Serum 1,5-anhydroglucitol (Glycomark) levels in children with and without type 1 diabetes mellitus

Abstract:  Postprandial hyperglycemia associated with diabetes is a risk factor for cardiovascular disease. Currently, glycated hemoglobin A_1c (HgbA_1c) and glycated protein fructosamine are not sensitive markers for acute and short-term hyperglycemia. 1,5-Anhydroglucitol (1,5-AG) (Glycomark™; Tomen America, New York, NY, USA) is reported in adults with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) as a marker for postmeal hyperglycemia. However, the reference ranges for 1,5-AG in normal children and children with T1DM are not known. We studied 1,5-AG levels in 10 control children (6 males and 4 females) and 10 children with T1DM (7 males and 3 females). The levels of 1,5-AG in the normal controls were higher than those in children with T1DM (24.60 ± 3.99 μg/mL vs. 4.75 ± 2.95 μg/mL; p < 0.0001). There were no gender differences noted. The 1,5-AG levels were negatively correlated with HgbA_1c (r =−0.9366; p < 0.0001) and the peak postmeal plasma glucose concentrations (Pearson r =−7230; p = 0.0003). Our findings suggest that despite good glycemic control, postprandial glucose concentrations are elevated and that 1,5-AG showed a difference between controls and children with T1DM. The data are comparable with previous studies in normal adults and in those with T1DM and T2DM. They support the use of 1,5-AG concentrations, together with HgbA_1c, to evaluate therapy, especially to target postprandial hyperglycemia.     

Hyperglycemia in celiac disease: not always pretype 1 diabetes?

Abstract:  Celiac disease (CD) is a T-cell-mediated enteropathy, triggered in genetically susceptible individuals by the ingestion of wheat gluten or related rye and barley proteins, whose clinical picture disease is considerably heterologous. Patients with CD are at high risk of autoimmune disorders; similarly, CD is frequent in patients with type 1 diabetes mellitus (T1DM), a disorder characterized by the immune-mediated β-cell destruction, with the cooperation of environmental factors in genetically susceptible individuals. The immunological markers of β-cell destruction are the autoantibodies to insulin, glutamic acid decarboxylase, and the protein tyrosine phosphatase. In absence of these markers, incidental hyperglycemia in children and adolescents appears unlikely to be associated with the progression to T1DM. We report a girl with CD and incidental hyperglycemia, without immunological markers of T1DM, with a family history for hyperglycemia, and diagnosed as maturity-onset diabetes of the young. We present this case as evidence that the possibility of monogenic forms of diabetes must be suspected in children with incidental hyperglycemia, a family history for mild hyperglycemia or diabetes, and absence of markers of β-cell destruction, even if the patients are affected by an autoimmune disease.     

Beta-cell autoantibodies in children with type 2 diabetes mellitus: subgroup or misclassification?

BACKGROUND: In adults, a fraction of diabetic individuals with beta-cell autoantibodies has initially non-insulin requiring diabetes clinically appearing as type 2 diabetes mellitus (T2DM), named latent autoimmune diabetes in adulthood (LADA). The occurrence of beta-cell autoantibodies in European children and adolescents with T2DM has not been reported so far. METHODS: The frequency of beta-cell autoantibodies (anti-GAD, anti-IA-2, and anti-ICA) was determined in 7050 diabetic children and adolescents. The type of diabetes was classified by paediatric diabetic specialists based on the clinical presentation. Children with non-insulin dependent T2DM over a one year period were studied separately. RESULTS: A total of 6922 children were clinically classified as having type 1 diabetes (T1DM) and 128 children as having T2DM. Thirty six per cent of the children with T2DM had at least one detectable beta-cell autoantibody. These children did not differ significantly from the children with T2DM and without autoantibodies in respect of age, gender, weight status, lipids, blood pressure, C-peptide, glucose, and HbA1c at manifestation, as well as frequency of anti-thyroidal antibodies and insulin treatment during follow up. In the subgroup of the 38 children with T2DM without insulin requirement over a one year period, autoantibodies occurred in 32%. These 12 children were predominantly obese (67%), female (67%), and in the pubertal age range. CONCLUSION: beta-cell autoantibodies were detectable in a subgroup of initially non-insulin dependent diabetic children and adolescents with the clinical appearance of T2DM. Following the terminology "latent autoimmune diabetes in adulthood (LADA)", this subgroup might be classified as "LADY" (latent autoimmune diabetes in youth).     

儿童 1型糖尿病 30年临床特征及随访观察

目的 分析儿童1型糖尿病（T1DM）的临床特征,探讨该病对儿童生长发育的影响程度及后期并发症发生的情况。方法 对发病年龄在13个月至14．7岁,经实验室检查确诊为T1DM的210例患儿的临床特征进行了回顾性分性,并对99例患儿进行了1～24年的并发症、生长发育、死因随访。结果 因单纯糖尿病人院者47例（22．4％）;伴酮血症入院者69例（32．9％）;伴酮症酸中毒入院者94例（44．7％）,其中农村患儿78例。起病时有诱因者43例,其中自停胰岛素15例。酮症酸中毒患儿住院时间明显比单纯糖尿病患儿长（P〈0．05）。随访的99例中出现各种并发症50例,其中以微血管病变发生率最高。病程长易并发各种并发症（P〈0．05）,病后的监测方法与并发症的发生也明显相关。患儿组身高明显低于对照组（P〈0．05）。结论 酮症酸中毒是儿童糖尿病的基本特征;病程长易并发各种并发症;加强对儿童糖尿病患者的血糖检测和病后教育,将对儿童糖尿病的治疗起重要作用。     

Thyroid autoimmunity in children with coexisting type 1 diabetes mellitus and celiac disease: a multicenter study

BACKGROUND: Children with type 1 diabetes mellitus (DM1) are more prone to developing thyroid autoimmunity (TAI); TAI also occurs more frequently in patients with celiac disease (CD). AIM: To determine whether TAI occurs more frequently in children with coexisting DM1 and CD compared to children with DM1 only, and whether the clinical course of DM1 is influenced by concomitant TAI. PATIENTS AND METHODS: We performed a multicenter retrospective case-control study comparing data from 84 diabetic children with CD (group 1) to 167 diabetic children without CD (group 2), matched by age at DM1 onset, duration of DM1 and center. Markers of TAI, thyroid function and HbA1c were recorded. The TAI follow-up lasted 4.9 +/- 2.8 years. RESULTS: TAI was diagnosed in 13% of children in group 1 and 19% of children in group 2 (ns). Diabetes control was not influenced by TAI in either group. CONCLUSIONS: Occurrence of TAI in diabetic children is not related to coexisting CD. TAI does not lead to worsening of metabolic control in children with DM1.     

Type 2 diabetes in a 5‐year‐old and single center experience of type 2 diabetes in youth under 10

The worrisome rise in pediatric type 2 diabetes (T2DM) is most prevalent among minority ethnic/racial populations. Typically, T2DM occurs during puberty in high risk obese adolescents with evidence of insulin resistance. Screening for T2DM in obese youth can be a daunting task for pediatricians and differentiating between pediatric T1DM and T2DM in obese youth can be challenging for pediatric endocrinologists. There is very limited data regarding the prevalence of T2DM among youth < 10 years of age. Here we present the case of a 5‐year‐old Hispanic male diagnosed with T2DM after referral by his pediatrician for abnormal weight gain, acanthosis nigricans and an elevated HbgA1c. He subsequently became symptomatic for diabetes with confirmed hyperglycemia and HbgA1c of 9.7% (83 mmol/mol) at the time of formal diagnosis. Type 1 diabetes autoantibodies (GAD65, Islet, and ZincT8) and monogenic diabetes genetic tests were negative. Due to elevated liver enzymes and baseline HbgA1c, he received basal insulin as his initial therapy. In this paper, we will discuss this case and present an IRB approved retrospective review of the characteristics of the 20 T2DM patients <10 years of age identified to date in our pediatric diabetes center. This review highlights that while uncommon, the diagnosis of T2DM merits consideration even in prepubertal children. This is especially true when working with a high risk population, such as our Hispanic South Texas youth.     

25-羟维生素D与儿童1型糖尿病及酮症酸中毒的相关性研究

目的探讨血清25-羟维生素D[25-(OH)D]水平与儿童1型糖尿病(T1DM)及酮症酸中毒(DKA)的相关性。方法选取2006年1月—2009年12月期间152例住院患儿,其中52例为首次发病的T1DM患儿,包括酮症酸中毒(DKA组)21例,以及非酮症酸中毒(非DKA组)31例,其余100例为非T1DM组。检测并比较三组患儿的血清25-(OH)D水平,分析血清25-(OH)D水平与儿童T1DM及DKA的相关性。结果 DKA组患儿的血清25-(OH)D平均为(53.6±27.8)nmol/L,显著低于非DKA组的(69.7±27.9)nmol/L和非T1DM组的(81.8±28.3)nmol/L(P<0.05);非DKA组患儿的血清25-(OH)D水平显著低于非T1DM组(P<0.05)。结论 T1DM患儿的血清25-(OH)D水平低,尤以DKA患儿最为明显,维生素D在儿童T1DM发病中的潜在保护效应值得关注。     

Pediatric stroke associated with new onset type 1 diabetes mellitus: case reports and review of the literature

Neurological deterioration in children with diabetic ketoacidosis (DKA) is commonly caused by cerebral edema. However, stroke should also be suspected when focal neurological deficits are apparent, because children with hyperglycemia and DKA are prone to thrombosis. We report three cases of pediatric stroke associated with new onset type 1 diabetes mellitus (T1DM). The first case presented with sinovenous thrombosis, and the other two cases presented in DKA and had a late diagnosis of ischemic stroke following neurological deterioration. Our recent experiences and review of the literature emphasize the importance of early diagnosis, investigation, and treatment for patients that present with new onset T1DM and stroke.     

Dendritic cell mediated therapy for immunoregulation of type 1 diabetes mellitus

Diabetes is a state of imbalance in insulin secretion and tissue sensitivity resulting in hyperglycemia and a host of other metabolic changes. Increased patient morbidity and mortality are caused in part by diabetic complications that include cardio-vascular complications, retinopathy, neuropathy, and nephropathy (1). The early onset of disease in type 1 diabetes mellitus increases the effects of these complications since the risk of development increases with disease duration. Clinical agents are currently available for type 2 diabetic patients to increase both secretion and sensitivity to insulin. These compounds are ineffective in type 1 diabetic patients due to the destruction of the insulin producing beta cells in the pancreatic islets of Langerhans, making type 1 and non-responsive type 2 diabetic patients dependent on insulin replacement therapy. Intensive insulin treatment delays onset of these complications, but does not eliminate them (1). Insulin replacement therapy is not a cure for type 1 diabetes; to establish a cure, the destruction of the beta cells themselves must be directly addressed. Here we will focus on immunoregulatory techniques to prevent beta cell loss due to the autoimmunity found in type 1 diabetes mellitus.     

Newly diagnosed T1 diabetes presenting with hypoglycemia due to simultaneous co‐existence of Addison disease

Type 1 diabetes mellitus (TIDM) classically presents with symptomatic hyperglycemia and many patients develop diabetic ketoacidosis prior to their diagnosis. However, non‐classical presentation or co‐presentation with associated diseases may delay diagnosis or lead to challenges in acute, clinical management. An 18‐yr‐old girl presented to hospital with severe, symptomatic hypoglycemia. Clinical history and serum electrolyte concentrations suggested a diagnosis of adrenal insufficiency. She remained hypoglycemic until glucocorticoid replacement was commenced, at which point she developed persistent hyperglycemia requiring insulin therapy. Subsequent follow up confirmed the diagnosis of Addison's disease (AD), the treatment of which unmasked co‐existing type 1 diabetes. Autoimmune diseases often cluster together in affected patients and first‐degree relatives. Approximately 1 in 200 patients with T1DM develop AD. However, months or more commonly years usually elapse between the presentation of different autoimmune conditions. The co‐diagnosis T1DM and AD in the acute setting is rare. Moreover, the first presentation of T1DM with severe hypoglycemia is even more exceptional. This case highlights the need for vigilance during the acute, emergency management of patients with autoimmune conditions and, in particular, to consider the possibility of concurrent antibody‐mediated diseases which may need to be addressed during resuscitation.     

1型糖尿病患儿血清干扰素γ诱导蛋白10水平的变化及其意义

目的观察趋化因子干扰素γ诱导蛋白10（IP-10）在儿童1型糖尿病（T1DM）发病中的变化。方法用ELISA法检测50例T1DM患儿和30例健康儿童的血清IP-10水平,根据自身抗体存在与否、自身抗体阳性种类数及不同病程对IP-10进行分组比较。结果T1DM患儿血清IP-10水平[（367±131）ng／L]显著高于对照组[（133±43）ng／L],差异有统计学意义（t=9．49,P〈0．01）。其中自身抗体阳性组IP-10[（385±147）ng／L]和自身抗体阴性组IP-10[（311±101）ng／L]均高于对照组（t=8．99,P〈0．01;t=8．67,P〈0．01）,但该两组间差异无统计学意义。1种、2种和3种自身抗体阳性患儿血清IP-10水平差异无统计学意义（F=1．46,P〉0．05）。初发组和病程〉12年组的T1DM患儿血清IP-10均高于对照组（t=10．34,P〈0．01;t=4．36,P〈0．01）,而病程〉12年组血清IP-10水平低于初发组（t=4．30,P〈0．01）。结论T1DM患儿血清IP-10水平高于对照组,血清IP-10水平不受自身抗体阳性存在与否、自身抗体阳性种类多少的影响,随病程延长,血清IP-10水平逐渐下降。     

Neurocognitive functioning in preschool‐age children with type 1 diabetes mellitus

Patiño‐Fernández AM, Delamater AM, Applegate EB, Brady E, Eidson M, Nemery R, Gonzalez‐Mendoza L, Richton S. Neurocognitive functioning in preschool‐age children with type 1 diabetes mellitus. 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.     

Diagnosis of MODY in the offspring of parents with insulin-dependent and non-insulin-dependent diabetes mellitus

Maturity Onset Diabetes of the Young (MODY) is an autosomal dominant monogenic form of type 2 diabetes mellitus (DM) representing 5% of youth-onset DM in the Caucasian population. In young adults the disease can be present as either non-insulin dependent or insulin-dependent DM. The diagnosis of this genetic disorder in children and adolescents is rare because of the mild glucose metabolism disorder at this time. We performed a metabolic, autoimmune and genetic study in 40 offspring of young parents affected by insulin-dependent DM (Group A) and in 35 offspring of young parents affected by early-onset non-insulin-dependent DM (Group B). Two children of Group A (5%) were found to be affected by fasting hyperglycemia and carry a GCK gene mutation that in one case was present also in the diabetic father. Eighteen offspring of Group B (51%) were positive for GCK or HNF-1alpha gene mutations present in the affected parents. All but two of these young patients had impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Eleven of them were younger than 16 years. We conclude that screening for DM in youth should be extended to MODY in young families with both non-insulin-dependent and insulin-dependent DM. The sensitivity of the metabolic tests will precede the genetic diagnosis.     

Low serum TNF-alpha levels in subjects at risk for type 1 diabetes

OBJECTIVE: The aim of our study was to determine whether serum TNF-alpha levels in individuals at risk of developing type 1 diabetes, such as first-degree relatives of diabetic patients and children with incidental hyperglycemia, underwent alterations, and also to establish whether these levels might be used to identify individuals prior to insulin dependence. RESEARCH DESIGN AND METHOD: We studied 71 healthy first-degree relatives (FDR) of type 1 diabetic patients and 11 children with incidental hyperglycemia. We looked for immunogenetic (HLA class II serologic alleles and HLA-DQ alpha/beta genomic polymorphisms), immunologic (islet-cell and insulin autoantibodies) and metabolic (FPIR to IVGTT) markers of type 1 diabetic risk. Serum concentrations of TNF-alpha were quantified using IRMA. RESULTS: We found significantly lower serum TNF-alpha levels in FDR of type 1 diabetic patients (median: 54.3 pg/ml) (p=0.01) and in children with incidental hyperglycemia (median: 10.83 pg/ml) (p<0.0001) compared to controls (median: 76.56 pg/ml). No significant difference was observed between subjects with or without immunogenetic, immunologic and metabolic markers of type 1 diabetic risk. A negative correlation was found between serum TNF-alpha and HbA1c levels (r=-0.27, p=0.023). Two children with incidental hyperglycemia, whose TNF-alpha levels were very low, developed type 1 diabetes 6 and 8 months after this study. CONCLUSION: Our results are compatible with an impaired immune system in the prediabetic period and suggest that serum TNF-alpha concentrations may be considered as an immunological marker useful to identify subjects at risk of developing type 1 diabetes.     

Diabetic retinopathy in childhood: long-term follow-up by fluorescein angiography beginning in the first months of disease

BACKGROUND: Little is known about minimal retinal lesions occurring in the first months of disease in children with type 1 diabetes mellitus (DM). OBJECTIVE: To detect any early retinal change and to evaluate its progression in children diagnosed with type 1 DM. PATIENTS: From 1979 to 1997 we examined by fluorescein angiography at diagnosis or within 15 months from the onset of DM 130 young patients with type 1 DM (mean age at diagnosis 10.08 +/- 2.62 yr). In 112 patients follow-up by fluorescein angiography was performed every 1.26 years with a mean of 5.41 fluorescein angiographies/patient. METHODS: The stage of retinopathy was graded to detect minimal lesions. We also considered sex, pubertal stage, HLA, family history of DM, disease duration and HbA1c levels. RESULTS: At first examination, 14 out of 127 (11%) readable angiographies showed minimal retinal changes. There was no statistically significant difference between the patients with or without lesions for all parameters considered. The 112 patients examined during follow-up were divided as follows: Group A: no retinopathy at first examination; Group A1: no retinopathy during follow-up; Group A2: retinal changes during follow-up; Group B: retinal changes at the first examination. Mean HbA1c value evaluated during the whole follow-up was lower in group A1 than in group A2. HbA1c levels at onset of the disease were significantly different in the three groups: in group A1 it was lower than in group A2 and in group B. CONCLUSIONS: The presence of early lesions in the first year of disease in 11% of patients is probably due to the method of examination, which may detect even minimal retinal changes. This may be correlated to the acute metabolic failure present at the onset of disease. The prolonged follow-up seems to demonstrate that the early changes are not necessarily a negative prognostic factor in the evolution of diabetic retinopathy. We confirm that duration of DM and metabolic control are the main factors influencing the course of retinopathy in these young patients. Early fluorescein angiography is not particularly useful in the management of children with DM.     

Hyperglykämie im Kindes- und Jugendalter

The ready availability of blood glucose measurement devices in everyday medical life often leads to the incidental discovery of hyperglycemic events, the long-term significance of which often remains unevaluated in the absence of additional tests. Although up to 4%–5% of children admitted to pediatric accident and emergency units present with transient hyperglycemia, only a minority of these subsequently develops diabetes or is already in a prediabetic stage. Both type 1 and type 2 diabetes, as well as rarer monogenetic forms of diabetes, can present as incidental hyperglycemia. Despite low incidence rates, a differential diagnostic work-up of incidental hyperglycemia is useful, since it may prevent severe diabetic events such as diabetic ketoacidosis; moreover, in the case of specific types of monogenetic diabetes, patients can use oral antidiabetic drugs and the further disease course can be predicted.     

Maternal type 1 and gestational diabetes: postnatal differences in insulin secretion in offspring at preschool age

Background: It is well known that children born to mothers with diabetes in pregnancy are more likely to develop metabolic abnormalities in later life. Most prior studies have not differentiated between offspring of mothers with type 1 diabetes (T1DM) and gestational diabetes (GDM) or lack a control group of non‐exposed offspring. Subjects: Offspring of T1DM (n = 16), GDM (n = 22) and mothers without diabetes (n = 25) born at Oulu University Hospital. Aim: To assess insulin secretion and insulin resistance in the offspring of T1DM and GDM at preschool age in comparison with offspring of non‐diabetic mothers. Methods: Anthropometric measurements and intravenous glucose tolerance testing were performed. First‐phase insulin response (FPIR) and homoeostasis model assessment (HOMA) values were calculated. Pregnancy and birth data were analysed in relation to later metabolic parameters in all three groups using one‐way analysis of variance (anova ) and analysis of covariance (ancova ). Results: At a mean age of 4.9 yr, offspring of T1DM had increased fasting serum insulin concentrations (p = 0.044), FPIR (p = 0.034) and HOMA‐B values (p = 0.008) compared with offspring of GDM or with offspring of healthy controls (statistically non‐significant). The GDM gained least weight during pregnancy, and when adjusted for maternal weight gain during pregnancy, there were no statistically significant differences between study groups. Conclusions: Prenatal exposures to maternal type 1 and gestational diabetes may have different effects on postnatal glucose metabolism in the offspring assessed at a mean age close to 5 yr. Maternal weight gain in pregnancy may affect the postnatal glucose metabolism in the offspring.     

Prevalence of components of the metabolic syndrome in schoolchildren with newly diagnosed type 2 diabetes mellitus

Objective: To examine the prevalence of components of the metabolic syndrome (MS) other than hyperglycemia at diagnosis in schoolchildren with type 2 diabetes mellitus (T2DM). Design: The study involved 112 Japanese schoolchildren, 45 males and 67 females aged 12.9 ± 1.5 yr, who were diagnosed as having T2DM. The body weight, blood pressure and fasting serum triglyceride (TG), and high‐density lipoprotein cholesterol cholesterol (HDL‐C) levels were also measured at diagnosis. The criteria adopted for the diagnosis of MS were as follows; i.e., TG ≥150 mg/dL, HDL‐C <40 mg/dL, systolic blood pressure ≥130 mmHg, and/or diastolic blood pressure ≥85 mmHg. Obesity was defined as percent overweight ≥20.0%. Results: As much as 83.0% of the patients had obesity. The prevalence of increased TG was 33.0% and that of decreased HDL‐C was 21.4% among the patients. Elevated blood pressure was identified in 11.6% of the patients. Of the total, 15.2% of the patients had no other components of MS besides hyperglycemia; 49.1% had only one other component, which was obesity in the majority; 17.0% had two other components of MS besides hyperglycemia, which were obesity and elevated TG in the majority; 18.8% of the patients had three or more components of MS besides hyperglycemia. Conclusions: We found a high prevalence of other components of MS besides hyperglycemia in the patients even at the time of diagnosis. Early detection of other components of MS would appear to be of importance for preventing the development of cardiovascular disease in children with T2DM.     

Sustained IL-1α, IL-4, and IL-6 elevations following correction of hyperglycemia in children with type 1 diabetes mellitus

Objective:  An imbalance of pro-/anti-inflammatory cytokines may accelerate diabetic vascular complications and interfere with proper wound healing. Currently, limited available literature suggests that plasma concentrations of certain pro- and anti-inflammatory cytokines may be altered during hyperglycemia/diabetes mellitus. It is still unclear, however, whether these concepts also apply to children with diabetes, and whether alterations in circulating cytokine levels are a permanent feature of diabetes or an acute effect of fluctuating glucose concentrations.
Methods:  Twenty-two children with type 1 diabetes mellitus (T1DM) were studied. In 13 children, postprandial morning plasma glucose was >11.1 mmol/L at least once (hyperglycemic group, or HyG group); in 9 subjects, plasma glucose never exceeded 10.6 mmol/L (non-hyperglycemic group, or non-HyG group). After admission, intensive euglycemia (5.0–6.1 mmol/L) was achieved in all participants via intravenous insulin and dextrose for at least 90 min. Blood samples were drawn every 30 min to determine plasma levels of 14 cytokines and chemokines.
Results:  Interleukin IL-1α, IL-4, and IL-6 were elevated in HyG group compared with non-HyG not only when plasma glucose was elevated but also during the first 2 h following return to euglycemia. The levels of the other 11 cytokines were not significantly different.
Conclusions:  Specific cytokines (IL-1α, IL-4, and IL-6) are acutely elevated during hyperglycemia in children with T1DM, and these elevations persist for hours after hyperglycemia has been corrected. Therefore, aside from glycemic control, additional therapeutic measures against elevated proinflammatory signals may be necessary for preventing vascular complications in children with hyperglycemic diabetes.     

Electrogastrography in children and adolescents with type 1 diabetes: weak correlation with metabolic control parameters

AIM: To evaluate gastric myoelectrical activity with respect to duration and metabolic control of type 1 diabetes mellitus (T1DM). METHODS: 172 children and adolescents with T1DM (mean 14.4+/-3.7 y), divided into subgroups depending on diabetes duration (< 5 and > 5 y), and 35 healthy controls (mean 13.93+/-3.59 y) were examined. All subjects underwent electrogastrography (EGG) performed after overnight fasting. In subjects with T1DM, haemoglobin A1c (HbA1c) and blood glucose levels during EGG records were measured. RESULTS: 15.69% of T1DM patients and 91.42% of the controls fulfilled normal EGG criteria (p < 0.001). T1DM subjects had a lower percentage of fasting normogastria (34.56+/-27.35% vs 69.84+/-18.16%, p = 0.0001) and higher bradygastria (51.97+/-30.24% vs 19.11+/-15.01%, p = 0.0001) compared to controls. In diabetic patients, an increase in postprandial normogastria (60.37+/-23.96% vs 76.68+/-12.38, p < 0.05) and a decrease in bradygastria percentage (25.67+/-21.01% vs 9.58+/-7.13%, p < 0.05) was observed. In children with disease < 5 y, diabetes duration correlated with power ratio (r = - 0.27, p = 0.01), postprandial normogastria (r = - 0.24, p = 0.03) and tachygastria (r = 0.25, p = 0.02). Weak correlations between EGG parameters and glucose (preprandial dominant frequency r = - 0.19, p < 0.05; postprandial normogastria r = 0.23, p < 0.01) and HbA1c levels (preprandial bradygastria r = 0.19, postprandial dominant power r = 0.23; p < 0.05) were observed. CONCLUSION: Gastric myoelectrical rhythm derangement is present in a large proportion of young diabetic patients. Bradygastria is the most prominent EGG abnormality. Weak correlation was found between EGG parameters and diabetes metabolic control.