Impact of neighbourhood-level inequity on paediatric diabetes care.

AIMS: To evaluate the association between neighbourhood-level inequity and glycaemic control in paediatric participants with Type 1 diabetes using the Neighbourhood Equity Index (NEI). METHODS: The NEI was linked to the clinical data of 519 children with diabetes followed at the Hospital for Sick Children (Toronto, Canada). The NEI is a composite measure of inequity developed using the World Health Organization's Urban Health Equity Assessment and Response Tool (HEART), which encompasses 15 weighted indicators evaluating economic, social, environmental and lifestyle factors. The geographic distribution of participants was determined using postal codes, and the relationship between HbA1c and NEI was evaluated using regression and spatial analysis techniques. RESULTS: Participants' mean HbA1c was significantly correlated with NEI (R = -0.24, P < 0.0001). Regression analysis demonstrated that NEI was a strong predictor of mean HbA1c (P < 0.0001), accounting for differences in HbA1c as large as 1.0% (11 mmol/mol) when controlled for age, sex, diabetes duration, insulin pump therapy and number of annual clinic visits. Geo-mapping using spatial scan testing revealed the presence of two clusters of low-equity neighbourhoods containing 3.22 (P = 0.001) and 2.83 (P = 0.02) times more participants with HbA1c ≥ 9.5% (80 mmol/mol) than expected. CONCLUSIONS: Our findings demonstrated that NEI was a significant predictor of HbA1c in our clinic population and a useful tool for investigating spatial trends related to inequities in health, providing evidence that a composite, area-based measure of overall inequity is well suited to the study of glycaemic control in urban paediatric Type 1 diabetes populations.

The effect of renal hyperfiltration on urinary inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes mellitus.

AIMS/HYPOTHESIS: High intraglomerular pressure causes renal inflammation in experimental models of diabetes. Our objective was to determine whether renal hyperfiltration, a surrogate for intraglomerular hypertension, is associated with increased excretion of urinary cytokines/chemokines in patients with type 1 diabetes mellitus. METHODS: Blood pressure, renal haemodynamic function (inulin and para-aminohippurate clearances for glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively) and urine samples were obtained during clamped euglycaemia in individuals with type 1 diabetes with either hyperfiltration (GFR determined using inulin [GFRINULIN] ≥ 135 ml min⁻¹ 1.73 m⁻², n = 28) or normofiltration (n = 21) and healthy control individuals (n = 18). RESULTS: Baseline clinical characteristics, dietary sodium and protein intake and blood pressure levels were similar in the diabetic and healthy control groups. In addition, HbA1c levels were similar in the two diabetic groups. As expected baseline GFR was higher in hyperfilterers than either normofiltering diabetic patients or healthy control patients (165 ± 9 vs 113 ± 2 and 116 ± 4 ml min⁻¹ 1.73 m⁻², respectively, p < 0.01). ERPF and renal blood flow were also comparatively higher and renal vascular resistance was lower in hyperfiltering patients (p < 0.01). Hyperfiltering diabetic patients had higher excretion rates for eotaxin, IFNα2, macrophage-derived chemokine, platelet-derived growth factor (PDGF)-AA, PDGF-AB/BB and granulocyte-macrophage colony-stimulating factor (p ≤ 0.01). Urinary monocyte chemoattractant protein (MCP)-1 and RANTES (regulated on activation, normal T expressed and secreted) excretion was also higher in hyperfiltering vs normofiltering diabetic individuals (p < 0.01) and fibroblast growth factor-2, MCP-3 and CD40K excretion was elevated in hyperfiltering diabetic individuals vs healthy controls (p < 0.01). CONCLUSIONS/INTERPRETATION: Renal hyperfiltration is associated with increased urinary excretion of inflammatory cytokines/chemokines in patients with uncomplicated type 1 diabetes.

Urinary markers of renal inflammation in adolescents with Type 1 diabetes mellitus and normoalbuminuria.

AIMS: Patients with the highest albumin:creatinine ratio within the normal range are at an increased risk for developing microalbuminuria. The mechanistic basis for this is unknown, but may be related to renal inflammation. Our goal was to characterize the urinary excretion of cytokines/chemokines in normoalbuminuric adolescents with Type 1 diabetes to determine whether higher range normoalbuminuria is associated with evidence of renal inflammation. METHODS: Forty-two urinary cytokines/chemokines were measured in subjects who were screened for the Adolescent Type 1 Diabetes Cardio-Renal Intervention Trial. Urinary cytokines/chemokines were compared across low (n = 50), middle (n = 50) or high (n = 50) albumin:creatinine ratio tertile groups. RESULTS: At baseline, participants in the upper tertile were younger and had shorter diabetes duration compared with the other groups. Other clinical characteristics were similar. Urinary levels of interleukin 6, interleukin 8, platelet-derived growth factor-AA and RANTES differed across albumin:creatinine ratio tertiles, with higher values in patients in the middle and high tertiles compared with the lower tertile (ANCOVA P ≤ 0.01). CONCLUSIONS: Within the normal albumin:creatinine ratio range, higher urinary albumin excretion is associated with elevated urinary levels of inflammatory markers. Ultimately, this may provide mechanistic insights into disease pathophysiology and stratify the risk of nephropathy in Type 1 diabetes.

Association between childhood obesity and subsequent Type 1 diabetes: a systematic review and meta-analysis.

AIMS: To review and synthesize the published evidence on the possible association between childhood obesity and the subsequent risk of Type 1 diabetes. METHODS: The PubMed database was systematically searched for studies using childhood obesity, BMI or %weight-for-height as the exposure variable and subsequent Type 1 diabetes as the outcome. Studies were only included if assessment of obesity preceded the diagnosis of Type 1 diabetes. RESULTS: Eight case-control studies and one cohort study were included, comprising a total of 2658 cases. Of these nine studies, seven reported a significant association between childhood obesity, BMI or %weight-for-height and increased risk for Type 1 diabetes. Meta-analysis of the four studies that reported childhood obesity as a categorical exposure produced a pooled odds ratio of 2.03 (95% CI 1.46-2.80) for subsequent Type 1 diabetes; however, in those studies, age at obesity assessment varied from age 1 to 12 years. A dose-response relationship was supported by a continuous association between childhood BMI and subsequent Type 1 diabetes in a meta-analysis of five studies (pooled odds ratio 1.25 (95%CI 1.04-1.51) per 1 sd higher BMI). CONCLUSION: There is overall evidence for an association between childhood obesity, or higher BMI, and increased risk of subsequent Type 1 diabetes. Several theories have been proposed for a causal relationship. Reduction in Type 1 diabetes should be considered as a potential additional benefit of preventing childhood obesity.

Distinct antibody specificities to a 64-kD islet cell antigen in type 1 diabetes as revealed by trypsin treatment.

Type 1 diabetes is associated with antibodies that immunoprecipitate a 64-kD islet cell membrane protein from detergent extracts of pancreatic islets. In this study we have determined whether mild trypsin treatment of islet membranes can release fragments of the antigen that bind antibodies in the serum of Type 1 diabetic patients. Partial tryptic proteolysis of [35S]methionine-labeled 64-kD antigen immunoprecipitated from detergent extracts of rat islets resulted in the formation of 50-, 40-, and 37-kD fragments. Similar sized fragments were recovered when sera from diabetic patients were employed to immunoprecipitate polypeptides solubilized by mild trypsin treatment of a particulate fraction of radiolabeled rat islets. Of 27 diabetic patients, 22 possessed antibodies to the 50-kD polypeptide and 21 to the 40- and 37-kD polypeptides. A positive association was found between 64k antibodies and antibodies to the 50-kD fragment but not between 64k antibodies and antibodies to the 40- or 37-kD fragments. Some 64k antibody negative patients possessed antibodies that efficiently immunoprecipitated the latter fragments. Serum from 25 of 27 (93%) diabetic patients immunoprecipitated at least one of the three tryptic polypeptides. One of 20 nondiabetic controls immunoprecipitated a 50-kD polypeptide and all controls were negative for antibodies to 40- and 37-kD fragments. Thus, Type 1 diabetes is associated with the presence of at least two antibody reactivities to distinct determinants of the 64-kD antigen, and some patients may possess antibodies to a cryptic epitope on the detergent-solubilized molecule. These data suggest that the detection of antibodies (present in 93% of patients) to epitopes on tryptic polypeptides of the 64-kD antigen may be of even greater diagnostic value for the onset of Type 1 diabetes than analyses of antibodies reactive with the intact 64-kD antigen.

Target setting in intensive insulin management is associated with metabolic control: the Hvidoere childhood diabetes study group centre differences study 2005.

OBJECTIVE: To evaluate glycaemic targets set by diabetes teams, their perception by adolescents and parents, and their influence on metabolic control. METHODS: Clinical data and questionnaires were completed by adolescents, parents/carers and diabetes teams in 21 international centres. HbA1c was measured centrally. RESULTS: A total of 2062 adolescents completed questionnaires (age 14.4 +/- 2.3 yr; diabetes duration 6.1 +/- 3.5 yr). Mean HbA 1c = 8.2 +/- 1.4% with significant differences between centres (F = 12.3; p < 0.001) range from 7.4 to 9.1%. There was a significant correlation between parent (r = 0.20) and adolescent (r = 0.21) reports of their perceived ideal HbA1c and their actual HbA1c result (p < 0.001), and a stronger association between parents' (r = 0.39) and adolescents' (r = 0.4) reports of the HbA1c they would be happy with and their actual HbA1c result. There were significant differences between centres on parent and adolescent reports of ideal and happy with HbA1c (8.1 < F > 17.4;p < 0.001). A lower target HbA1c and greater consistency between members of teams within centres were associated with lower centre HbA1c (F = 16.0; df = 15; p < 0.001). CONCLUSIONS: Clear and consistent setting of glycaemic targets by diabetes teams is strongly associated with HbA1c outcome in adolescents. Target setting appears to play a significant role in explaining the differences in metabolic outcomes between centres.

Are family factors universally related to metabolic outcomes in adolescents with Type 1 diabetes?

AIMS: To assess the importance of family factors in determining metabolic outcomes in adolescents with Type 1 diabetes in 19 countries. METHODS: Adolescents with Type 1 diabetes aged 11-18 years, from 21 paediatric diabetes care centres, in 19 countries, and their parents were invited to participate. Questionnaires were administered recording demographic data, details of insulin regimens, severe hypoglycaemic events and number of episodes of diabetic ketoacidosis. Adolescents completed the parental involvement scale from the Diabetes Quality of Life for Youth--Short Form (DQOLY-SF) and the Diabetes Family Responsibility Questionnaire (DFRQ). Parents completed the DFRQ and a Parental Burden of Diabetes score. Glycated haemoglobin (HbA(1c)) was analysed centrally on capillary blood. RESULTS: A total of 2062 adolescents completed a questionnaire, with 2036 providing a blood sample; 1994 parents also completed a questionnaire. Family demographic factors that were associated with metabolic outcomes included: parents living together (t = 4.1; P < 0.001), paternal employment status (F = 7.2; d.f. = 3; P < 0.001), parents perceived to be over-involved in diabetes care (r = 0.11; P < 0.001) and adolescent-parent disagreement on responsibility for diabetes care practices (F = 8.46; d.f. = 2; P < 0.001). Although these factors differed between centres, they did not account for centre differences in metabolic outcomes, but were stronger predictors of metabolic control than age, gender or insulin treatment regimen. CONCLUSIONS: Family factors, particularly dynamic and communication factors such as parental over-involvement and adolescent-parent concordance on responsibility for diabetes care appear be important determinants of metabolic outcomes in adolescents with diabetes. However, family dynamic factors do not account for the substantial differences in metabolic outcomes between centres.

Evidence-based review of treatment and follow up of pediatric patients with differentiated thyroid carcinoma.

Childhood onset differentiated thyroid cancer (DTC) is distinct from the adult-onset disease being more aggressive at the time of initial evaluation with a higher risk category for disease recurrence; however, it is ultimately less lethal. International groups have outlined consensus statements detailing follow up and management guidelines for adult DTC, but since disease progression and markers are significantly different in childhood DTC compared to adults, management protocols may differ. Unfortunately, there is no consensus regarding the means of follow up, timing and management strategy regarding pediatric DTC. We performed an evidence-based review of DTC in children targeted to address the following questions: What is the most appropriate initial treatment? What is the goal of thyroid hormone replacement management? What is the approach to follow-up of childhood DTC? and, How should tumor recurrence/persistence be assessed and treated? We conducted a literature search using PubMed, Cochrane databases, guidelines from various international groups, and studies pertaining to pediatric DTC management and outcome in order to answer these questions. We suggest a pre-set algorithm and approach for the management of children with DTC according to our review.

Insulin-stimulated glucose transport in circulating mononuclear cells from nondiabetic and IDDM subjects.

The objectives of this study were 1) to evaluate glucose transport and its regulation by insulin in easily accessible human cells, 2) to investigate the glucose transporter isoforms involved, and 3) to establish whether a defect in glucose transport is associated with peripheral insulin resistance, which is common in insulin-dependent diabetes mellitus (IDDM) patients. We measured 2-deoxyglucose (2-DG) uptake in circulating mononuclear cells from 23 nondiabetic adults, 16 adults with IDDM, and 10 children with IDDM. Circulating mononuclear cells were separated from whole blood by Ficoll gradients and incubated with +/- 1 nM insulin. 2-DG uptake was measured after incubation with [3H]2-DG and cell separation through corn oil-phthalate. Cytochalasin B-inhibitable 2-DG uptake (basal and insulin stimulated) was higher in control than in IDDM subjects (P less than 0.001). Insulin significantly increased 2-DG uptake or 3-O-methylglucose uptake in both groups. Basal and insulin-stimulated 2-DG uptake was similar for adults and children with IDDM and did not correlate with age or body mass index in any group or disease duration, insulin dosage, or HbA1c in IDDM. In separated monocytes and lymphocytes, 2-DG uptake increased in response to insulin only in the monocyte population. Insulin dose-response curves indicated maximal stimulation of hexose uptake at 1-2 nM insulin for both control and diabetic subjects and demonstrated a significant decrease in maximal insulin response in the latter. Immunoblotting with specific antibodies revealed that circulating mononuclear cells and separated monocytes express the GLUT1 but not the GLUT4 isoform of the glucose transporter.(ABSTRACT TRUNCATED AT 250 WORDS)

Persistence of serum antibodies to 64,000-Mr islet cell protein after onset of type I diabetes.

Antibodies to an islet protein of 64,000 Mr (64K antibodies) were measured in 15 diabetic children who were followed prospectively for up to 3 yr after onset of type I (insulin-dependent) diabetes. Of the 15 children, 12 were positive for 64K antibodies at diagnosis. Those patients who were negative for these antibodies at onset remained negative throughout the study. Modest increases in 64K antibodies were observed in 7 patients within 1 mo of diabetes onset, concomitant with an increase in C-peptide concentrations. All antibody-positive patients were still positive at the end of the study, with no significant decrease in antibody levels relative to those at diagnosis, whereas C-peptide concentrations decreased between 3 and 24 mo after onset. Islet cell antibodies, measured by immunochemical staining on sections of rat pancreas, were detected in 9 of 15 patients at onset, whereas only 3 of 11 patients were still positive after 3 yr. In an additional group of 11 patients with diabetes for 6-7 yr, when basal and stimulated C-peptide concentrations were undetectable, 4 patients were still positive for 64K antibodies. These results demonstrate that levels of 64K antibodies persist during the first 3 yr of diabetes, despite declining beta-cell function and decreased immune responses to other islet antigens, but decrease during the next 3-4 yr as the remaining functional beta-cells disappear.

Contribution of growth hormone and IGF-I to early diabetic nephropathy in type 1 diabetes.

In children and adolescents with type 1 diabetes, we have reported an association between duration of puberty and the prevalence of nephromegaly and microalbuminuria (MA), which are early markers of diabetic nephropathy. Growth hormone (GH), IGF-I, testosterone, and prorenin are potential mediators of this effect. This study examined the relationship of these hormonal factors to kidney volume (KV) and MA in 155 subjects (78 males, age 13.2 +/- 3.5 years [mean +/- SD]) with similar diabetes duration (6.83 +/- 1.6 years) but varying pubertal experience (0-10 years). KV (by ultrasound), plasma IGF-I, testosterone, prorenin, and NaLi countertransport, and urinary albumin, urinary GH, and urinary IGF-I from three 24-h collections were measured. Multiple regression analysis showed that BSA (P < 0.0001) and urinary IGF-I (P = 0.001) were significantly associated with KV. MA subjects (albumin excretion rate 15-200 microg/min) had higher urinary IGF-I (P = 0.005) and urinary GH (P = 0.05) compared with normoalbuminuric subjects. Only 9% of the variance in urinary IGF-I could be attributed to plasma IGF-I (r = 0.30, P < 0.0001). Testosterone and prorenin were not associated with MA, but they were associated with KV in univariate analyses. The strong association of urinary IGF-I with KV, a marker for glomerular hypertrophy, and of both urinary IGF-I and urinary GH with MA suggests a role for these growth factors in the development of human diabetic nephropathy. Together, these data support animal studies that have shown that renal GH and IGF-I may contribute significantly to the pathogenesis of early diabetic nephropathy.

Effect of puberty on markers of glomerular hypertrophy and hypertension in IDDM.

Epidemiological data implicate puberty as a factor in the initiation of diabetic nephropathy. However, the mechanism remains unclear. We hypothesized that puberty would result in an increase in glomerular hypertrophy and hypertension; these two early concomitant events are seen as pivotal to the pathophysiology of diabetic nephropathy. We studied the effect of pubertal duration on three surrogate markers of glomerular hypertrophy/hypertension: kidney volume (KV), microalbuminuria (MA), and Na-Li countertransport (CT). We recruited 177 subjects (87 female and 90 male; aged 6.2-22.1 years) with IDDM of 5 to 10 years' duration (6.8 +/- 1.6 years) into three groups with different pubertal duration: prepubertal since IDDM diagnosis; prepubertal at diagnosis, now pubertal; or early puberty at diagnosis, now postpubertal. KV was measured by ultrasound and corrected for body surface area; MA was defined as urinary albumin excretion of 15-200 micrograms/min in two of three 24-h samples, and Na-Li CT was measured in erythrocytes. As pubertal duration increased, there was a disproportionate increase in mean KV (prepubertal, 247 +/- 6 [SE] ml/1.73 m2; pubertal, 282 +/- 7/1.73 m2; postpubertal, 295 +/- 7/1.73 m2, P = 0.001), prevalence of nephromegaly (KV > 300 ml/1.73 m2) (14, 31, and 45%, respectively, P = 0.001), and prevalence of MA (0, 9.7, and 20.5%, respectively, P = 0.003). Subjects with KV > 300 ml/1.73 m2 were eight times more likely to have MA than those with KV < 300 (odds ratio 8.1, 95% confidence interval 2.4-27.4, P = 0.0001). There was no effect of pubertal duration on Na-Li CT. Multiple regression with KV as the dependent variable found an association with pubertal duration, MA, Na-Li CT, and current HbA1c (P < 0.0001). Our findings indicate that pubertal duration is an important determinant of both KV and MA and suggest that nephromegaly precedes microalbuminuria. We postulate that these effects are attributable to the influence of the pubertal milieu on glomerular hypertrophy/hypertension.

Relationship of insulin autoantibodies to presentation and early course of IDDM in children.

Insulin antibodies have been documented before (insulin autoantibodies [IAAs]) and after (insulin antibodies) insulin administration in children with new-onset insulin-dependent diabetes mellitus (IDDM). Whereas the relationship of IAA to various factors at presentation has been studied in some detail, little is known about their relationship to events during the 1st yr after diagnosis. Furthermore, the course and factors affecting insulin-antibody response to human insulin administration in children with newly diagnosed IDDM remain poorly defined. To study these questions, we measured serum glucose, pH, bicarbonate, C-peptide, and IAA at diagnosis in 84 children between 0.5 and 18 yr of age. Basal and peak C-peptide responses to Sustacal ingestion, glycosylated hemoglobin (HbA1c), and IAA were then measured in 33 of these patients at 10 days and 1, 3, 6, and 12 mo after diagnosis. At presentation, IAAs were absent (binding below the mean + 3SD of the binding of control serums) in 51 patients (61%) and present (binding above the mean + 3SD) in 33 patients (39%). Multiple regression analysis showed a significant nonlinear relationship between IAAs and both age (P less than .005) and blood glucose (P less than .05) at onset. There was a stepwise increase in median insulin-antibody binding throughout the 1st yr. This increase was most marked during the 1st mo of insulin therapy and showed a statistically significant difference between successive measurements only during this period.(ABSTRACT TRUNCATED AT 250 WORDS)

Eating disorders and IDDM. A problematic association.

IDDM and eating disorders are common conditions in young women. Whether a specific association exists between these two disorders remains controversial. Some studies have suggested an increased incidence of eating disorders in young women with IDDM, whereas others have not detected such an increase. These differences may be attributable, at least in part, to methodological issues in study design, measurement tools, and relatively small sample sizes. Whether the prevalence of eating disorders in IDDM is increased will be resolved only by larger studies that use standardized diagnostic interviews. We suspect that certain aspects of IDDM and its management may trigger the expression of an eating disorder in susceptible individuals. Required dietary restraint and weight gain related to diabetes management are the factors most likely to be implicated. Eating disorders are relatively common in young women with IDDM and may contribute to impaired metabolic control with hypoglycemia and DKA, and to long-term microvascular complications of diabetes. Omission or reduction of required insulin, an extremely common means of weight control in these young women, is likely an important factor in this regard. Further research is required to determine more precisely the relationship between IDDM and eating disorders, and the effects of eating disorders on metabolic control and chronic complications of IDDM.

Residual beta-cell function in children with IDDM: reproducibility of testing and factors influencing insulin secretory reserve.

Reproducibility of C-peptide secretion was assessed in 20 children (group 1) by their responses to two Sustacal- (a mixed liquid meal) stimulation tests performed 7-14 days apart. For the 12 C-peptide-positive children (basal C-peptide greater than or equal to 0.03 pmol/ml) there were no differences in the basal or stimulated values between tests 1 and 2. The effect of exogenous insulin on C-peptide secretion was assessed in 20 other children (group 2) by their responses to two Sustacal tests, one test without and one with soluble insulin (0.25 U/kg) injected subcutaneously before testing. Eleven children were C-peptide positive and had no differences in C-peptide response between tests 1 and 2. The results from test 1 in groups 1 and 2 were combined with those from 44 others undergoing a single Sustacal test (group 3, N = 84). There was a close correlation between basal and peak C-peptide concentrations in the 44 C-peptide-positive children (r = .88, P less than .001). Peak C-peptide concentrations correlated inversely with HbA1 (r = -.29, P less than .01), insulin dose in units per kilogram (r = -.40, P less than .001), and duration of diabetes (r = .33, P less than .001) and positively with age at onset of diabetes (r = .34, P less than .001). The C-peptide-positive children had reduced glucose response to Sustacal, lower HbA1 concentration, lower insulin requirement, later age of onset, and shorter duration of diabetes than children who were C-peptide negative.

Sodium-lithium transport in adolescents with IDDM. Relationship to incipient nephropathy and glycemic control.

OBJECTIVE: The aims of this study were to examine genetic and environmental influences in the development of early diabetic nephropathy and to assess the value of measuring membrane sodium transport as a marker for early nephropathy. RESEARCH DESIGN AND METHODS: We measured erythrocyte sodium-lithium (Na-Li) countertransport, blood pressure (BP), HbA1c, and microalbuminuria (MA) in 84 adolescents with insulin-dependent diabetes mellitus (IDDM), 29 of whom had MA. Twenty-nine non-MA patients were selected and matched for age, sex, and IDDM duration with the 29 diabetic subjects with MA. The 84 diabetic adolescents were also compared with 85 nondiabetic siblings. RESULTS: The erythrocyte Na-Li countertransport was significantly greater in the IDDM group than in the sibling group (mean +/- SD, 0.41 +/- 0.14 vs. 0.30 +/- 0.11 mmol Li.liters of erythrocytes-1.h-1, respectively, P < 0.0001), but a significant correlation was noted between the results in IDDM subjects and their siblings (r = 0.42, P < 0.0008). Na-Li countertransport was not different in the diabetic subjects with or without MA (0.43 +/- 0.13 vs. 0.37 +/- 0.13 mmol Li.liters of erythrocytes-1.h-1, respectively). There was a significant correlation in the IDDM group between recent diabetic control (HbA1c) and Na-Li countertransport (r = 0.37, P < 0.003). Diastolic BP was significantly higher in the IDDM group with MA than in those without MA (60 +/- 6 vs. 55 +/- 6 mmHg, respectively, P < 0.03). CONCLUSIONS: These results suggest that erythrocyte Na-Li countertransport is influenced by the diabetic milieu. However, there was also evidence in our subjects of a genetic contribution to Na-Li countertransport as seen by the correlation between levels in the IDDM subjects and their siblings. Using Na-Li countertransport, we were not able to segregate those IDDM adolescents with and without early nephropathy.

The role of self-monitoring of blood glucose in the routine management of children with insulin-dependent diabetes mellitus.

We report a double-crossover study to assess the impact of self-monitoring of blood glucose (SMBG) on the glycemic control of children with insulin-dependent diabetes mellitus (IDDM) on a conventional therapeutic regimen. Sixteen children were assigned to one of two groups--group A, period 1 (wk 1-13): urine testing plus SMBG; period 2 (wk 14-26): urine testing only; group B, period 1: urine only; period 2: urine testing plus SMBG. Frequent telephone contact was maintained throughout to help optimize insulin dose adjustment. At the outset, the two groups were similar in age, diabetes duration, and glycosylated hemoglobin levels (10.5 +/- 0.6% and 9.5 +/- 0.3% in groups A and B, respectively). No significant differences could be detected between the two groups at any stage of the study. There was, however, a trend toward lower mean blood glucose (MBG) concentration in both groups toward the end of the SMBG period. No complications of SMBG were noted, but compliance was a major problem in three children. SMBG confirmed symptoms of hypoglycemia in all children, and detected asymptomatic hypoglycemia (BG less than or equal to 40 mg/dl) in 11. Sixty-nine percent preferred SMBG to urine testing. We conclude that SMBG is an acceptable part of routine diabetes care in children. It is associated with very few complications and helps to confirm symptomatic hypoglycemia and detect asymptomatic hypoglycemia. However, the addition of SMBG to routine diabetes care does not necessarily lead to improved metabolic control.

Self-monitoring of blood glucose: how accurate are children with diabetes at reading chemstrip bG?

Accuracy of self-monitoring of blood glucose (SMBG) using Chemstrip bG (Bio-Dynamics, Indianapolis, Indiana) was studied in 90 randomly selected children with insulin-dependent diabetes mellitus (IDDM). For 28 children (mean age 8.3 +/- 3.6 yr) a parent routinely read the Chemstrip at home. The remaining 62 children (mean age 13.7 +/- 2.8 yr) read the Chemstrip themselves. Each child or parent analyzed 20 capillary blood samples using Chemstrips and answered a questionnaire on SMBG. The accuracy of SMBG of the group was high (mean correlation coefficient = 0.89 +/- 0.05), but consistency of measurement was variable (mean standard deviation = 1.90 +/- 0.57) and there was a general tendency to underread Chemstrips (mean y-intercept = 1.05 +/- 1.48; mean slope = 0.80 +/- 0.17). For each subject, 0-65% (mean of 34%) of readings were within 10% of the laboratory measurement, and 17-100% (mean 68%) within 20%. These results indicate that most subjects were fairly accurate in reading Chemstrips; however, analysis of accuracy is useful in identifying individuals who are inaccurate or inconsistent in SMBG. Continuing supervision of SMBG is necessary in children with IDDM.

Relationship of self-efficacy and binging to adherence to diabetes regimen among adolescents.

OBJECTIVE: To test the hypothesis that poorer adherence to diabetes care is related to four variables associated with self-concept in adolescents with diabetes: self-esteem, self-efficacy, depression, and binging behavior. In addition, we expected adolescent females to be less adherent to diabetes care. RESEARCH DESIGN AND METHODS: We recruited 193 consecutive patients (aged 13-18 yr) with insulin-dependent diabetes mellitus during their regular quarterly visit to a diabetes clinic in a large urban hospital. Participants completed the Rosenberg Self-Esteem Scale, the Children's Depression Inventory, an assessment of the frequency of binging in the past 3 mo, and parallel forms of an adherence scale and a self-efficacy scale that were developed for use in this study. RESULTS: Adolescents who reported lower adherence tended to report lower self-esteem (r = 0.45, P less than 0.001) and self-efficacy (r = 0.57, P less than 0.001), more depressive symptoms (r = -0.50, P less than 0.001), more binging (r = -0.36, P less than 0.001), and had higher HbA1c (r = -0.24, P less than 0.001) than those with higher adherence scores. Together, the psychological variables accounted for 50% of the variance in adherence. There was no sex difference in reported binging, but, as expected, adolescent females reported less adherence overall (F[7,184] = 2.5, P = 0.018). CONCLUSIONS: Treatment adherence in adolescents with insulin-dependent diabetes mellitus is associated with behavioral and psychological variables. These findings suggest that specific behavioral and cognitive interventions could be used to improve adherence in those individuals who lack confidence in their ability to perform diabetes-related tasks.

Effects of enhanced conventional therapy on metabolic control in children with insulin-dependent diabetes mellitus.

We implemented a three-phase, 32-wk program to improve both self-regulation of adherence behaviors and insulin delivery in children with diabetes. Twenty children, aged 8-12 yr (mean duration 3.6 yr), enrolled. Phase 1 (wk 1-12) used behavior modification to improve diet, exercise, urine testing, and insulin adjustment, targeting an increased percentage negative urines. Feedback training and parent checks were used to improve reliability; adherence was measured using Clinitest placebos. Phase 2 (wk 13-20) was a stabilization period. Phase 3 (wk 21-32) studied the effect of insulin dose adjustment, comparing once-versus twice-daily shots in 10 pairs of children matched for %GHb. GHb, fasting plasma glucose, and lipids were measured at baseline and at the end of each phase. Results revealed a significant and sustained increase in negative urine tests, but no change in % GHb or FBG. Reliability of and adherence to urine tests were 83% and 76%, respectively. During phase 3, no significant differences were noted between groups receiving once- or twice-daily insulin injections. Thus, behavior modification resulted in increased reliability and adherence to routines, associated with a reliable increase in negative urines. This did not, however, produce changes in other control measures. Furthermore, no differences between those receiving 1 or 2 daily shots were evident.