Abstract:OBJECTIVE: To review the incident status of childhood type 1 diabetes mellitus hospitalized in the Children′s Hospital of Zhejiang University School of Medicine from 1999 to 2009 and to explore the clinical value of IL-10 in diabetic ketoacidosis. METHODS: The clinical data of 263 children with type 1 diabetes mellitus hospitalized in the Children′s Hospital of Zhejiang University School of Medicine from January 1999 to February 2009 were retrospectively reviewed. Serum lipid levels were measured in 48 children with type 1 diabetes mellitus and in 24 healthy children. The diabetic children were classified into two subgroups, with or without ketoacidosis. Serum lipid and cytokines levels were compared. RESULTS: Childhood type 1 diabetes mellitus was common in females (56.3%). The peak incident age of the disease was between 6 and 11.9 years. Diabetic ketoacidosis was as the presenting symptom for the first visit in 86 cases (32.7%). The levels of serum lipid, blood glucose and HbA1c in diabetic children with ketoacidosis were significantly higher than those without ketoacidosis (P<0.05). Logistic analysis demonstrated that the increased levels of blood glucose, serum lipid and HbA1c were risk factors for diabetic ketoacidosis. The level of serum IL-10 in diabetic children with ketoacidosis was significantly higher than that in patients without ketoacidosis (P<0.01), while there were no differences in serum levels IL-2, IL4, IL-6, TNF-α and IFN-γ between them. Serum levels IL-2, IL-4, IL-6, IL-10, TNF-α and IFN-γ in diabetic children were significantly higher than those in healthy children (P<0.01). CONCLUSIONS: Ketoacidosis is a common acute complication of type 1 diabetes mellitus. The disorders of glucose and lipid metabolism are the risk factors for ketoacidosis in diabetic children. IL-10 may be a sensitive index of diabetic ketoacidosis in children with type 1 diabetes mellitus.[Chin J Contemp Pediatr, 2010, 12 (11):849-854]
DAI Yang-Li,FU Jun-Fen,LIANG Li et al. A 10-year review of childhood type 1 diabetes mellitus and the clinical value of interleukin-10 in diabetic ketoacidosis[J]. CJCP, 2010, 12(11): 849-854.
[2]Mohamed-Ali V, Armstrong L, Clarke D, Bolton CH, Pinkney JH. Evidence for the regulation of levels of plasma adhesion molecules by proinflammatory cytokines and their soluble receptors in type 1 diabetes[J]. J Intern Med, 2002, 250 (5): 415-421.
[3]Erbagci AB, Tarackioglu M, Coskun Y, Sivasli E, Namiduru ES. Mediators of inflammation in children with type 1 diabetes mellitus:cytokines in type 1 diabetic children[J]. Clin Biochem, 2001(34): 645-650.
[4]Geerlings SE, Brouwer EC, van Kessel KC, Gaastra W, Stolk RP, Hoepelman AL. Cytokine secretion is impaired in women with diabetes mellitus[J]. Eur J Clin Invest, 2000, 30(11): 995-1001.
[5]Foss NT, Foss-Freitas MC, Ferreira MA, Cardili RN, Barbosa CM, Foss MC. Impaired cytokine production by peripheral blood mononuclear cells in type diabetic patients[J]. Diabetes Metab, 2007(33): 439-443.
[7]Kukreja A, Cost G, Marker J, Zhang C, Sun Z, Lin-Su K, et al. Multiple immuno-regulatory defects in type-1 diabetes[J]. Clin Invest, 2002, 109(1):131-140.
[8]Gabir MM, Hanson RL, Dabelea D, Imperatore G, Roumain J, Bennett PH, et al.The 1997 American Diabetes Association and 1999 World Health Organization criteria for hyperglyccmia in the diagnosis and prediction of diabetes[J]. Diabetes Care, 2000, 23(8):1108-1112.
[9]Wolfsdorf J, Glaser N, Sperling MA. Diabetic ketoacidosis in infants, children, and adolescents.A consensus statement from the American Diabetes Association[J]. Diabetes Care, 2006, 29(5):1150-1159.
[10]Yoon JW,Jun HS.Viruses in type 1 diabetes:brief review[J]. ILAR J, 2004, 45(3):343-348.
[11]Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg RA, Malone JI, et al. American Diabetes Association. Hyperglycemic crises in diabetes[J]. Diabetes Care, 2004, 27(Suppl 1): s94-s102.
[12]van der Werf N, Kroese FG, Rozing J, Hillebrands JL.Viral infections as potential triggers of type 1 diabetes[J]. Diabetes Metab Res Rev, 2007, 23(3):169-183.
[16]Heptulla RA, Stewart A, Enocksson S, Rife F, Ma TY, Sherwin RS, et al. In situ evidence that peripheral insulin resistance in adolescents with poorly controlled type 1 diabetes is associated with impaired suppression of lipolysis: a microdialysis study[J]. Pediatr Res, 2003, 53(5):830-835.
[17]Enoksson S, Caprio SK, Rife F, Shulman GI, Tamborlane WV, Sherwin RS. Defective activation of skeletal muscle and adipose tissue lipolysis in type 1 diabetes mellitus during hypoglycemia[J]. J Clin Endocrinol Metab, 2003, 88(4):1503-1511.
[18]White NH. Diabetic ketoacidosis in children[J]. Endo Metab Clin North Am, 2000, 29(4):657-682.
[19]Mosser DM, Zhang X.Interleukin-10:new perspectives on an old cytokine[J]. Immunol Rev, 2008, 226(1): 205-218.
[20]Cai G, Kastelein RA, Hunter CA. IL-10 enhances NK cell proliferation, cytotoxicity and production of IFN-gamma when combined with IL-18[J]. Eur J Immunol, 1999, 29(9): 2658-2665.
[21]Lauw FN, Pajkrt D, Hack CE, Kurimoto M, van Deventer SJ, van der PT. Proinflammatory effects of IL-10 during human endotoxemia[J]. J Immunol, 2000(165): 2783-2789.
[22]Hoffman WH, Burek CL, Waller JL, Fisher LE, Khichi M, Mellick LB. Cytokine response to diabetic ketoacidosis and its treatment[J]. Clin Immunol, 2003, 108(3): 175-181.