Segovia LDA, Vargas AG, Márquez SM

Language: Spanish
References: 14
Page: 4-8
PDF size: 209.33 Kb.

ABSTRACT

Introduction: Diabetic ketoacidosis (DKA) is an acute metabolic complication which affects diabetic patients. DKA metabolic abnormalities promote the increase of lipase and amylase serum levels, as well as the overproduction of ketone bodies, worsening the acidosis state and hydroelectrolytic balance. These abnormalities, together with the clinical features associated with DKA are potential sources for misinterpreting the symptoms as acute abdomen. Although the clinical meaning is unclear, hyperlipasemia levels seem to vary according to the severity of DKA; hence, this likely correlation is assessed in this study.
Material and methods: Observational cross-sectional analytic comparative study, including internal medicine patients from the following general hospitals: Xoco, Balbuena and Ticomán (SSDF). The patients were diagnosed with DKA, showing different lipase levels with no acute pancreatitis, gastric and/or parotid gland pathology. The severity of DKA was assessed based on the clinical record. Hyperlipasemia was considered as a lipase serum level of ›38 UI/L.
Results: Forty-five patients with DKA were included and 4 were excluded. The 41 patients studied were divided in 3 groups according to their DKA severity. The general prevalence of hyperlipasemia was 51.2%, with a distribution of 42.8%, 33.3% and 23.9% among patients with mild, moderate and severe DKA, respectively. Lipase levels between the groups with mild and severe DKA were different; however, no difference was found when comparing only patients showing hyperlipasemia. Furthermore, a low inverse correlation was found between DKA severity and serum lipase levels (r=0.37), HCO3 (r=0.3) and anion gap (r=0.23), according to multiple regression analysis. This study suggests that the presence of hyperlipasemia is not a good marker to indicate the severity of DKA.
Conclusion: Lipase levels and DKA severity show an inverse correlation, which, according to current knowledge, should have no significant value for clinical interpretation.

REFERENCES

1. Thomas WD, Kristin M F. Diabetes Management in the Hospital. Med Clin N Am. 2008;92:407-25.

2. Guzmán-Juárez N, Madrigal-Bujaidar E. Revisión de las características clínicas, metabólicas y genéticas de la diabetes mellitus. Bioquimia. 2003;28(2):14-23.

3. Bracho F. Cetoacidosis Diabética. Medicrit. 2005;2(1):9-16.

4. Tavera HM, Coyote N. Cetoacidosis diabética. An Med (Mex). 2006;51(4):180-7.

5. Abbas EK, Ebenezer A. Nyenwe. Hyperglycemic Crises in Diabetes Mellitus: Diabetic Ketoacidosis and Hyperglycemic Hyperosmolar State. Endocrinol Metab Clin N Am. 2006;35:725-51.

6. Trachtenbarg DE. Diabetic Ketoacidosis. Am Fam Physician. 2005;71:1705-14.

7. Chiasson JL, Aris-Jilwan N, Belanger R, Bertrand S, Beauregard H, Ekoe JM, et al. Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state. CMAJ. 2003;168(7):859-66.

8. Magee M, Bhatt B. Endocrine and metabolic dysfunction syndromes in the critically ill. Management of decompensated diabetes. Crit Car Clin. 2001;17:1.

9. Haddad NG, Croffie JM, Eugster EA. Pancreatic enzyme elevations in children with diabetic ketoacidosis. J Pediatr. 2004;145(1):122-4.

10. Sánchez-Lozada R, Acosta-Rosero AV. Chapa-Azuela O, Hurtado-López LM. Etiology on determining the severity of acute pancreatitis. Gac Med Mex. 2003;139:27-31.

11. Sánchez-Ramírez CA, Larrosa-Haro A, Flores-Martínez S, Sánchez-Corona J, Villa-Gómez A, Macías-Rosales R. Acute and recurrent pancreatitis in children: etiological factors. Acta Paediatr. 2007;96:534-7.

12. Nøjgaard C, Bendtsen F, Matzen P, Becker U. The aetiology of acute and chronic pancreatitis over time in a hospital in Copenhagen. Dan Med Bull. 2010;57:A4103.

13. Quiros JA, Marcin JP, Kuppermann N, Nasrollahzadeh F, Rewers A, DiCarlo J, et al. Elevated serum amylase and lipase in pediatric diabetic ketoacidosis. Pediatr Crit Care Med. 2008;9:418-22.

14. Rizvi AA. Serum amylase and lipase in diabetic ketoacidosis. Diabetes Care. 2003;26:3193-3194.