Non-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogenetics

  • dose appropriately
  • pick the right drug and formulation?
    • Choose Cox-2 selective.
    • enteric coating (., aspirin) - a little protection, variable absorption
    • buffers (., aspirin) - a little protection, enhanced absorption
  • GI Protection?
    • PGE 2 analog - Misoprostol ® (Good evidence of efficacy)
    • Protectants (sucralfate) - no clear evidence
    • Omeprazole - no clear evidence
    • Cimetidine et al. - do not appear to be particularly effective for prevention.

NSAIDS have antipyretic activity and can be used to treat fever. [75] [76] Fever is caused by elevated levels of prostaglandin E2 , which alters the firing rate of neurons within the hypothalamus that control thermoregulation. [75] [77] Antipyretics work by inhibiting the enzyme COX, which causes the general inhibition of prostanoid biosynthesis ( PGE2 ) within the hypothalamus . [75] [76] PGE2 signals to the hypothalamus to increase the body's thermal set point. [76] [78] Ibuprofen has been shown more effective as an antipyretic than paracetamol (acetaminophen). [77] [79] Arachidonic acid is the precursor substrate for cyclooxygenase leading to the production of prostaglandins F, D & E.

Non-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogenetics

non-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogenetics

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non-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogeneticsnon-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogeneticsnon-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogeneticsnon-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogeneticsnon-steroidal anti-inflammatory drugs for cancer prevention promise perils and pharmacogenetics

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