Omeprazole is almost useless for potentiation; use cimetidine.
Hydrocodone is primarily metabolized via CYP3A4, into norhydrocodone, an inactive metabolite. It is also metabolized, to a much lesser extent, into hydromorphone via 2D6. Whether or not 2D6 inhibition matters is a point of contention; BUT 3A4 metabolism is definitely a good thing, as it extends duration.
Best bet with hydrocodone is to drink 1.5-2 liters of white grapefruit juice, an hour beforehand, and then take the hydro with baking soda. I personally recommend Ocean Spray. This will push BA to near 100%, and make the hydro stronger, and last slightly longer. Cimetidine, or better yet a 3A4 selective inhibitor like erythromycin will extend duration.
But, IME, only WGJ significantly enhances hydro, and it still isn't as dramatic of an effect as say, methadone.(with WGJ)
And FYI, 1 glass of grapefruit, or 400mg of cimetidine won't do shit. You really need 1.5-2ltr WGJ, and 800mg Cimetidine.
Firstly, to a previous poster, may I ask if 'diclazepam' is actually CHLORDIAZEPAM? I looked it up and it does not appear to be a drug which is marketed anywhere at all, but was one of Sternbach's discoveries for ROCHE when investigating chlorination and fluoridation of classical BZDs in the early 1960s.
I have looked and looked and still can not find any (to me) valid chemical reasoning why a PPI such as lansoprazole or Omeprazole would potentiate any opioid at all. Anyone able to provide a good reason?
I am glad to see that you have correctly identified the secondary metabolite of Hydrocodone, which first metabolite is simply the dihydromorphine and codeine produced also by its parent drug, dihydrocodeine (Hydrocodone is more properly chemically named dihydrocodeineone). Usually encountered as the tartrate, the ketonal version you discuss is molecularly a natural for the BItartrate due to the structure, which may be seen in 3D on the relevant article on Wikipedia. Note also the extremely small changes to that molecule which result in the dihydrocodeineone having a potency of around three or four times that of the original dihydrocodeine.
Your dosage of cimetidine is way too high for anybody to take for any reason whatever. The stuff. DOES have a ceiling you know, and 800mg is way above that.
Having required thanks to insufficient prescribing over the past few years to potentiate my opioids (OxyContin, being in the UK that means REAL OxyContin, not the pretend stuff sold now in the USA which uses an MR formulation which actually inhibits the bioavailability and therefor the overall analgesia obtained from any dosage given; and my rescue drugs, dipipanone with cyclizine tabs 10/30mg three prn, dextromoramide tartrate tabs 5mg FOUR or FIVE prn, Oxynorm caps 20/10/5mg dosage 35mg, hydromorphone hydrochloride caps IR 2.6mg four or five prn and diamorphine hydrochloride tabs 10mg four prn, 200mg cimetidine plus 25-50mg cyclizine and carisoprodol tabs either 350 or 500mg (if you can find it since the almost worldwide ban in 2007 - India and a couple of Soth American countries appear to be the only places where it may now be procured, oh, and South Africa as well but the carisoprodol I have had originating there has always been of the worst possible quality - Argentina produces the finest, Listaflex brand - is quite sufficient to bring my analgesia back up to former levels.
The banning of carisoprodol was also a great blow to me as it is, because of drug interactions with current Rx and side effects of all other available SMRs it is the ONLY medicine which is able to help with my long standing lumbar muscular problem. The potentiation factor was really a great bonus, now I must pay vastly inflated costs for this once cheap and common drug which is now one of the most difficult to find in the entire world. And the Indian brands which are affordable (just - they appear to be targetting US customers with their profiteering there) are not exactly as good as the CARISOMA that I used to be prescribed in 350mg tabs. Opioid analgesics do nothing for that kind of pain, I use those for completely different conditions.
Grapefruit juice, as far as I can make out, has little effect on metabolism of drugs acting at opioid receptors but a huge effect on those which process benzo and thieno diazepines, barbiturates and alcohol. Can you refer me to any study which connects the use of these enzymes with opiates, semi synthetics and synthetic opioids or any other drug acting at mu-receptor sites?
As far as antihistamine potentiators are concerned, dipipanone tablets are not combined with cyclizine just for the enhanced antiemesis but because cyclizine has been known for over sixty years to enhance the potency of synthetic opioids. It is also used by 'recreational' users of opiates/oids as such, and is available OTC as VALOID but now only in 50mg dosage.
I need potentiation because of bad doctoring principally. And the opiophobia of the UK NHS which has grown over the past 20 years, as has benzophobia, to the extent that there are now only NINE of the 45 (or 46) marketed BZDs listed in the BNF, and the withdrawal of opiates and opioids carries on apace - the newer combo SNRI opioids (tramadol, tapentadol) which are effective in only around 50-60% of the population, SNRIs being almost as badly tolerated as SSRIs to what is an absolutely MASSIVE clinical degree given that 1/100 is described as 'extremely common' when discussing side effects in academic parlance. 1/1,000 'common'.
Let us hope that the people who are most interested in this thread are so because of the clinical implications of insufficient prescribing now taking place and not purely for the pleasure principle.