Article Text

  1. L. R. Nematollahi1,
  2. E. Taheri1,
  3. B. Larijani1,
  4. M. Mohajeri1,
  5. M. Gozashti1,
  6. J. Y. Wan1,
  7. A. E. Kitabchi1
  1. 1The University of Tennessee Health Science Center, Memphis, TN.


Background Our previous study confirmed the well-known phenomenon of leukocytosis in hyperglycemic crises, without obvious infection. We hypothesized that stimulation of sympathetic nervous system, secondary to any acute stress, would be a possible mechanism. Therefore, in this study, we attempted to create the stress of hypoglycemia by insulin-induced hypoglycemic test and evaluate the stimulation of sympathetic nervous system and leukocytosis.

Materials and Methods Thirteen healthy subjects (age from 20-32 years) without cardiovascular diseases or metabolic syndrome or acute infection were selected. Hypoglycemia was induced by IV injection of 0.1 unit of insulin/kg of body weight. The levels of counterregulatory hormones (cortisol, growth hormone, norepinephrine, epinephrine, and ACTH) and white blood cells were measured at 0, 30, 45, 60, 90, 120, and 240 minutes. The means ± SD were calculated for all continuous variables. A two-tailed p value < .05 is considered statistically significant.

Results During the test, no severe adverse effects were detected. The mean nadir of hypoglycemia was 38.23 ± 19.9 mg/dL in 30 minutes. The highest levels of cortisol, growth hormone, and ACTH were detected in 60 minutes. For norepinephrine and epinephrine, the highest levels were in 45 minutes. By applying Pearson correlation method, leukocytosis in 60 and 120 minutes were significantly associated with the rising of norepinephrine and was also associated with rising cortisol in 45 minutes (p values were .0034 and .021, respectively).

Conclusion Our results demonstrated that the stimulation of the sympathetic nervous system secondary to the acute stress of hypoglycemia is responsible for significant leukocytosis in our study.

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