Utilization of these drugs is common in patients with HF. In a study from Denmark, 34 percent of patients received at least one nonsteroid anti-inflammatory agent or cyclooxygenase-2 inhibitor after discharge for first hospitalization for HF [ 2 ]. Use of some of these drugs may be increasing. As an example, a review of Medicare beneficiaries hospitalized with the diagnoses of HF and diabetes mellitus found that the proportion using metformin and/or a thiazolidinedione increased from percent in 1998 to 1999 to percent in 2000 to 2001 [ 3 ].
In the end when we examine the various steroid drugs there is an important note we must discuss and to leave this out would be somewhat irresponsible. Anabolic androgenic steroids, while often referred to as drugs should not be viewed in the same typical light. Anabolic androgenic steroids are hormones, they are derived and based on hormones your body already naturally produces placing them in a bit of a unique category as compared to many of the other items you might find at your local RX. Of course the specific definitions can be a bit fuzzy at times, especially when we look at the manner in-which drugs are defined in the . Under . law drugs are defined as any substance that alters the body other than food from its normal function but guess what, alcohol is excluded from this rule and while anabolic androgenic steroids are a part of the normal human bodily function they are by no means excluded. Its a bit of a paradox as even the simplest minded can see.
A number of arguments counted against the COX-3 hypothesis: COX-2-selective inhibitors react weakly with the COX-3 enzymatic site, because the site is identical to that in COX-1, but they are as good at reducing fever as older NSAIDs. The fever response has also been clearly associated with a rapid induction of COX-2 expression and an associated increase in prostaglandin E2 production, with no role for COX-1 or a COX-1 gene product (., COX-3). Finally, the sites of COX-3 expression do not appear to fit in well with those sites associated with fever, and the protein should be present within the hypothalamus rather than the cerebral cortex . All these considerations appeared to argue against COX-3 being the site of the antipyretic actions of NSAIDs and COX-2-selective agents. However, the results could be read as showing that paracetamol acts at a different site than the other NSAIDs and that more than one COX isoform contribute to the fever response.