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Neurocognitive functioning may be compromised in children with type 1 diabetes mellitus (T1DM). The factor most consistently implicated in the long-term neurocognitive functioning of children with T1DM is age of onset. The pediatric literature suggests that glycemic extremes may have an effect on the neurocognitive functioning of children, but findings are mixed. The purpose of this study was to compare the neurocognitive functioning of young children with T1DM diagnosed before 6 yr of age and healthy children (i.e., without chronic illness). Additionally, in the children with T1DM, we examined the relationship between their neurocognitive functioning and glycemic control. Sixty-eight (36 with T1DM and 32 without chronic illness) preschool-age children (M age = 4.4 yr ) were recruited and administered a battery of instruments to measure cognitive, language, and fine motor skills. Children with T1DM performed similar to the healthy controls and both groups' skills fell in the average range. Among children with diabetes, poor glycemic control [higher hemoglobin A1c (HbA1c)] was related to lower general cognitive abilities (r = -0.44,p < 0.04), slower fine motor speed (r = -0.64,p < 0.02), and lower receptive language scores (r = -0.39,p < 0.04). Such findings indicate that young children with T1DM already demonstrate some negative neurocognitive effects in association with chronic hyperglycemia.

Increased chromosomal rearrangements and chromosomal fragility have been previously observed in lymphocytes of children treated with human GH, implying that treatment could predispose to malignancy. Twenty-four children with classic GH deficiency, neurosecretory GH dysfunction, and Turner syndrome were treated with recombinant human GH (0.3 mg x kg(-1) x wk(-1)). Metaphase cells were assessed for spontaneous chromosomal and chromatid aberrations at baseline and 6 mo into treatment. There were no significant differences in aberrations between baseline and the 6-mo samples. However, the mean frequency of chromatid-type aberrations on a per cell basis was significantly higher than at baseline, 0.0088 versus 0.0064 aberrations per cell (p < 0.024). Two patients contributed inordinately to this increase. A third sample from these two patients was almost identical to their baseline samples. Cells were also irradiated in vitro (3 Gy) to assess chromosomal fragility. After irradiation, no patient showed a significant difference for any aberration type, although there was a significantly lower frequency of ring chromosomes on a per cell basis in the 6-mo samples (p < 0.001). We find no evidence that GH therapy influences spontaneous chromosomal aberrations or chromosomal fragility.

Maternal glycosylated hemoglobin and glycosylated protein and cord glycosylated protein were measured at delivery in 20 normal mothers of 20 macrosomic neonates over 4000 g (group I) and compared with values in two groups of mother/infant pairs: 20 normal/20 appropriate for gestational age (group II) and nine diabetic mothers/ten neonates (group III). Infants in group I, by design, weighed more (mean +/- SD 4403 +/- 337 g) than those in group II (2902 +/- 278 g) or group III (3365 +/- 898 g) (P less than .001). There was no significant difference in weight between group II and group III infants. Birth weight ratio was greater (P less than .001) in group I than in group II or group III (1.39 +/- 0.1, 0.9 +/- 0.08, and 1.08 +/- 0.25, respectively); group III infants had a higher birth weight ratio (P less than .05) than those in group II. Hematocrit (%) was higher (P less than .05) in group III (62 +/- 3) than in group I (59 +/- 5) or group II (57 +/- 6) infants. Glycosylated hemoglobin values were similar in all three groups. Mean serum glycosylated protein was higher (P less than .001) in group III (13.8 +/- 2%) than in group I (10 +/- 2%) or group II (9.8 +/- 2.5%) mothers. Cord glycosylated protein was also higher (P less than .001) in group III (12.3 +/- 1.9%) than in group I (9 +/- 1.3%) or group II (8.6 +/- 1.7%) neonates.(ABSTRACT TRUNCATED AT 250 WORDS)