Digitoxin Unit Converter
Digitoxin Unit Converter
Convert digitoxin between ng/mL, µg/L and nmol/L — and start from the fact the page exists for: digitoxin is not digoxin. Different molecule, half-life measured in days, hepatic rather than renal clearance, and a therapeutic range more than ten times higher.
Digitoxin converter
Mass ⇄ molarSerum digitoxin 18 ng/mL at steady state, six hours post-dose
The conversion — and the two molecular weights that must not be swapped
ng/mL = nmol/L ÷ 1.30729
because 1.30729 = 1 ng/mL ÷ 764.94 g/mol, the molecular weight of digitoxin
- ng/mL = µg/L
- the same concentration written two ways, so nothing needs calculating between them. Continental European reports often print nmol/L
- MW 764.94 — digitoxin
- C₄₁H₆₄O₁₃. Factor 1.30729 nmol/L per ng/mL
- MW 780.94 — digoxin, a different drug
- C₄₁H₆₄O₁₄, one oxygen heavier because digoxin carries a 12β-hydroxyl group that digitoxin lacks. Factor 1.28051. The masses differ by only 2%, so the conversion factors are nearly the same and converting the wrong drug’s level looks entirely plausible — the error is never in the arithmetic, it is in which drug you thought you were converting
- the ranges are what differ
- digitoxin 10–30 ng/mL; digoxin roughly 0.8–2.0 ng/mL, and 0.5–0.9 ng/mL in heart failure. A digitoxin concentration of 20 ng/mL is mid-range and unremarkable; a digoxin concentration of 20 ng/mL is ten times the top of its range and life-threatening. This is the one fact to take from the page
- the assay
- digitoxin is measured by its own assay. A digoxin immunoassay is not a digitoxin assay, cross-reactivity between the two glycosides in immunoassays is variable, and a specific request is needed. Digoxin-like immunoreactive substances and digoxin-specific antibody fragments also interfere with glycoside immunoassays
Worked example
Serum digitoxin 18 ng/mL at steady state, six hours post-dose
18 ng/mL = 18.0 µg/L — the same concentration
18 × 1.30729 = 23.5 nmol/L
23.5 nmol/L sits inside the 10–30 ng/mL range, which is 13.1–39.2 nmol/L
Now the error the page exists to prevent. Suppose that 18 ng/mL was actually a digoxin level, mislabelled or misread. Against digoxin's range of about 0.8–2.0 ng/mL, 18 ng/mL is nine times the upper limit — a potentially fatal concentration that reads as comfortably mid-range if it is checked against the digitoxin band
The arithmetic gives no warning, because the two factors are nearly identical: 18 × 1.28051 (digoxin's factor) = 23.0 nmol/L against 23.5. A 2% difference. The molecular weights protect nobody here; only reading the drug name does
Timing matters differently too. With a half-life of six to eight days, a digitoxin level taken a week after starting the drug is roughly halfway to steady state, and the same dose will produce a considerably higher concentration a month later
Digitoxin against digoxin — the comparison that matters
| Digitoxin | Digoxin | |
|---|---|---|
| Molecular weight | 764.94 | 780.94 (one extra oxygen: a 12β-hydroxyl) |
| Conversion, ng/mL → nmol/L | × 1.30729 | × 1.28051 |
| Therapeutic range | 10 – 30 ng/mL (13.1 – 39.2 nmol/L) | about 0.8 – 2.0 ng/mL; 0.5 – 0.9 ng/mL in heart failure |
| Elimination half-life | 6 – 8 days | 36 – 48 hours with normal renal function, much longer in renal failure |
| Time to steady state | About a month | About a week |
| Route of elimination | Hepatic metabolism, with enterohepatic recirculation; some conversion to digoxin | Renal, largely excreted unchanged |
| Effect of renal impairment | Relatively little — historically the reason it was preferred in chronic kidney disease | Major; the dose must be reduced and levels rise readily |
| Plasma protein binding | About 90–97% | About 25% |
| Availability | Not marketed in the UK or the US; still used in parts of continental Europe, particularly Germany | Widely used worldwide |
What a long half-life does to monitoring
| Question | Digitoxin | Why |
|---|---|---|
| When is steady state reached after a dose change? | About a month | Five half-lives at six to eight days each |
| When can a level be acted on? | At steady state, six hours or more after the dose | An earlier sample catches distribution and reads high; the MLabs catalogue advises resampling 48–96 hours after a dose change for early information, with the definitive level later |
| How quickly does a high level fall if the drug is stopped? | Over weeks | Elimination is slow, and enterohepatic recirculation slows it further |
| Does renal failure change the level much? | Not greatly | Elimination is chiefly hepatic — the historical argument for using digitoxin in chronic kidney disease |
Things that cause glycoside toxicity at an ordinary level
| Factor | Effect |
|---|---|
| Hypokalaemia | The classic sensitiser. Digitalis and potassium compete at the Na⁺/K⁺-ATPase, so a low potassium produces toxicity at concentrations that would otherwise be harmless — and diuretics supply both the hypokalaemia and the indication |
| Hypomagnesaemia | Also lowers the threshold for glycoside arrhythmias, and is often present alongside hypokalaemia |
| Hypercalcaemia | Increases the risk of arrhythmia |
| Hypothyroidism | Increases sensitivity; hyperthyroidism reduces it |
| Myocardial ischaemia, hypoxia, advanced age, cardiac amyloid | A vulnerable myocardium is more arrhythmogenic at any given concentration |
| Interacting drugs — amiodarone, verapamil, quinidine, macrolides, and for digitoxin also enzyme inducers and inhibitors | Raise or lower concentrations, sometimes considerably |
Not digoxin: a different molecule, a different half-life, a different range
Digitoxin is reported in nanograms per millilitre, identically in micrograms per litre, or in nanomoles per litre on many continental European reports. The conversion uses a molecular weight of 764.94, so one nanogram per millilitre is 1.30729 nanomoles per litre and a mid-range level of 18 ng/mL is 23.5 nmol/L. That is the arithmetic, and it is the easy part. The reason this page exists is that digitoxin and digoxin are constantly confused, and the confusion is dangerous in a specific direction.
They are different molecules. Digoxin is digitoxin plus one hydroxyl group at the 12β position, which is why its molecular weight is 780.94 against digitoxin’s 764.94 — a difference of about two per cent. That similarity is exactly the problem. The conversion factors, 1.28051 for digoxin and 1.30729 for digitoxin, are so close that converting the wrong drug’s level produces an answer that looks entirely reasonable. What differs by more than an order of magnitude is the therapeutic range. Digitoxin’s is 10 to 30 ng/mL; digoxin’s is roughly 0.8 to 2.0 ng/mL, and post-hoc analysis of the DIG trial supports aiming lower still, around 0.5 to 0.9 ng/mL, in heart failure. So a digoxin concentration of 18 ng/mL — around nine times the top of its range, and potentially fatal — reads as comfortably mid-therapeutic if it is checked against digitoxin’s band. No arithmetic check catches that. Only reading the drug name on the report and on the prescription catches it.
The pharmacokinetics differ just as sharply. Digoxin is cleared by the kidney, largely unchanged, with a half-life of a day and a half in normal renal function; it reaches steady state in about a week, and a high level falls within days of stopping. Digitoxin is cleared by hepatic metabolism with enterohepatic recirculation, and part of it is converted to digoxin. Its half-life is six to eight days, steady state takes about a month, and a raised concentration falls over weeks rather than days. Renal impairment barely alters it, which was historically the argument for preferring digitoxin in chronic kidney disease. It is also around 90 to 97 per cent protein-bound against digoxin’s 25 per cent. In practical terms: a level drawn a week after starting digitoxin is roughly halfway to where it will end up, and a level drawn less than six hours after a dose is inflated by the distribution phase.
Digitoxin is now little used. It is not marketed in the United Kingdom or the United States, and prescribing survives mainly in parts of continental Europe, Germany in particular — so most clinicians who encounter a digitoxin level encounter it on a patient who has moved, travelled or brought their own supply. That rarity is itself a hazard: an unfamiliar drug name beside a number in the twenties invites the assumption that something has gone badly wrong, when for digitoxin it has not. It also means the assay must be requested specifically. A digoxin immunoassay is not a digitoxin assay; cross-reactivity between the two glycosides varies between platforms and is not something to rely on in either direction. Whichever glycoside is involved, the level supports a clinical judgement and never replaces it: toxicity depends on potassium, magnesium, calcium, thyroid status, renal function and the state of the myocardium, so a patient with a hypokalaemia can be thoroughly toxic at a concentration inside the range, and a dose is never changed on the strength of a number alone.
Frequently asked questions
How do you convert digitoxin from ng/mL to nmol/L?
Multiply by 1.30729, which is one nanogram per millilitre divided by digitoxin’s molecular weight of 764.94 g/mol. A level of 18 ng/mL is 23.5 nmol/L, and dividing by the same factor goes back. ng/mL and µg/L are the same number. Make sure the report says digitoxin: digoxin’s factor is 1.28051, only 2% different, so the arithmetic gives no clue that you have converted the wrong drug.
Is digitoxin the same as digoxin?
No. Digoxin is digitoxin with an extra hydroxyl group, which makes it 780.94 g/mol against 764.94. The clinically important differences are everywhere else: digitoxin’s therapeutic range is 10–30 ng/mL against digoxin’s roughly 0.8–2.0 ng/mL, its half-life is six to eight days against a day and a half, it is cleared by the liver rather than the kidney, and it is about 90–97% protein-bound against 25%. Confusing them is a real prescribing hazard, because a digoxin level of 18 ng/mL looks mid-therapeutic against the digitoxin range and is in fact around nine times the top of its own.
What is the therapeutic range for digitoxin?
10–30 ng/mL, equivalently 10–30 µg/L or 13.1–39.2 nmol/L, as published by the University of Michigan MLabs test catalogue, which also advises taking the sample six hours after the dose and resampling 48 to 96 hours after a dose change. Being inside that range does not exclude glycoside toxicity: hypokalaemia, hypomagnesaemia, hypercalcaemia, hypothyroidism and a vulnerable myocardium all produce toxicity at ordinary concentrations.
Why does digitoxin take so long to reach steady state?
Because its half-life is six to eight days. Concentrations need roughly five half-lives to plateau, so steady state takes about a month, and a level drawn a week after starting or changing the dose is only around halfway there. The same slow elimination works against you when a level is high: stopping the drug does not bring the concentration down quickly, and it is still falling weeks later. Digoxin, by contrast, reaches steady state in about a week.
Can a digoxin assay measure digitoxin?
Not reliably. Digitoxin has its own assay and has to be requested specifically. Cross-reactivity of digoxin immunoassays with digitoxin varies between platforms and is not a basis for interpreting a result in either direction. Glycoside immunoassays are also affected by digoxin-like immunoreactive substances and by digoxin-specific antibody fragments given as treatment, so an unexpected glycoside level is worth discussing with the laboratory before it is acted on.
Why is digitoxin still used anywhere?
Because its elimination is chiefly hepatic, so its concentrations are far less affected by renal impairment than digoxin’s — historically an attraction in chronic kidney disease — and its long half-life makes concentrations stable and forgiving of a missed dose. It is not marketed in the UK or the US and its use is now largely confined to parts of continental Europe, particularly Germany. Most clinicians outside those countries meet it on a patient who has moved or brought their own supply.
Related calculators
References
- University of Michigan MLabs. Test catalogue: Digitoxin. Therapeutic range 10–30 ng/mL; optimal sampling six hours after dose administration; resample 48–96 hours after a dose change.
- Rathore SS, Curtis JP, Wang Y, Bristow MR, Krumholz HM. Association of serum digoxin concentration and outcomes in patients with heart failure. JAMA. 2003;289(7):871–878.
- Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997;336(8):525–533.
- Belz GG, Breithaupt-Grögler K, Osowski U. Treatment of congestive heart failure — current status of use of digitoxin. Eur J Clin Invest. 2001;31(Suppl 2):10–17.
- Joint Formulary Committee. Digoxin — Monitoring requirements and Digoxin-specific antibody fragments. British National Formulary. London: BMJ Group and Pharmaceutical Press.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.