**Complications**

[132] Wautier, M.P., Chappey, O., Corda, S., Stern, D.M., Schmidt, A.M & Wautier, J.L. (2001). Activation of NADPH oxidase by AGE links oxidant stress to altered gene ex‐

[133] Weber, P., Bendich, A. & Machlin, L.J. (1997). Vitamin E and human health: rationale for determining recommended intake levels. Nutrition Vol. 13, pp. 450-460.

[134] Wegner, M., Pioruńska-Stolzmann, M., Araszkiewicz, A., Zozulińska-Ziołkiewicz, D. & Wierusz-Wysocka, B. (2011). Evaluation of paraoxonase 1 arylesterase activity and lipid peroxide levels in patients with type 1 diabetes. Pol Arch Med Wewn Vol. 121,

[135] West, I.C. (2000). Radicals and oxidative stress in diabetes. Diabetic Med Vol. 17, pp.

[136] Wild, S., Roglic, G., Green, A., Sicree, R. & King, H. (2004). Global prevalence of dia‐ betes: estimates for the year 2000 and projections for 2030. Diabetes Care Vol. 27, pp.

[137] Winterbourn, C.C. & Metodiewa, D. (1994). The reaction of superoxide with reduced

[138] Witko-Sarsat, V., Friedlander, M., Capeillère-Blandin, C., Nguyen-Khoa, T., Nguyen, A.T., Zingraff, J., Jungers, P., Descamps-Latscha, B. (1996). Advanced oxidation pro‐ tein products as a novel marker of oxidative stress in uraemia. Kidney Int Vol. 49, pp.

[139] Yamagishi, S. (2009). Advanced glycation end products and receptor-oxidative stress system in diabetic vascular complications. Ther Apher Dial Vol. 13, p. 534-539.

[140] Yan, S.D., Schmidt, A.M., Anderson, G.M., Zhang, J., Brett, J., Zou, Y.S., Pinsky, D. & Stern, D. (1994). Enhanced cellular oxidant stress by the interaction of advanced gly‐ cation endproducts with their receptors/ binding proteins. J Biol Chem Vol. 269, pp.

[141] Yung, L.M., Leung, F.P., Yao, X., Chen, Z.Y. & Huang, Y. (2006). Reactive oxygen species in vascular wall. Cardiovascular and Hematological Disorders Vol. 6, pp.

[142] Zivić, S., Vlaski, J., Kocić, G., Pesić, M., Cirić, V. & Durić, Z. (2008). The importance of oxidative stress in pathogenesis of type 1 diabetes-determination of catalase activity

in lymphocytes of diabetic patients. Med Pregl Vol. 61, pp. 458-463.

pression via RAGE. Am J Physiol Vol. 280, pp. E685-E694.

glutathione. Arch Biochem Biophys Vol. 314, pp. 284-290.

pp. 448-455.

171-180.

248 Type 1 Diabetes

1047-1053.

1304-1313.

9889-9897.

1-19.

**Chapter 10**

**Diabetic Ketoacidosis**

Mustafa Cesur and Irmak Sayin

http://dx.doi.org/10.5772/53199

**1. Introduction**

**2. Epidemiology**

years will rise by 70% in 2020 [15].

Additional information is available at the end of the chapter

tions, it may also influence the later outcome of diabetes [11].

A chronic autoimmune destruction of the pancreatic beta cells results in decreasing endoge‐ nous insulin secretion and the clinical manifestation of type 1 diabetes mellitus (T1DM). The clinical onset of the disease is often acute in children and adolescents and diabetic ketoaci‐ dosis (DKA) is present in 20-74% of the patients [1-7]. DKA is a serious condition that re‐ quiring immediate intervention. Even with appropriate intervention, DKA is associated with significant morbidity and possible mortality in diabetic patients in the pediatric age group [8]. Young age and female sex have been associated with an increased frequency of DKA [3,9]. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA [10]. In addition to possible acute complica‐

Worldwide, an estimated 65 000 children under 15 years old develop T1DM each year, and the global incidence in children continues to increase at a rate of 3% a year [12,13]. The cur‐ rent incidence in the UK is around 26/100 000 per year [14]. Patterson et al. were aimed to establish 15-year incidence trends for childhood T1DM in European centres with EURO‐ DIAB study. 29 311 new cases of T1DM were diagnosed in children before their 15th birth‐ day during a 15-year period between 1989-2003. The overall annual increase was 3.9% and the increases in the age groups 0-4 years, 5-9 years, and 10-14 years were found to be 5.4%, 4.3%, and 2.9% respectively. If present trends continue, prevalent cases younger than 15

The incidence of DKA was found to be 5-8% in large community-based studies [16]. Ap‐ proximately 115 000 patients admitted to the hospital because of DKA in one year in USA

and reproduction in any medium, provided the original work is properly cited.

© 2013 Cesur and Sayin; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

**Chapter 10**
