^ I'll be honest and say that I don't know what the mechanism of this observation could be, but it is from a study in dogs - dogs do not have the exact same biochemistry as humans (all mammals have slightly different biochemisty, meaning that they respond differently to the same drug). It's possible that dogs do not possess significant amounts of plasma pseudoesterase to metabolize the GBL to GHB.
My reason for the above comment is based on the following study
Journal of Toxicology: : Volume 39, Number 6 / 2001 Pages: 653 - 654 DOI: 10.1081/CLT-100108502
"During GHB poisoning, acidosis can be due to respiratory acidosis (1), metabolic acidosis has also been reported (2)..."
The above was from an article about GHB intoxication in people admitted to emergency rooms. GBL was also stated to produce metabolic acidosis in large doses, so unlike in dogs (which was also using intravenous infusion of the drugs)
both GHB and GBL have been found to produce acidosis in humans (so GBL isn't inherently more dangerous in humans than GHB).
This observation (that both produce acidosis in humans as well as 1,4-BDO) is also confirmed in the following:
Gamma-hydroxybutyrate, gamma-butyrolactone, and 1,4-butanediol: A case report and review of the literature.
Pediatric Emergency Care. 16(6):435-440, December 2000.
This leads to the conclusion that it must be GHB that is responsible for the acidosis as the only metabolite that GBL & 1,4-BDO have in common is GHB. As to how GHB causes the acidosis, that's still up for discussion as far as I know, but I'm still putting money on endocrine effects until all the evidence is in.
Incidentally, 1,4-BDO is much more toxic than either GHB or GBL as it requires the liver to convert it to GHB via alcohol dehydrogenase in a manner analogous to the metabolism of ethanol to acetic acid, thereby putting a 'load' on the liver in the same way alcohol does (and we all know the damage large doses of alcohol can have on the liver). It also appears to be similar to other polyhydric alcohols in irritating the lining of the GI tract
With regard to you & your g/f's admission to hospital, was she on any meds that you were not (I'm including the contraceptive pill)? This can alter the bone density for women (which is why women are many times more likely to suffer from oesteoporosis after the menopause), leading to easier fracturing of bones. Such conditions can also occur due to things like mineral/vitamin deficiency from poor diet (a common cause of ill health in persons dependant upon drugs of abuse) and inhertited risk factors.
I did a search for other threads re GBL/GHB and found this comment that you posted a while ago
Note how acidic compounds (which GBL is) in the human diet causes acidosis.
GBL isn't an acidic compound as it does not alter the concn of hydrogen ions in solution. While I agree with the statement in your post that consuming acidic compounds can lead to Ca++ depletion because of reduction of plasma pH (consequently solublizing Ca++ ions from bone), I don't think you can make the logical jump to GBL causes Ca++ depletion because it's acidic because of the fact that GBL isn't acidic, nor does it 'leave behind' an excess of H+ during conversion to GHB as the hydrolysis of GBL to GHB consumes a H+ and an OH- ion therefore leaving the concn of H+ ions unaltered.