The relationship between the occurrence of caries and diabetes was explored in 80 children and adolescents with insulin-dependent diabetes mellitus. The mean age of the subjects was 14.5 years (range 11.7–18.4 years) and duration of diabetes 0.3–15.0 years (mean 6.0 years). DFS indices in poorly controlled subjects (gly-cosylated haemoglobin, HbA₁, values over 13%) were significantly higher than in moderately (HbA₁ 10.0–12.9%) or in well-controlled cases (HbA₁ values < 10%). However, the difference was not statistically significant if adjustments were made for age, age at the onset of diabetes and duration of diabetes (p = 0.1, Ancova). Subjects with caries and/or fillings had significantly higher short- and long-term HbA₁ values than subjects with intact teeth, both if all subjects or subjects with long-term disease (duration of diabetes of at least 2 years, n = 62) were included. This finding was valid after adjustments for age, duration of diabetes and age at the onset of diabetes. Association between poor control and the loss of intact dentition was also demonstrated in subjects whose diabetes was diagnosed before the age of 7. Presence of yeasts was highly associated with poor control of diabetes, and yeasts were more frequently found in the saliva samples of subjects with decayed and/or filled teeth. Instead, salivary flow rates, salivary lactobacilli and Streptococcus mutans counts, buffering capacity and pH were not different between the subjects. As well, home care practices were similar, and all subjects had received similar regular dental treatment. In conclusion, poor control of diabetes was found to be associated with caries. The presence of yeasts may be a caries risk indicator in subjects with diabetes, since diabetes may enhance yeast growth, particularly if poorly controlled.

The hypothalamo-pituitary-insulin-like growth factor I (IGF-I) axis was studied in 24 prepubertal children with insulin-dependent diabetes mellitus (IDDM) and 12 non-diabetic children. There were no significant differences between the diabetic and control subjects in basal concentrations of immunoreactive growth hormone releasing hormone (ir-GHRH), growth hormone (GH) or stimulated GH levels, but after exercise ir-GHRH concentrations were higher in the diabetic children. Peripheral IGF-I levels were significantly lower in the diabetic children, and even lower in those with poor metabolic control. A positive correlation was found between IGF-I levels and circulating free insulin concentrations in the diabetic subjects (r = 0.49, p < 0.05). These observations suggest that the GH response to physiological stimulation is normal in prepubertal diabetic children. Exercise-induced GH response may not be mediated by GHRH. IGF-I levels were reduced in prepubertal children with IDDM and even more so in subjects with poor metabolic control. This may be a consequence of transitory hypoinsulineamia, emphasizing the importance of adequate insulinization to facilitate optimal growth in children and adolescents with IDDM.

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Seventeen children aged 5 months to 3 years with recurrent or chronic otitis media complicated by Pseudomonas aeruginosa were treated with ceftazidime. All patients had been previously treated with several antibiotics. All strains of Pseudomonas were initially sensitive to ceftazidime. In four of the six cases which failed bacteriologically, the Pseudomonas was found to be of intermediate sensitivity after treatment. In 11 patients the Pseudomonas was eradicated during treatment but reappeared in 4 during the follow-up period. All 11 patients were clinically cured or improved. Three of the six children whose Pseudomonas was not eliminated from aural discharge showed some clinical improvement whereas the remaining three showed no clinical response to treatment. The range of MIC values of ceftazidime, gentamicin and carbenicillin for the Pseudomonas isolated were respectively 0.5 to 4.0, 0.25 to 2.0 and 4.0 to 125 mg/l. The mean ceftazidime serum level at 1 h after the first injection of 50 mg/kg was 74.12 (S.D. 12.84) mg/l and at 12 h post injection 1.93 (S.D. 4.14) mg/l.

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