Bone calcium changes during diabetic ketoacidosis: a comparison with lactic acidosis due to volume depletion.
In this study, we aimed to compare bone calcium system changes from children with diabetic ketoacidosis or acute metabolic acidosis due to dehydration to find out the relative contribution of metabolic acidosis and diabetes-related factors on expected negative calcium balance. We studied a set of non-invasive parameters of bone remodeling in 16 children with diabetic ketoacidosis due to new onset type 1 diabetes and 25 children with acute metabolic acidosis due to dehydration complicating acute gastroenteritis before and after the correction of acidosis. The two groups of subjects were matched for age, sex, pubertal status, and degree of metabolic acidosis and dehydration. A group of 18 age and sex-matched healthy children served as the control group. Plasma ionized calcium levels were increased in both groups, significantly more so in diabetic ketoacidosis. While osteoblastic markers, osteocalcin and alkaline phosphatase, were depressed to a comparable degree in both groups, urinary calcium/creatinine ratio and hydroxyproline excretion were significantly greater in diabetic ketoacidosis. No significant changes in calcitrophic hormone (intact PTH, calcitonin, 25-hydroxy vitamin D3) levels were observed. All study parameters except for serum phosphate levels behaved in parallel in both clinical conditions, and abnormalities disappeared with the correction of acidosis except for IGF-1, which remained low in diabetic subjects. In conclusion, our results suggest that, in diabetic ketoacidosis, the observed severe negative calcium balance occurred through diminished bone formation mediated by metabolic acidosis per se and increased bone mineral dissolution and bone resorption because of severe insulin deficiency and secondarily via metabolic acidosis. Observed changes appear to be independent of calcitrophic hormones.
Topaloglu
A Kemal
AK
Division of Pediatric Endocrinology and Metabolism, Cukurova University, Faculty of Medicine, Balcali, Adana 10330, Turkey. ktopaloglu@cu.edu.tr
Yildizdas
Dincer
D
Yilmaz
H Levent
HL
Mungan
Neslihan O
NO
Yuksel
Bilgin
B
Ozer
Guler
G
D000140:Acidosis, Lactic / Q000097:blood / Q000209:etiology / Q000378:metabolism*; D000469:Alkaline Phosphatase / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D001842:Bone and Bones / Q000378:metabolism*; D002118:Calcium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D002648:Child; D002675:Child, Preschool; D003401:Creatine / Q000097:blood / Q000652:urine; D003681:Dehydration / Q000150:complications; D016883:Diabetic Ketoacidosis / Q000097:blood / Q000378:metabolism* / Q000652:urine; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006909:Hydroxyproline / Q000652:urine; D007223:Infant; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D015675:Osteocalcin / Q000097:blood; D012044:Regression Analysis; D018709:Statistics, Nonparametric
D001786:Blood Glucose; D015675:Osteocalcin; D007334:Insulin-Like Growth Factor I; D000469:Alkaline Phosphatase; D003401:Creatine; D006909:Hydroxyproline; D002118:Calcium