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Background and purpose: Aspirin reduces the risk of myocardial infarction and stroke by inhibiting thromboxane production in platelets. This inhibition can be competitively antagonized by some non-steroidal anti-inflammatory drugs (NSAIDs). Experimental approach: By measuring thromboxane B2 production in healthy volunteers, we investigated whether ibuprofen (800 mg three times daily for 7 days) or diclofenac (50 mg three times daily for 7 days) taken concurrently with aspirin 80 mg (once daily for 7 days) influenced the inhibitory effect of aspirin. The effects were compared with aspirin 30 mg (once daily for 7 days), which is the lowest dose of aspirin with a proven thromboprophylactic effect. Key results: The median percentage inhibition of thromboxane B2 levels by 30 mg or 80 mg aspirin was 90.3% (range 83.1-96.0%) and 98.0% (range 96.8-99.2%) respectively. The inhibition by concurrent administration of slow release diclofenac and 80 mg aspirin was 98.1% (range 97.2-98.9%), indicating no interference between aspirin and diclofenac. The inhibition decreased significantly by concurrent administration of immediate release ibuprofen and 80 mg aspirin (86.6%; range 77.6-95.1%) to a level less than 30 mg aspirin. Conclusions and implications:As alternatives are easily available, NSAIDs such as diclofenac should be preferred to ibuprofen for combined use with aspirin.

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The influence of co-trimoxazole on colonization resistance of the bowel was investigated in six healthy volunteers, by measuring the numbers of indigenous aerobic flora and of a co-trimoxazole resistant challenge strain of Klebsiella pneumoniae. Impairment of colonization resistance of the bowel was shown by a significant increase in the numbers of yeasts in the faeces of five of six volunteers, by a significant increase in the numbers of Gram-negative bacilli in the faeces of two of six volunteers, and by facilitation of colonization of the bowel by the challenge strain in all volunteers. Impairment of colonization resistance of the mouth was shown by the development of glossitis caused by Candida albicans in two volunteers, and by a significant increase in the numbers of yeasts in mouth washings from four volunteers. It is concluded that co-trimoxazole impairs colonization resistance of the gastro-intestinal tract.

The influence of cefotaxime 1000 mg given intravenously bd on microbial colonization resistance was investigated in six healthy volunteers. Administration of cefotaxime allowed colonization of the bowel by a resistant challenge strain of Enterobacter cloacae in all volunteers. The faecal concentration of aerobic flora increased significantly in five of six volunteers. In one the numbers of Gram-negative bacilli, enterococci and yeasts also increased. In the other four the faecal concentration of enterococci and yeasts increased, but Gram-negative bacilli did not rise above pre-treatment level. It is concluded that cefotaxime impairs colonization resistance, although to a variable degree. Therefore the term 'selective decontamination' is not fully justified for prophylactic regimens that include cefotaxime.