Codeine and Tramadol CYP2D6 Conversion Interpreter

Codeine and Tramadol CYP2D6 Conversion Interpreter

Codeine and tramadol are prodrugs activated by CYP2D6, so a fixed oral morphine equivalent factor is wrong in both tails — far too low in an ultrarapid metaboliser and far too high in a poor one. This page reads the published factor against the CPIC phenotype.

What CYP2D6 phenotype does to a fixed conversion factor

3 drug groups, 5 phenotypes
Only the first two are the prodrugs this page is about. The last three are here because they are what a reader reaches for next, and because the honest answer for each of them is that CPIC does not make a recommendation — which is different from saying the genotype does not matter.
These are the current bands, which moved in the 2019 to 2020 CPIC and Dutch Pharmacogenetics Working Group consensus: an activity score of exactly 1 — the score of the common CYP2D6 *1/*4 genotype — is now an intermediate metaboliser where it used to be a normal one. The activity score page computes the score from the two allele values.
A strong inhibitor converts a genotypic normal metaboliser into a phenotypic poor one, and the activity score cannot see it. This is the commonest reason a genotype result and a patient’s actual response disagree, and it is why a genotype alone is not a phenotype.
Not genotyped: the fixed factor is a population average, wrong in both tailsExample

Codeine, CYP2D6 phenotype not known, no strong CYP2D6 inhibitor — the ordinary case

Advertisement

Why a fixed factor is wrong at both ends

Codeine → morphine, and tramadol → O-desmethyltramadol, both by CYP2D6
Published factors, applied identically to everybody: codeine 0.1 (Faculty of Pain Medicine, Scottish Palliative Care Guidelines, BNSSG, Severn Hospice) or 0.15 (CDC 2022 and pre-2022); tramadol 0.1 (Faculty of Pain Medicine, Scottish Palliative Care Guidelines, BNSSG, CDC pre-2022), 0.15 (Severn Hospice) or 0.2 (CDC 2022)
CYP2D6 activity score bands: 0 poor; above 0 and below 1.25 intermediate; 1.25 to 2.25 normal; above 2.25 ultrarapid
the prodrug problem
CPIC states that codeine and tramadol “are O-demethylated by CYP2D6 to the more active metabolites morphine and O-desmethyltramadol, respectively”. The dose on the chart is the prodrug; the exposure that matters is the metabolite, and the step between them varies between people by more than any disagreement between conversion tables
the ultrarapid tail
“Increased formation of morphine leading to higher risk of toxicity”, and CPIC’s strong recommendation is “Avoid codeine use because of potential for serious toxicity”. The published factor understates the exposure here, and nobody has published a corrected factor for this phenotype
the poor tail, and why it is the dangerous one for conversion
“Greatly reduced morphine formation leading to diminished analgesia”. The published factor overstates the exposure, so converting such a patient off codeine credits them with an opioid history they do not have — and the arithmetic then implies a tolerance that is not there
phenoconversion
paroxetine, fluoxetine, bupropion, quinidine and terbinafine are strong CYP2D6 inhibitors and turn a genotypic normal metaboliser into a phenotypic poor one. An activity score computed from alleles cannot see this, which is why a genotype is not a phenotype
the boundary that moved
the 2019 to 2020 CPIC and Dutch Pharmacogenetics Working Group consensus made an activity score of exactly 1 an intermediate metaboliser where it had been a normal one. That is the score of the common CYP2D6 *1/*4 genotype, so the same report means different things before and after the consensus
tramadol’s second mechanism
tramadol is not only an opioid prodrug; it also inhibits serotonin and noradrenaline reuptake. A poor metaboliser may therefore get a partial response that does not prove the CYP2D6 pathway is working, and the serotonergic action brings a hazard that no opioid conversion factor represents
what CPIC does not recommend
for oxycodone and methadone, “There is insufficient evidence and confidence to provide a recommendation to guide clinical practice at this time”; for OPRM1 and COMT, “There are no therapeutic recommendations for dosing opioids based on either OPRM1 or COMT genotype”. Dihydrocodeine appears only in the literature-search list

Worked example

Codeine, CYP2D6 phenotype not known, no strong CYP2D6 inhibitor — the ordinary case
The published factor is applied identically to everybody: 240 mg of codeine a day × 0.1 is 24 mg of oral morphine equivalent by every United Kingdom source read here, and × 0.15 is 36 mg by both CDC sets — a 1.5-fold disagreement before any genotype is considered
In an ultrarapid metaboliser, CPIC's implication is "Increased formation of morphine leading to higher risk of toxicity" and its strong recommendation is "Avoid codeine use because of potential for serious toxicity". The real exposure is above what either factor implies, and no source publishes a corrected factor
In a poor metaboliser, "Greatly reduced morphine formation leading to diminished analgesia", and the exposure is far below either factor. The same 240 mg a day is still scored as 24 or 36 mg of oral morphine equivalent on every chart
That second case is the one that bites on a conversion. Convert such a patient off codeine using the factor and the arithmetic credits them with an opioid history they never had, which implies a tolerance that is not there
Tramadol repeats the problem with a wider factor disagreement on top: 400 mg a day is 40 mg by the Faculty of Pain Medicine, the Scottish Palliative Care Guidelines, the BNSSG chart and CDC's pre-2022 file, 60 mg by Severn Hospice's 0.15, and 80 mg by CDC's 2022 table — a 2.00-fold spread that is entirely independent of the genotype
Add paroxetine and the genotype stops being the answer: a strong CYP2D6 inhibitor turns a genotypic normal metaboliser into a phenotypic poor one, and an activity score computed from alleles cannot see it
Switch the drug to hydrocodone and CPIC's table changes shape — "No recommendation for hydrocodone therapy because of minimal evidence regarding adverse events or analgesia" at the ultrarapid end. Switch to oxycodone or methadone and CPIC says "There is insufficient evidence and confidence to provide a recommendation". Switch to dihydrocodeine and the guideline does not cover it at all
Advertisement

CPIC’s positions, by drug and phenotype

DrugPhenotypeImplication, in CPIC’s wordsRecommendation, in CPIC’s words
CodeineUltrarapid, above 2.25“Increased formation of morphine leading to higher risk of toxicity”“Avoid codeine use because of potential for serious toxicity. If opioid use is warranted, consider a non-tramadol opioid.” Strong
CodeineNormal, 1.25 to 2.25“Expected morphine formation”Label-recommended age-specific or weight-specific dosing. Strong
CodeineIntermediate, above 0 and below 1.25“Reduced morphine formation”Label dosing; if no response and an opioid is warranted, consider a non-tramadol opioid. Moderate
CodeinePoor, 0“Greatly reduced morphine formation leading to diminished analgesia”“Avoid codeine use because of possibility of diminished analgesia.” Strong
TramadolUltrarapid, above 2.25“Increased formation of O-desmethyltramadol (active metabolite) leading to higher risk of toxicity”“Avoid tramadol use because of potential for toxicity. If opioid use is warranted, consider a non-codeine opioid.” Strong
TramadolPoor, 0“Greatly reduced O-desmethyltramadol (active metabolite) formation leading to diminished analgesia”“Avoid tramadol use because of possibility of diminished analgesia.” Strong
HydrocodoneUltrarapid, above 2.25not stated“No recommendation for hydrocodone therapy because of minimal evidence regarding adverse events or analgesia”
Oxycodone and methadoneAnynot stated“There is insufficient evidence and confidence to provide a recommendation to guide clinical practice at this time”. CPIC level C
Any opioid, OPRM1 or COMT genotypeAnynot stated“There are no therapeutic recommendations for dosing opioids based on either OPRM1 or COMT genotype”
DihydrocodeineAnynot discussedAppears only in the list of opioids the literature review searched
Every cell quoting CPIC is quoted from the 2021 guideline’s own tables. Note that the intermediate and normal recommendations for codeine and tramadol are the same, which CPIC states explicitly after the 2019 phenotype changes — the activity score moved but the advice at that end did not. Nothing in this table is a dose and nothing in it is this page’s own opinion.

The published conversion factors these phenotypes sit underneath

DrugFactorSources that publish it
Codeine0.1Faculty of Pain Medicine; Scottish Palliative Care Guidelines; BNSSG 2024; Severn Hospice
Codeine0.15CDC 2022 and CDC pre-2022; MSD’s 200 mg oral codeine against 30 mg oral morphine implies the same
Tramadol0.1Faculty of Pain Medicine; Scottish Palliative Care Guidelines; BNSSG 2024; CDC pre-2022
Tramadol0.15Severn Hospice conversion table
Tramadol0.2CDC 2022 guideline table
Dihydrocodeine0.1Faculty of Pain Medicine; Scottish Palliative Care Guidelines; BNSSG 2024; Severn Hospice. No CDC factor and no CPIC position
Hydrocodone1CDC 2022 and CDC pre-2022. No United Kingdom figure read
Any of them, corrected for CYP2D6 phenotypenone publishedNo source read for this page publishes a phenotype-specific conversion factor for any opioid
The last row is the finding that matters most on this page. The pharmacogenomics is well enough established for CPIC to issue strong recommendations to avoid two of these drugs in two phenotypes, and yet not one conversion table adjusts its factor for phenotype — so the arithmetic and the pharmacogenomics are, in practice, two separate literatures that do not meet.

A conversion factor for a drug that is not the active drug

Codeine and tramadol are the two opioids a conversion table is most often asked about, and they are the two for which a fixed factor is least defensible. Neither is the active drug. CPIC’s guideline states that both “are O-demethylated by CYP2D6 to the more active metabolites morphine and O-desmethyltramadol, respectively”, so the dose written on the chart is a prodrug and the exposure that produces analgesia depends on an enzyme whose activity varies enormously between people.

The size of that variation dwarfs everything else in this category. At the top end, a CYP2D6 ultrarapid metaboliser converts more of the prodrug and CPIC’s implication is “Increased formation of morphine leading to higher risk of toxicity”, with a strong recommendation to “Avoid codeine use because of potential for serious toxicity”. At the bottom end, a poor metaboliser converts almost none: “Greatly reduced morphine formation leading to diminished analgesia”, and again a strong recommendation to avoid. The same milligram dose is therefore scored identically by every conversion table in the world and means two completely different exposures.

For this category the poor-metaboliser end is the more dangerous one, and in a way that is easy to miss. Converting such a patient off codeine or tramadol using the published factor credits them with an opioid history they never actually had — and the arithmetic then implies a tolerance that does not exist, which is exactly the situation the reduction for incomplete cross-tolerance exists to protect against and is not sized for. Tramadol adds a complication of its own: it also inhibits serotonin and noradrenaline reuptake, so a poor metaboliser may get a partial response that does not prove the CYP2D6 pathway is working at all, and that second mechanism brings a serotonergic hazard — see the Hunter criteria — that no opioid conversion factor represents.

Two further things keep a genotype from settling the question. A strong CYP2D6 inhibitor — paroxetine, fluoxetine, bupropion, quinidine or terbinafine — turns a genotypic normal metaboliser into a phenotypic poor one, and an activity score computed from alleles cannot see it. And the phenotype boundaries themselves moved: the 2019 to 2020 CPIC and Dutch Pharmacogenetics Working Group consensus made an activity score of exactly 1 — the score of the common CYP2D6 *1/*4 genotype — an intermediate metaboliser where it used to be a normal one. The activity score interpreter computes the score from the two allele values and reads it against the current bands. What no source read for this page publishes is a phenotype-adjusted conversion factor for any opioid, which is the real state of the field: the arithmetic and the pharmacogenomics are two literatures that have not yet met. Every published conversion factor on this page is a population approximation with wide interindividual variability. The factor that fits the average of a cohort can be out by twofold or more in one person, because opioid absorption, clearance, active-metabolite handling and receptor pharmacology all differ between individuals. The equianalgesic tables these factors descend from were largely derived from single-dose studies in opioid-naive or acute-pain patients, and they are applied in practice to chronic, repeated dosing in people who are already tolerant — a use the original studies were never designed to support. Published practice when changing from one opioid to another is to reduce the calculated equivalent, and the reduction is applied after the equivalence rather than instead of it. The reason is incomplete cross-tolerance: tolerance to one opioid does not transfer fully to another, so the arithmetic equivalent over-estimates what the patient already tolerates. The Faculty of Pain Medicine puts the cut at 25 to 50 per cent, and at least 50 per cent above about 500 mg of oral morphine equivalent a day or in the frail and elderly; the other five sources read for this page put the first cut between 25 and 50 per cent and none puts it at zero; and MSD’s table raises it to 75 to 90 per cent for methadone. The figure this page returns is an arithmetic equivalence and nothing else. It is not a dose, not a target and not a limit, and no part of this page says what any patient’s dose ought to be. Your own formulary, local conversion chart or specialist pain or palliative care service governs: where it differs from anything here, it wins. The factors themselves, and the sources that disagree about them, are on the oral morphine equivalent page.

Frequently asked questions

Why is a fixed conversion factor wrong for codeine and tramadol?

Because neither is the active drug. CPIC states that both “are O-demethylated by CYP2D6 to the more active metabolites morphine and O-desmethyltramadol, respectively”, and CYP2D6 activity varies from none to several times normal between individuals. A single factor assumes the conversion is identical in everybody, so it understates the exposure in an ultrarapid metaboliser and overstates it in a poor one. No source read for this page publishes a phenotype-adjusted factor for any opioid.

What does CPIC say about codeine in an ultrarapid metaboliser?

The implication is “Increased formation of morphine leading to higher risk of toxicity” and the recommendation, graded strong, is “Avoid codeine use because of potential for serious toxicity. If opioid use is warranted, consider a non-tramadol opioid.” The tramadol table is the same shape with O-desmethyltramadol in place of morphine, and the alternative named is a non-codeine opioid — because the two drugs share the pathway.

Which end is more dangerous for a conversion?

The poor-metaboliser end, counter-intuitively. An ultrarapid metaboliser’s hazard is from the codeine or tramadol itself and is well described. The conversion hazard is at the other end: a poor metaboliser’s published oral morphine equivalent credits them with an opioid exposure they never had, so the arithmetic implies a tolerance that is not there — and the standard reduction of 25 to 50 per cent for incomplete cross-tolerance was not sized for a patient who is effectively opioid-naive.

Does a genotype result settle the question?

No, for two reasons. A strong CYP2D6 inhibitor — paroxetine, fluoxetine, bupropion, quinidine or terbinafine — phenoconverts a genotypic normal metaboliser into a phenotypic poor one, and an activity score computed from alleles cannot see it. And the bands themselves changed: the 2019 to 2020 consensus moved an activity score of exactly 1, the score of the common CYP2D6 *1/*4 genotype, from normal to intermediate.

What does CPIC say about oxycodone, methadone and dihydrocodeine?

For oxycodone and methadone it reviewed the evidence and concluded that “There is insufficient evidence and confidence to provide a recommendation to guide clinical practice at this time”. For hydrocodone it does publish a table, with “No recommendation for hydrocodone therapy because of minimal evidence regarding adverse events or analgesia” at the ultrarapid end. Dihydrocodeine appears only in the list of opioids its literature review searched, so nothing on this page applies to it. It also states that there are no dosing recommendations based on OPRM1 or COMT genotype.

Related calculators

References

  1. Crews KR, Monte AA, Huddart R, Caudle KE, Kharasch ED, Gaedigk A, et al. Clinical Pharmacogenetics Implementation Consortium Guideline for CYP2D6, OPRM1, and COMT Genotypes and Select Opioid Therapy. Clin Pharmacol Ther. 2021. doi:10.1002/cpt.2149. Codeine and tramadol “are O-demethylated by CYP2D6 to the more active metabolites morphine and O-desmethyltramadol, respectively”. Ultrarapid metaboliser, activity score above 2.25: “Increased formation of morphine leading to higher risk of toxicity” and, graded strong, “Avoid codeine use because of potential for serious toxicity”. Poor metaboliser, score 0: “Greatly reduced morphine formation leading to diminished analgesia” and “Avoid codeine use because of possibility of diminished analgesia”. The tramadol table is the same shape. Hydrocodone, ultrarapid: “No recommendation for hydrocodone therapy because of minimal evidence regarding adverse events or analgesia”. Oxycodone and methadone: “There is insufficient evidence and confidence to provide a recommendation to guide clinical practice at this time”. OPRM1 and COMT: “There are no therapeutic recommendations for dosing opioids based on either OPRM1 or COMT genotype”.
  2. Caudle KE, et al. Standardizing CYP2D6 Genotype to Phenotype Translation: Consensus Recommendations from the Clinical Pharmacogenetics Implementation Consortium and Dutch Pharmacogenetics Working Group. Clin Transl Sci. 2020. doi:10.1111/cts.12692. The consensus that moved the intermediate-to-normal boundary, so that an activity score of exactly 1 — the score of the common CYP2D6 *1/*4 genotype — is now an intermediate metaboliser where it used to be a normal one. The current bands are 0, above 0 and below 1.25, 1.25 to 2.25 inclusive, and above 2.25.
  3. Faculty of Pain Medicine of the Royal College of Anaesthetists. Opioids Aware: dose equivalents and changing opioids. Oral potencies, reviewed March 2023 against the BNF: codeine 0.1, dihydrocodeine 0.1, hydromorphone 5, morphine 1, oxycodone 1.5, tapentadol 0.4, tramadol 0.1, methadone “varies” with specialist advice required. Transdermal fentanyl 12, 25, 50, 75 and 100 micrograms an hour against 30, 60, 120, 180 and 240 mg of oral morphine a day. Conversion factors are an approximate guide only “because data are incomplete and individual variation is significant”; in most switches the calculated equivalent is cut by 25 to 50 per cent, and by at least 50 per cent above about 500 mg of oral morphine equivalent a day or in the elderly or frail; and “Opioid rotation is not recommended if a patient has responded to one opioid”.
  4. Dowell D, Ragan KR, Jones CM, Baldwin GT, Chou R. CDC Clinical Practice Guideline for Prescribing Opioids for Pain — United States, 2022. MMWR Recomm Rep. 2022;71(RR-3). Its conversion table, reproduced in CDC’s own 2022 Implementation Guide, reads: codeine 0.15, transdermal fentanyl 2.4 per microgram an hour, hydrocodone 1, hydromorphone 5, methadone 4.7, morphine 1, oxycodone 1.5, oxymorphone 3, tapentadol 0.4, tramadol 0.2. Of its seven cautions, the second is “Equianalgesic dose conversions are only estimates”, the third “Do not use the calculated dose in MMEs to determine the doses to use when converting one opioid to another”, and the seventh “These conversion factors should not be applied to dosage decisions related to the management of opioid use disorder”.
  5. Severn Hospice. Opioid Conversion Table, version 07.19. Oral potencies of 0.1 for codeine and dihydrocodeine but 0.15 for tramadol, and oral oxycodone reached by dividing oral morphine by 2 — two figures that disagree with the Faculty of Pain Medicine’s 0.1 and 1.5 for the same drugs. Transdermal fentanyl “approx. 100 to 150 times more potent than oral morphine” with the table built at 100:1; buprenorphine 5 micrograms an hour matched to 12 mg of oral morphine a day. Puts the switching reduction at 25 to 30 per cent, and at 50 per cent when converting high doses, to avoid toxicity.
  6. MSD Manuals Professional Version. Equianalgesic Doses of Opioid Analgesics. Parenteral against oral: morphine 10 to 30 mg, codeine 130 to 200, hydromorphone 1.5 to 7.5, methadone 10 to 20, oxycodone 15 to 20, oxymorphone 1 to 15. Its footnotes state that the equivalences come from single-dose studies and clinical experience and are approximations; that on changing opioid the equianalgesic dose is cut by 50 per cent, and by 75 to 90 per cent for methadone; and that the morphine-to-methadone ratio is non-linear, rising from about 2:1 below 30 mg of oral morphine equivalent a day to about 20:1 at 1000 mg a day and above. Its oral oxymorphone figure of 15 mg against 30 mg of morphine implies a potency of 2, where CDC publishes 3.

Not medical advice. For healthcare professionals and education. Reference intervals vary by laboratory and assay — always use your own laboratory's. Never base a dose or a treatment decision on this page alone. Full disclaimer at calcengines.com/disclaimer/