© The Board of Management and Trustees of the British Journal of Anaesthesia 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Amsterdam, The Netherlands
*E-mail: f.o.kooij{at}amc.uva.nl
Editor—With interest, we have read the article by Hans and colleagues1 entitled ‘Blood glucose concentration profile after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients undergoing abdominal surgery’. In recent years, an increasing amount of attention has been directed at perioperative and critical illness hyperglycaemia, as hyperglycaemia has been associated with higher morbidity and mortality rates.2 3 Several risk factors have been identified that increase the risk of hyperglycaemia in the perioperative period, including abnormal glucose homeostasis, obesity, duration of fasting and type of surgery.4 In addition, administration of dexamethasone may affect normal glucose homeostasis resulting in hyperglycaemia.
To date the effect of the low dose of dexamethasone that is commonly used for PONV prophylaxis on blood glucose concentration is not known. Therefore, the conclusion of this study that 10 mg dexamethasone may increase blood glucose concentration in non-diabetic and type 2 diabetic patients is potentially very relevant.
However, we feel that Hans' conclusion is not entirely justified by the data that are presented. Besides the possible effect of dexamethasone, several other factors may have contributed to the increase in blood glucose concentration, of which surgical stress is probably the most important. That blood glucose concentration has previously been shown to increase significantly over the course of surgery in patients who did not receive dexamethasone may by itself explain the results, whether patients had diabetes or not.5 6 Therefore, the lack of a control group of patients that did not receive dexamethasone or preferably a control group receiving a placebo precludes any conclusion about the effect of dexamethasone on blood glucose concentration.
Hence, the hyperglycaemia found could have been caused by other factors than the low dose dexamethasone. This is supported by others showing that in normal subjects, high dose dexamethasone indeed increased insulin resistance, but did not increase blood glucose concentration.7 Once more, this illustrates the importance of including a control group in the design of the study. Without such a control group, interpretation of the data of this study remains difficult.
Blood glucose concentration profile after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients
Liege, Belgium
*E-mail: Pol.hans{at}chu.ulg.ac.be
Editor—We thank Drs Kooij and Kal for their interest and comments regarding our paper on blood glucose concentration profile after dexamethasone administration in diabetic and non-diabetic patients undergoing abdominal surgery. They first noted that several risk factors including abnormal glucose homeostasis, obesity, duration of fasting and type of surgery, may be responsible for hyperglycaemia in the perioperative period. We completely agree with that comment for two reasons: (i) as mentioned in their letter, this particular point has already been highlighted and published; and (ii) we demonstrated and confirmed in our study that severe obesity is a determinant factor of glucose increase, regardless of the metabolic status of patients. Their second point is that they consider 10 mg of dexamethasone as a low dose. However, there is still some controversy regarding the optimal dose of dexamethasone to be used for PONV prophylaxis and a 10 mg injection is probably in the upper part of the prophylactic range. They also noted that surgical stress is another very important contributing factor to the increase in blood glucose concentration. Once again, we agree with that point which was clearly mentioned and discussed in our paper. In our study, we addressed this issue by looking at the CRP level measured in all patients the day after surgery and failed to find any difference between groups. However, given the disparity of surgery in our patients, we think that surgical stress cannot be considered as a minor risk factor and agree that it should be evaluated specifically and in a different way in a further study.
Finally, the last and most important comment questions the role of dexamethasone as the primary cause of hyperglycaemia and stresses the importance of including a control group in the design of the study. As mentioned in the paper, our study was not designed to investigate the effect of dexamethasone on blood glucose level. This question has already been answered in the literature, even if dexamethasone is certainly not the only factor that should be incriminated. We did not conclude that dexamethasone was responsible for hyperglycaemia. We actually demonstrated that after dexamethasone administration, blood glucose profile significantly differs in non-diabetic and type 2 diabetic patients undergoing elective abdominal surgery early in the morning. In addition, the main message the reader should keep in mind is that in the course of dexamethasone injection, severe obesity and poor-controlled diabetes rather than diabetes per se are determinant factors of hyperglycaemia and should incite to a close monitoring of blood glucose level.
References
1 Hans P, Vanthuyne A, Dewandre PY, et al. Blood glucose concentration profile after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients undergoing abdominal surgery. Br J Anaesth 2006; 97:164–70
2 Van den Berghe GH, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001; 345:1359–67
3 McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia. Crit Care Clin 2001; 17:107–24[CrossRef][Web of Science][Medline]
4 Cely CM, Arora P, Quartin AA, et al. Relationship of baseline glucose homeostasis to hyperglycemia during medical critical illness. Chest 2004; 126:879–87
5 Pasternak JJ, McGregor DG, Lanier WL. Effect of single-dose dexamethasone on blood glucose concentration in patients undergoing craniotomy. J Neurosurg Anesthesiol 2004; 16:122–5[CrossRef][Web of Science][Medline]
6 Sicardisalomon Z, Rodhe P, Hahn RG. Progressive decrease in glucose clearance during surgery. Acta Anaesthesiol Scand 2006; 50:848–54[CrossRef][Web of Science][Medline]
7 Nicod N, Giusti V, Besse C, Tappy L. Metabolic adaptations to dexamethasone-induced insulin resistance in healthy volunteers. Obes Res 2003; 11:625–31[Web of Science][Medline]
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