BMJ 1994;309:1512 (3 December)

Letters

Authors' reply

EDITOR,--A S Wierzbicki and colleagues think that trends in glycated haemoglobin concentration should be used with little referral to their absolute value. Accordingly, they must think that a patient with a stable haemoglobin A1c concentration of 12% should be treated in a similar manner to one with a stable value of 6%. In the light of the diabetes control and complications trial, which showed an impressive reduction in microvascular complications with improved absolute glycated haemoglobin values,1 this opinion must be held by only a minority of clinicians.

How are we to achieve reductions in the incidence of long term diabetic complications without establishing a standard by which we can compare the glycaemic control of our own diabetic patients with those participating in complications trials? It is well known that standardisation for glycated haemoglobin does not exist, but what we showed was the extent to which the same diabetic patients may have their glycaemic control categorised differently because of this lack of standardisation between assays.

With regard to our statistical analysis, our way of comparing the glycated haemoglobin methods had no relevance to the European classification of patients into good, borderline, or poor control. Likewise patients' concentrations of fetal haemoglobin were not pertinent to our chosen assay by high performance liquid chromatography since fetal haemoglobin was not included in the result for glycated haemoglobin. We read with interest the findings of Hassan and colleagues, which are at odds with those of our study and previous publications.2 3 While there is little doubt that their Glycomat results are analytically correct, their interpretation may be artefactual owing to the inclusion of fetal haemoglobin concentrations in this glycated haemoglobin assay. The random error introduced by fetal haemoglobin is likely to have a greater relative effect on the bias and standard deviation of their reference range population when using haemoglobin A1c than it is when measuring haemoglobin A1.4 Therefore, this may affect the subsequent classification of diabetic control when European guidelines are used. We too found a significant correlation between nonglucose haemoglobin adducts and haemoglobin A1c concentration (r=0.66), but this disguised the fact that these adducts did not rise as quickly as haemoglobin A1c in diabetic patients, which was part of the reason for the discrepancy we found when comparing haemoglobin A1 and haemoglobin A1c.

Eric S Kilpatrick, Alan G Rumley, Marek H Dominiczak, Michael Small 

Career registrar Principal biochemist Consultant biochemist Department of Pathological Biochemistry, Gartnavel General Hospital, Glasgow G12 0YN Consultant physician Diabetic Unit, Gartnavel General Hospital.


  1. Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulindependent diabetes mellitus. N Engl J Med 1993;329:977-86. [Abstract/Free Full Text]
  2. Rumley AG, Kilpatrick ES, Dominiczak MH, Small M. Evaluation of glycaemic control limits using the Ames DCA 2000 HbA1c analyser. Diabet Med 1993;10:976-9. [Medline]
  3. Paterson JR, Barrington H, Malcolm EA, Lawrence JR. Evaluation of glycaemic control limits. Diabet Med 1994;11:715.
  4. Kilpatrick ES, Rumley AG, Small M, Dominiczak MH. Increased fetal haemoglobin in insulin-treated diabetes mellitus contributes to the imprecision of glycohaemoglobin measurements. Clin Chem 1993;39:833-5. [Abstract/Free Full Text]

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