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Shock NSAIDs

Antibacterial agents, vaccines and non-steroidal anti-inflammatory drugs (NSAIDs) may all lead to anaphylactic shock if the patient is allergic to these products. [Pg.299]

Acetyls alley lie acid was shown to prevent cirrhosis under certain experimental conditions [125]. Naproxen and indomethacin partially protected against LPS and D-galactosamine-in-duced hepatotoxicity [126] Acetylsalicylic acid and ibuprofen were also protective in endo-toxic shock [127]. Endotoxaemia is one of the complications in cirrhotic patients [128] and is probably caused by an impaired ability of the liver to take up and detoxify gut-derived LPS [116]. The presence of portosystemic shunts in cirrhotic patients may also contribute to this spill-over of LPS into the systemic circulation [129]. NSAIDs, however, are also reported to provoke deleterious effects on renal function in cirrhosis [130], and can therefore not be used in cirrhotic patients. Cell-specific delivery of NSAIDs to SECs and/or KCs may make application of these drugs in cirrhosis feasible by circumventing the renal side-effects. [Pg.104]

A small number of individuals exhibit aspirin intolerance or supersensitivity.84 These individuals comprise approximately 1 percent of the general population, but the incidence is considerably higher (10%-25%) in people with asthma or other hypersensitivity reactions.84,94 People with aspirin intolerance will display allergiclike reactions, including acute bronchospasm, urticaria, and severe rhinitis, within a few hours after taking aspirin and aspirinlike NSAIDs.45,76 These reactions may be quite severe, and cardiovascular shock may occur. Likewise, sensitivity to aspirin often indicates a concomitant sensitivity to other NSAIDs, including COX-2 selective drugs.92 Consequently, the use of all NSAIDs is contraindicated in these individuals.84... [Pg.206]

While the pattern of alclofenac toxicity resembles that of other NSAIDs, the frequency of adverse effects differs widely. Allergic reactions have been reported more frequently and skin rashes have been particularly common. Hypersensitivity reactions, including anaphylactic shock, severe generalized vasculitis, hepatotoxicity, and nephrotoxicity, have been observed. Alclofenac has therefore been withdrawn in several countries (1). Blood dyscrasias and neurological symptoms are rare. [Pg.57]

Among the anaphylactic reactions to NSAIDs that result in different types of reaction (urticaria, angioedema, asthma, or hypotension), there have been very few reports of anaphylactic shock. However, anaphylaxis has been described in patients taking celecoxib (135,136) or rofecoxib (137). Rofecoxib caused anaphylaxis in a patient who had had a similar reaction to diclofenac, suggesting that COX-2 inhibitors may be not safe in all individuals who have adverse reactions to non-selective COX inhibitors. It also suggests that different mechanisms may be involved in patients with asthma and in those with anaphylactoid reactions to NSAIDs. [Pg.1010]

Asthma and anaphylactic shock are the most dangerous acute hypersensitivity reactions. There is cross-sensitivity with other NSAIDs (18). Rash, urticaria, and pruritus accompany more serious reactions. [Pg.2231]

NSAIDs can mask signs of infection, such as fever and pain, which can delay appropriate treatment. Furthermore they can impair the host defence mechanism against infection and can modulate the acute inflammatory response in such a way as to alter the course of infection, predisposing the patient to bacteremia, shock, and multiorgan failure (212,213). Until appropriate studies have defined the relation between NSAIDs and severe soft tissue infections, it is better to avoid using them, if possible, until the cause of the fever is known. [Pg.2572]

Stevens DL. Could nonsteroidal antiinflammatory drugs (NSAIDs) enhance the progression of bacterial infections to toxic shock syndrome Clin Infect Dis 1995 21(4) 977-80. [Pg.2581]

Acute renal failure 4pg,4rbe,4gpr Hemodynamic disruption CHF, renal disease, hepatic disease, diuretic use, advanced age, dehydration, SEE, shock, sepsis, hyperreninemia, hyperaldosteronemia Discontinue NSAID, support with dialysis and steroids, if needed... [Pg.424]

To summarize patient a risk of NSAID-induced AKI. Frequency will be greater in patient populations with restricted renal blood flow, e.g. CHF, cirrhosis, nephrotic syndrome, shock. However, for absolute numbers, the elderly are probably most at risk since they are the primary group who take NSAIDs for re-heve rheumatic complaints [3]. [Pg.427]

Certain individuals display hypersensitivity to aspirin and NSAIDs, as manifested by symptoms that range from vasomotor rhinitis with profuse watery secretions, angioedema, generalized urticaria, and bronchial asthma to laryngeal edema, bronchoconstriction, flushing, hypotension, and shock. Aspirin intolerance is a contraindication to therapy with any other NSAID because cross-sensitivity can provoke a life-threatening reaction. [Pg.438]


See other pages where Shock NSAIDs is mentioned: [Pg.445]    [Pg.174]    [Pg.177]    [Pg.36]    [Pg.269]    [Pg.82]    [Pg.94]    [Pg.101]    [Pg.152]    [Pg.186]    [Pg.200]    [Pg.230]    [Pg.235]    [Pg.250]    [Pg.267]    [Pg.287]    [Pg.317]    [Pg.327]    [Pg.82]    [Pg.94]    [Pg.101]    [Pg.152]    [Pg.186]    [Pg.200]    [Pg.230]    [Pg.235]    [Pg.250]    [Pg.267]    [Pg.287]    [Pg.317]    [Pg.327]    [Pg.368]    [Pg.2571]    [Pg.427]    [Pg.253]    [Pg.179]    [Pg.1971]    [Pg.286]    [Pg.287]   
See also in sourсe #XX -- [ Pg.427 ]

See also in sourсe #XX -- [ Pg.286 ]




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