fenspiride, a non-steroidal anti-inflammatory agent, on neurogenic mucus secretion in ferret trachea in vitro, Pulm. Pharmacol. Then, 12, 363-368, 1999. 

Celecoxib, a non-steroidal anti-inflammatory drug, is a cyclo-oxygenase-2 selective inhibitor that is as effective as diclofenac and naproxen. It should be used for the shortest period required to control symptoms. Use is associated v/ith an increased risk of thrombotic events and the cyclo-oxygenase-2 selective inhibitors are contraindicated in cerebrovascular disease. Mobic is the proprietary preparation of meloxicam. 

Concomitant administration of methotrexate and Voltarol, a proprietary preparation of diclofenac, a non-steroidal anti-inflammatory drug, may result in accumulation of methotrexate as its excretion is reduced. The use of diclofenac and diuretics such as bendroflumethiazide may increase the risk of nephrotoxicity. Concomitant use of alcohol and an angiotensin-converting enzyme inhibitor such as lisinopril (Zestril) may result in an enhanced hypotensive effect. Alcohol and the benzodiazepine diazepam (Valium) may result in enhanced sedation. 

Indometacin, which is a non-steroidal anti-inflammatory drug, inhibits the enzyme cyclo-oxygenase implicated in inflammatory reactions. Indometacin is more effective as an anti-inflammatory agent than ibuprofen and tends to have a higher side-effect profile, including headache, diarrhoea and gastrointestinal disturbances. Rectal administration reduces but does not prevent gastrointestinal tract disturbances. 

Indometacin is an indole acetic acid derivative, while naproxen is a propionic acid derivative. Both are non-steroidal anti-inflammatory drugs (NSAIDs). Indometacin is associated with a higher incidence of side-effects, particularly gastrointestinal as well as headache and dizziness. 

The first-line agents in the treatment of rheumatoid arthritis are non-steroidal anti-inflammatory drugs such as diclofenac. Diclofenac and indometacin, another NSAID, tend to have similar activity hov/ever, indometacin has a higher incidence of side-effects and therefore diclofenac is more appropriate for initial treatment. Sodium aurothiomalate is classified as a disease-modifying antirheumatic drug and is used as a second-line treatment in rheumatoid arthritis, but has been superseded by methotrexate, administered v/eekly. Paracetamol is often indicated in the management of osteoarthritis. Local intra-articular injections of dexamethasone may be administered for the relief of soft-tissue inflammatory conditions. 

Naproxen, a non-steroidal anti-inflammatory drug, inhibits prostaglandin release through inhibition of the cyclo-oxygenase-2 enzyme, producing an analgesic and anti-inflammatory effect. 

Beta-adrenoceptor blockers block the sympathetic system antagonising the effect on the lungs, resulting in bronchoconstriction. Non-steroidal anti-inflammatory drugs inhibit prostaglandin synthesis, which may lead to bronchoconstriction. 

Alternative products to diclofenac include naproxen and mefenamic acid, both of which are non-steroidal anti-inflammatory drugs. Co-codamol is a mixture of the opioid analgesic codeine and paracetamol and it does not possess the anti-inflammatory component. It may be used in pain management either where NSAIDs are contraindicated or in patients who are intolerant to the effects of NSAIDs. 

Acetylsalicylic acid and related non-steroidal anti-inflammatory drugs (NSAIDs) selectively inhibit the cyclooxygenase activity of prostaglandin synthase [2] and consequently the synthesis of most eicosanoids. This explains their analgesic, antipyretic, and antirheumatic effects. Frequent side effects of NSAIDs also result from inhibition of eicosanoid synthesis. For example, they impair hemostasis because the synthesis of thromboxanes by thrombocytes is inhibited. In the stomach, NSAIDs increase HCl secretion and at the same time inhibit the formation of protective mucus. Long-term NSAID use can therefore damage the gastric mucosa. 

Flurbiprofen 622 (Froben , Cebutid ) is a non-steroidal anti-inflammatory whose structure makes it an ideal target for synthesis using a combination of the powerful deproto-nating ability of the superbases and the weakly directing effects of a fluoro or an aryl substituent (Scheme 243)" . 

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