Young Children with Type 1 Diabetes Mellitus Have Low Rate of Partial Remission Sasigarn A. Bowden, Mary Duck, Robert P Hoffman Division of Endocrinology, Department of Pediatrics, College of Medicine and Public Health, The Ohio State University, Columbus Children’s Hospital, Columbus, Ohio Young children (group 1) had the lowest rate of partial remission (26.8%) Adolescents (group 3) also had low rate of partial remission (29%). School age children (group 3) had the highest rate of partial remission (56%) There were no differences in the rate of diabetic ketoacidosis (DKA), autoantibody frequency and HbA1C at diagnosis between age groups. DKA at diagnosis is a predictor for less likelihood of having partial remission (p<0.001). There were no association between gender, autoantibodies, HbA1C at diagnosis and the rate of partial remission. SUMMARY There are data suggesting heterogeniety in the etiology and pathogenesis of type 1 diabetes mellitus (T1DM) between children and adults. The process of beta-cell destruction is faster in affected children than in affected adults. There are also data suggesting that the extent of beta cell damage differs between patients diagnosed before and after puberty. It has been our observation that young children (<5 years) do not have high rate of partial remission (or honeymoon phase) as compared to older children. BACKGROUND RESULTS Variables Group 1 (age <5) Group 2 (age 5-12) Group 3 (age >12) P value No. of patients (Total N=152) 41 60 51 Percentage of total 27% 39.5% 33.5% Mean age ± SD 2.95 ± 1.36 8.28 ± 2.29 14.52 ± 1.41 Male/female (%male) 24/17 (58.5%) 30/30 (50%) 34/17 (66.7%) No. of patients with partial remission (%) 11 (26.8%)a 34 (56.6%)a 15 (29.4%) a a P=0.002 Rate of DKA at diagnosis (%) (N) 46.3% (19) 28.3% (17) 27.4% (14) P=0.092 HbA1C at diagnosis (%) 10.4 ± 1.7b 11.7 ± 2.2 11.7 ± 2.1 bp<0.01 vs Gr 2, Gr3 HbA1C at 6 months 8.2 ± 1.5c, d 7.3 ± 1.7 6.8 ± 1.4 c p<0.01 vs Gr2 d p<0.001 vs Gr3 HbA1C at 9 months 8.0 ± 1.3 7.7 ± 1.4 7.8 ± 2.1 HbA1C at 12 months 8.5 ± 1.2 8.6 ± 2.1 8.4 ± 2.5 TDD at 6 months 0.50 ± 0.13e 0.66 ± 0.98 0.75 ± 0.32 eP<0.001 vs Gr 3 TDD at 9 months 0.58 ± 0.19 0.58 ± 0.24 0.89 ± 1.00 TDD at 12 months 0.55 ± 0.19f 0.64 ± 0.25 0.78 ± 0.33 fP<0.05 vs Gr 3 1. To test the hypothesis that young children with T1DM are less likely to have partial remission. 2. To identify clinical characteristics that predict partial remission. OBJECTIVE A total of 152 consecutive patients with newly diagnosed T1DM at Columbus Children’s Hospital in 2004 were studied. The Columbus Children’s Hospital at Columbus, Ohio is the only children’s hospital in central Ohio caring for children with new onset T1DM. We categorized patients to 3 age groups: Group 1: age < 5 years Group 2: age 5-12 years Group 3: age >12 years Clinical characteristics at diagnosis, the presence of diabetes ketoacidosis, initial blood glucose, initial HbA1C, islet cell antibodies, total daily insulin dose (TDD) along with HbA1C at 3-month interval follow for 1 year were analyzed in each age group. Partial remission was defined as TDD (total daily insulin dose) <0.5 units/kg/day with HbA1C <8%. Diabetes ketoacidosis: Bicarb < 15 with presence of ketonuria Pearson’s correlation coefficient was used for statistical analysis DESIGN/METHODS Patients with partial remission Patients without partial remission Total patients (N=152) 60 92 Rate of DKA at diagnosis% (n) 15% (9) 43.4% (40) P<0.001 Age (mean ± SD) 8.8 ± 4.2 9.0 ± 5.3 0.778 HbA1C at Diagnosis 11.0 ± 1.9 11.7 ± 2.2 0.097 GAD-65 Autoantibodies 200.9 ± 527 93.0 ± 672 0.37 Young children and adolescent children with T1DM were less likely to have partial remission or honeymoon phase as compared to prepubertal children. Metabolic control was poorest in young children, whereas, higher dose insulin in adolescents due to insulin resistance contributed to less likelihood of having partial remission. DKA at diagnosis was a strong predictor for lack of partial remission. It is possible that the low frequency of honeymoon phase in young children reflects more aggressive beta cell destruction in young children. CONCLUSION