OGTT Growth Hormone Suppression Interpreter
OGTT Growth Hormone Suppression Interpreter
The growth hormone nadir after 75 g of glucose is read against a cut-off that has moved twice and depends on the assay and on the patient’s body mass index. This page puts the current consensus thresholds and the historical one side by side, reads them alongside the IGF-I, and treats a raised IGF-I with a suppressed nadir as a named result rather than a contradiction.
OGTT growth hormone suppression
GH nadir + IGF-I → interpretationGH nadir 0.9 µg/L after 75 g glucose, IGF-I 1.6 × the age-specific upper limit, cut-off 0.4 µg/L
Two numbers, three cut-offs, and one that does not exist
Nadir ≥ cut-off = failure to suppress · cut-off = 0.4 µg/L (BMI < 25) or 0.2 µg/L (BMI ≥ 25)
IGF-I > 1.3 × age-specific ULN with typical features = acromegaly confirmed
There is no GH nadir that excludes acromegaly
- 75 g glucose
- the standard load, given after a fast. Growth hormone is sampled every 30 minutes for two hours and the lowest value is the nadir — not the value at any single timepoint
- 0.4 and 0.2 µg/L
- the 2024 consensus position, stratified by body mass index: “BMI-based GH nadir cutoffs can be considered for diagnosis, with <0.4 µg/L for BMI <25 kg/m2 and <0.2 µg/L for BMI ≥25 kg/m2, although this may be assay dependent". Obesity blunts growth hormone secretion, which is why the heavier patient gets the lower threshold
- 1.0 µg/L
- the older criterion, used before ultrasensitive assays and still printed on some reports. It is not a harmless alternative: moving from 1.0 to 0.4 µg/L dropped reported remission rates from 89–99% to 61–79%, which is the same patients reclassified
- IGF-I > 1.3 × ULN
- confirms the diagnosis in a patient with typical acromegalic features, without an OGTT. The reference range must be age-stratified and the assay calibrated to the international standard 02/254; growth hormone assays should be calibrated to 98/574
- no exclusionary cut-off
- the consensus states in terms that “there is no cutoff for glucose-suppressed GH that definitively excludes a diagnosis of acromegaly”. A suppressed nadir is therefore evidence, not a negative test
Worked example
GH nadir 0.9 µg/L after 75 g glucose, IGF-I 1.6 × the age-specific upper limit, cut-off 0.4 µg/L
0.9 µg/L is above the 0.4 µg/L consensus cut-off for a body mass index under 25 — growth hormone did not suppress
IGF-I at 1.6 × the age-specific upper limit is above the 1.3 × threshold that confirms the diagnosis in a patient with typical features
→ acromegaly, both criteria met
Now switch the cut-off to the older 1.0 µg/L and the nadir of 0.9 becomes "suppressed". The diagnosis still stands on IGF-I, but the result string changes to the discordant one — which is exactly what happened to reported remission rates when the field moved from 1.0 to 0.4
The third selectable cut-off, 0.2 µg/L, applies at a body mass index of 25 or over, because obesity blunts growth hormone secretion and a heavier patient should suppress further
The nadir cut-offs, side by side
| Cut-off | Where it comes from | Applies to | What it costs |
|---|---|---|---|
| 0.4 µg/L | 2024 consensus, and the post-2010 standard | Body mass index under 25 kg/m² | More patients classified as not in remission; reported remission fell to 61–79% |
| 0.2 µg/L | 2024 consensus | Body mass index 25 kg/m² or over | Recognises that obesity blunts GH secretion; fewer false reassurances in heavier patients |
| 1.0 µg/L | Pre-2010 criterion, and the Endocrine Society’s 2014 random-GH therapeutic goal | Legacy reports and older records | Reported remission of 89–99%, some of it spurious |
Discordant growth hormone and IGF-I: real, common, and not a contradiction
| Pattern | Frequency | What it usually means |
|---|---|---|
| Raised IGF-I, suppressed GH nadir | 14 of 16 discordant cases in a recent surgical series | Mild ongoing disease activity, or IGF-I that has not finished falling after surgery |
| Non-suppressed GH nadir, normal IGF-I | 2 of 16 in the same series | Often the cut-off or the assay; also diabetes, adolescence, pregnancy, liver or kidney disease |
| Discordance overall after surgery | 19.5% of that cohort | A grey zone between cure and active disease, warranting monitoring rather than reflex treatment |
A moving threshold, and a test that cannot say no
In health, a glucose load suppresses growth hormone. In acromegaly it does not, and that observation has underpinned the diagnosis for half a century. The test is simple — 75 g of oral glucose after a fast, growth hormone every 30 minutes for two hours, take the lowest value — and its difficulty is entirely in the number it is read against. That number has moved from 5 µg/L to 2, to 1, and now to 0.4 µg/L or 0.2 µg/L depending on body mass index, as assays became more sensitive and more specific for the 22 kDa isoform. Each move reclassified patients without anything changing in them: when the remission criterion went from 1.0 to 0.4 µg/L, reported remission rates fell from 89–99% to 61–79%.
The 2024 consensus is careful about what the nadir can and cannot do. It offers body-mass-stratified cut-offs for diagnosis — below 0.4 µg/L for a BMI under 25 and below 0.2 µg/L at or above it — while adding that these “may be assay dependent”, and it states plainly that there is no glucose-suppressed growth hormone value that definitively excludes acromegaly. It also moves the centre of gravity of the diagnosis onto IGF-I: in a patient with typical features, an IGF-I more than 1.3 times the age-specific upper limit confirms acromegaly, and the OGTT is reserved for equivocal cases where the interpretative difficulties may still be worth accepting.
That reordering is what makes the discordant result a normal finding rather than a paradox. A patient can have a clearly raised IGF-I and a growth hormone nadir that suppresses below any of the three thresholds, and this is neither a laboratory error nor grounds for dismissing the diagnosis. In a recent surgical series 19.5% of patients were biochemically discordant after surgery, and 14 of the 16 discordant patients had exactly this pattern. The consensus reads it as dysregulated but still partly suppressible somatotroph secretion with preserved tissue responsiveness — mild ongoing disease activity — or, in the first weeks after surgery, as IGF-I that has not yet finished falling, which is why success is assessed at 12 weeks and not before.
Several things legitimately disturb the test and should be excluded before a failure to suppress is taken at face value. Hyperglycaemia itself suppresses growth hormone, so in uncontrolled diabetes both random and post-glucose values need caution. Growth hormone nadirs in healthy adults vary with sex, body mass index and oestrogen-containing oral contraceptives. Adolescence and pregnancy raise growth hormone physiologically, and chronic liver disease, chronic kidney disease, malnutrition and anorexia nervosa all uncouple growth hormone from IGF-I. Assay standardisation matters in both directions: growth hormone assays should be calibrated to the international standard 98/574 and IGF-I to 02/254, and even then reference ranges are assay-specific, with the largest differences at the highest values.
Frequently asked questions
What GH nadir confirms acromegaly?
The 2024 consensus says body-mass-stratified cut-offs can be used for diagnosis: a nadir below 0.4 µg/L for a body mass index under 25 kg/m² and below 0.2 µg/L at 25 or over, adding that this may be assay dependent. A nadir at or above the applicable cut-off is a failure to suppress. The older criterion, still seen on reports, was 1.0 µg/L.
Can acromegaly be diagnosed without an OGTT?
Yes. In a patient with typical acromegalic features, an IGF-I more than 1.3 times the age-specific upper limit of normal confirms the diagnosis, and the consensus says the interpretative difficulties of the OGTT then outweigh its advantages. The OGTT is for equivocal IGF-I results.
Is a normal GH nadir with a raised IGF-I a contradiction?
No, and it is common. The consensus states that no glucose-suppressed growth hormone value definitively excludes acromegaly. Discordance affected 19.5% of patients in a recent postoperative series, and 14 of the 16 discordant cases were a raised IGF-I with a normal growth hormone. It usually means mild ongoing disease activity, or IGF-I that has not finished falling after surgery.
Why did the GH nadir cut-off change from 1.0 to 0.4 µg/L?
Because assays became more sensitive and more specific for the 22 kDa isoform, so healthy people were shown to suppress further than the old assays could measure. The change was not cosmetic: reported remission rates fell from 89–99% to 61–79%, meaning a substantial group was reclassified from cured to persistently active.
What defines remission after pituitary surgery?
IGF-I normalisation measured 12 weeks after surgery is what generally defines surgical success, using an age-stratified reference range. An early postoperative GH nadir below 0.4 µg/L at two to five days and again at three to six months correlates better with long-term remission than the older 1.0 µg/L figure did.
What else can stop GH suppressing after glucose?
Poorly controlled diabetes, adolescence, pregnancy, chronic liver disease, chronic kidney disease, malnutrition and anorexia nervosa. Growth hormone nadirs in healthy adults also vary with sex, body mass index and oestrogen-containing oral contraceptives, which is part of why the consensus stratifies the cut-off by body mass index.
Related calculators
References
- Giustina A, Biermasz N, Casanueva FF, et al. Consensus on criteria for acromegaly diagnosis and remission. Pituitary. 2024;27(1):7–22.
- Giustina A, Chanson P, Bronstein MD, et al. A consensus on criteria for cure of acromegaly. J Clin Endocrinol Metab. 2010;95(7):3141–3148.
- Pennlund A, Olsson Bontell T, Skoglund T, et al. Prevalence and patterns of biochemical discordance in patients with surgically treated acromegaly. Pituitary. 2026;29:93. — discordance in 19.5%, of which 14 of 16 were a raised IGF-I with a normal growth hormone; nadir cut-offs of 1.0 µg/L before 2010 and 0.4 µg/L after.
- Katznelson L, Laws ER, Melmed S, et al. Acromegaly: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2014;99(11):3933–3951.
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.