i don't know anything specific about liver metabolism of this compound vs others, but my guess is that unless there is a unique reason for degredation it souldn't be worse than other compounds. for example testolactone has a similar oxygen in the D ring and that compound to my knowledge has no super rate of breakdown. i suspect that the 17aa gives a lot longer than normal breakdown times which lead to such little amounts being required. however even those little amounts are enough to mess up the liver, while much larger amounts of non 17aa do not. the whole concept of first pass breakdown has been blown a little out of proportion. everything is going to have some first pass breakdown, the question is how much. even if we can prevent that, we have learned that some of the modifications which do this are in fact much more harmful than using more of the unmodified hormone especially with a time release delivery achieved by injection of esterified hormones or transdermal application of the base. testosterone is degraded quickly by the liver but we get around it by the time release delivery to keep the level constant. i believe that liver is better off removing 2 or 3 times as much unmodified hormone than a 17aa version. that leaves the question of is the unmodified version able to exhibit the same effects.
a side note:
people always talk about steroids increasing muscle protein synthesis. but what does this really mean? it can refer to the contractile apparatus, but this is only one aspect of increased synthesis of muscle proteins. how about if the enzymes responsible for replenishment of ATP from creatine phosphate or the transport of creatine into the muscle cell. if a hormone would cause the synthesis of these proteins (enzymes are proteins) to increase which would lead to increased muscle mass since you could lift more (assuming you ate enough). i assume anavar works through one of these pathways. why is this so? well you have to understand how hormones affect protein synthesis. basically they bind to proteins which allow them to bind to DNA segments in front of the coding region for the gene (any gene). the place where this binding occurs is very specific and there are also binding areas for other factors and different types of hormones, some of which can block or intensify the signal (obviously testosterone intensifies muscle building signals) - by signal, i mean the production of protein mediated through the production of RNA. in the case of anavar, it just happens that whatever binding occurs in the upstream region for that gene happens to be stronger than that of testosterone. why? there are too many possible mechanisms, but whatever it is the mechanisms are similar for any gene, it just happens that for some reason due to its unique 3D structure, anavar causes bigger protein synthesis in a specific protein involved in the creatine metabolism. the how and why may not be known to a detailed level, but once researched it would be elucidated quite quickly as all such systems are variations of the same basic idea (once again something simple adds up to be complicated.