Posted on 04/28/2003 5:35:00 AM PDT by TaxRelief
(This is a very technical article: See translation in comment, below.)
Assuming that, as in the case of mouse hepatitis coronavirus (MHV), activation of p38 MAP-kinase contributes to SARS virus replication, these results suggest that salicylates (aspirin) should NOT be given to SARS patients. In view of the antipyretic effects of ASA (acetylsalicylic acid, aspirin) this drug is likely to be in widespread use among early-stage SARS patients. It could be a factor contributing to the severity of the syndrome. For this reason I believe it imperative that ASA use among SARS patients be assessed as rapidly as possible in order to determine whether it has contributed to the severity of individual cases.
It gets more complicated, but interesting:
In a follow-up to my earlier posting [see part 1 above] concerning the possible utility of p38 MAP-kinase inhibitors in the treatment of SARS, I have located a number of references where p38 MAP-kinase has been reported to be ACTIVATED by salicylates.
Two publications have described the effect of the p38 MAP-kinase (mitogen-activated protein kinase) inhibitor SB203580 on mouse hepatitis virus strain 3 (MHV)(McGilvray ID, et al. J Biol Chem 1998; 273(48): 32222-9 and Banerjee S, et al. J Virol 2002; 76(12): 5937-48). In the latter paper the authors state that MHV activation of the p38 MAP-kinase pathway results in phosphorylation of the translation initiation factor eIF4E, which in turn contributes to a high level production of virus. SB203580 reduced MHV particle production by a factor of 3.
Although there is as yet no direct evidence to suggest that the SARS coronavirus uses the p38 MAP-kinase pathway, phosphorylation of eIF4E is likely to prove a conserved coronaviral mechanism for directing cellular protein synthesis towards production of viral particles. SB203580 also has potent anti-inflammatory activity: (see: Ermert M, et al. Cyclooxygenase-2-dependent and thromboxane-dependent vascular and bronchial responses are regulated via p38 mitogen-activated protein kinase in control and endotoxin-primed rat lungs. Lab Invest 2003; 83(3): 333-47).
These findings suggest p38 MAP-kinase may prove a useful target for the control of SARS symptoms and possibly also to limit replication of the virus. Perhaps p38 MAP-kinase inhibitors could have application in in the treatment of SARS? I gather that 3 such compounds (SB281832, BiRB0797, and Ro320-1195) have gone through phase II clinical trials for treatment of asthma and/or rheumatoid arthritis and that pharmacokinetics and potential toxicities of these compounds must therefore have been characterized.
If it turns out that the worse cases did use aspirin in the early stages, then research should be directed towards how "activation of p38 MAP-kinase " affects the reproduction of the SARS virus, which in turn will lead to possible treatment drugs.
He is not suggesting that aspirin is a factor, but suggests research concerning uses of aspirin should commence immediately.
Thus when the possibility is alleged to exist that aspirin is somehow a negative in connection with spreading of a virus, we tend to be very very skeptical.
Fine to study and assess the possibility at somebody elses expense. But until demonstrated otherwise, this is just another argument by the medical profession that people shouldn't use aspirin.
An unaccountably silly remark. Tell that to the thousands who are recommended to take a baby aspirin every day by their doctors. Also, it's a standard now for treatment in the presentation of heart attacks.
Aspirin is a powerful med.
Docs do not have a proprietary interest in the drugs they prescribe. AAMOF, they'd like to use the cheaper drugs in some cases, but are frightened away by the prospect of litigation. Case in point, there was a cheaper treatment for heart attacks available a few years back, but the drug company with the more expensive med managed to create a better (slightly, slightly better) record on paper. The hospitals were forced to use the more expensive drug for fear that they'd end up in court--a matter of documentary evidence. As a result, treatment for heart failure suddenly cost $2700 more than it had to. Multiply that by hundreds of thousands, and it's just one example.
It's a lawyer thing, not a doctor thing.
Another reason to research whether or not anyone has taken aspirin in the early stages of SARS.
Reyes syndrome used to kill 6000+ kids a year. Then they discovered that aspirin was the culprit behind Reyes. Now it only kills a handful of kids a year.
The problem may be an obsession with suppressing fever, rather than allowing a carefully monitored fever to do the job God intended it to do.
It's a good blood thinner, for preventing clots and strokes.
Viruses stop reproducing at a 101 temp which gives the body's natural defense a chance to kill them off. Taking any drug to drop the temp caused by a fever, which in turn allows the virus to reproduce , isn't the best idea. Letting the fever run it's course , even if you feel rotten , is the best thing to do. A temp over 104 is a different story.
We're talking a baby aspirin , every other day or less. Ask a doctor.
Ditto...and I do.
Example? Water retention. There's a drug women can buy to "combat" water retention during their menstrual cycles. This highly profitable drug (for the makers) "gets rid of the bloating caused by water retention."
Question? Do these medical quacks ever pause and ask "why"? Why is the body retaining water? Could it be, and this is just a wild guess, that the body is "starved" for water? Hmmm, do ya think so?
Maybe, "water retention" is a "sign" that the person is not drinking enough water. So the medicos say; "Gee, you're retaining water, here's a drug to suppress that awful symptom. Cha-ching." What they don't say is; "You need to increase your daily water consumption."
Maybe drug companies are willing to invest $200 million dollars developing a new drug because "they care about you". Caring and sharing.
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