Peter, I book-marked the site.
C3=< More aggressive regimens, containing experimental therapies, will likely be necessary in order to achieve durable, complete viral suppression in patients no longer responding to indinavir.>. I reckon that means none of the current drugs, combinations, &/or regimes are effective for all patients. New drugs against unique targets will certainly be well-comed.
C4=<However, data presented at these meetings, and at the recent St. Petersburg Resistance Workshop in Florida, suggests that that the G48V and L90M mutations commonly seen after saquinavir therapy confers significant cross-resistance to indinavir. Therefore, indinavir (with dual nucleoside analogues) may not always be sufficient for patients previously treated with saquinavir.>. G48V mutation is highly conservative, how came it confers resistance? L90M is further apart. Damn........
C4=<t Merck 035 remains a valuable source of clinical data. Indinavir, as part of an initial three-drug combination, is extremely effective at suppressing viral replication. This effect appears to be durable. Unfortunately, the long-term ability of indinavir to suppress viral replication is limited when added to a pre-existing nucleoside regimen. This data supports current recommendations that protease inhibitor therapy should be used initially in aggressive three-drug combinations.> I hope all MDs will follow it.
C5=<In minimally pre-treated patients, the combination of AZT, 3TC and nelfinavir has a potent and durable anti-viral response, with long-term results comparable to that seen with AZT, 3TC and indinavir in Merck 035. >. Like I said before AGPH is as good as anybody else. But not good enough for the patients. We all should/could be better in that sense.
C6=<This data set is the first independent analysis correlating pharmacokinetic parameters with antiviral activity. Limited or inconsistent exposure to indinavir may explain a large proportion of drug failures. If confirmed in larger studies, individual drug monitoring may become a necessary clinical tool in managing HIV disease. >. That is why I asked PB about AGPH's efford in improving its baby? anything new about that?
C7=< Ritonavir continues to be an impressive agent when used in combination with other protease inhibitors, largely due to its powerful and predictable effect on cytochrome P450.> P450 is responsible for drug clearance. Inhibition of its activity will help drug effect.
C9=<: Both of these studies strongly suggest that protease inhibitors exert an anti-HIV effect in the central nervous system. The University of Washington data suggests that this effect is due to penetration of the drug past the blood-brain barrier (at least for indinavir). > Has AGPH tried to improve its BBB penetration ability?
Conclusion=<The antiviral activity of potent protease inhibitor therapy in the "real world" setting is likely to be less than that reported in small, controlled clinical trials.> In the treatment of HIV or any other diseases, progress is incremental, any new addition or the understanding of the necessity of new addition in any way, by themselves, is revolutionary. Shall I feel guilt about myself a job not well-done enough?
This is just too long, & it is getting late.
regards |
