The primary clinical use of insulin measurement is in the differential diagnosis of documented spontaneous hypoglycaemia. Further tests, such as those for ketones, proinsulin, growth hormone and the insulin-like growth factors may also be required to complete the diagnostic process.
Causes of hypoglycaemia in adults
Ill or medicated individual
Seemingly well individual
Drugs other than antihyperglycemic agents and alcohol reported to cause hypoglycemia
Moderate quality of evidence (+++):
Low quality of evidence (++):
Very low quality of evidence (+):
Ref: J Clin Endocrinol Metab, March 2009, 94(3):709–728 jcem.endojournals.org 713
Blood should be collected when patient is hypoglycaemic.
Please note: Exogenous Insulin preparations have been shown to cross-react with the Architect insulin assay, but to varying degrees. The human sequence insulin preparations (Actrapid, Humulin S, Insulatard, Humulin I and Humulin M3) demonstrated similar levels of recovery (between 81 and 89%), indicating extensive cross-reactivity in the insulin assay. The insulin analogues (NovoRapid, Apidra, Humalog, Levemir and Lantus) demonstrated variable degrees of recovery with Apidra, showing the lowest recovery at 12 and 14%, while Lantus, over-recovered at 127 and 140%, demonstrating significant cross-reactivity with the assay.
If glucose is above 3.1 mmol/L, insulin analysis is not usually carried out.
Please send separate EDTA sample for this test.
Haemolysed samples are not suitable for analysis
No associated reference range. Should be interpreted alongside with glucose and c-peptide.
Non- diabetic hypoglycaemia
Evaluation of hypoglycaemia should only be undertaken for patients in whom Whipple’s triad has been documented. Firstly, review the history and physical findings to exclude more common hypoglycaemic aetiologies such as; drugs (insulin, insulin secretagogues, alcohol ingestion), critical illness (sepsis, organ failure), cortisol deficiency and non-islet cell tumours.
Once these have been excluded, in the seemingly well individual, the differentials lie between accidental/ surreptitious hypoglycaemia and endogenous hyperinsulinaemia. Further evaluation is warranted and should involve the following concomitant tests in the event of an ongoing episode of hypoglycaemia; plasma glucose (for confirmation of hypoglycaemia), insulin, C-peptide, beta-hydroxybutyrate as well as the measurement of circulating oral hypoglycaemic agents (if there is a degree of suspicion). When spontaneous hypoglycaemia cannot be observed, a prolonged fast or mixed meal test may recreate the environment in which hypoglycaemia is likely to occur.
Table 1: Taken from the Endocrine Society Guideline in 2009
Sxs/Signs |
Glucose (mmol/L) |
Insulin (pmol/L) | C-peptide (pmol/L) | BHB (mmol/L) | Circulating OHA | Ab to insulin | Interpretation |
No | <3.1 | <21 | <200 | >2.7 | No | No | Normal |
Yes | <3.1 | >>21 | <200 | ≤2.7 | No | Neg (Pos) | Exogenous insulin |
Yes | <3.1 | ≥21 | ≥200 | ≤2.7 | No | Neg | Insulinoma, NIPHS, PGBH |
Yes | <3.1 | ≥21 | ≥200 | ≤2.7 | Yes | Neg | Oral hypoglycaemic agent |
Yes | <3.1 | >>21 | >>200 | ≤2.7 | No | Pos | Insulin autoimmune |
Yes | <3.1 | <21 | <200 | ≤2.7 | No | Neg | IGF mediated |
Yes | <3.1 | <21 | <200 | >2.7 | No | Neg | Not insulin (or IGF) mediated |
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