Gender Difference and Changes in the Prevalence of Obesity Over Time in Children Under 12 Years Old: A Meta-analysis.

Objective: Evaluating changes over time in the odds of obesity according to sex. Methods: PubMed, Embase, Cochrane Library, and China National Knowledge Database were searched for relevant studies. Full-text studies evaluating the influence of sex on obesity were analyzed. We used R 3.4.3 to assess the impact of results in the selected studies, calculated pooled prevalence and odds ratio (OR) with their respective 95% confidence intervals (CIs). P<0.10 and I2>50% indicated high heterogeneity, and the random-effects model was used, otherwise, the fixed-effects model was used. Results: The included studies reported the prevalence of obesity in children covering 1987-2017 intervals. The pooled prevalence of obesity in boy and girl groups were 0.13 (95% CI: 0.08, 0.20) and 0.10 (95% CI: 0.07, 0.13). In the analysis of the boy group, the pooled OR in earlier time (1987-2013) vs. recent time (2011-2017) was 0.98 (95% CI: 0.76, 1.26). The estimated OR for girls in earlier vs. recent time was 1.01 (95% CI: 0.80, 1.28). In the analysis of studies with follow-up period ≥ 10 years, the pooled OR for obesity in earlier vs. recent time period was 0.99 (95% CI: 0.76, 1.30). For those with follow-up period < 10 years, the pooled OR in earlier vs. recent time period was 0.94 (95% CI: 0.57, 1.54). Conclusions: Comprehensive measurements are required to control obesity among children albeit with nonsignificant gender difference and time trend for obesity rates in children.

Application of tandem mass spectrometry in the screening and diagnosis of mucopolysaccharidoses.

Mucopolysaccharidoses (MPSs) are caused by a deficiency in the enzymes needed to degrade glycosaminoglycans (GAGs) in the lysosome. The storage of GAGs leads to the involvement of several systems and even to the death of the patient. In recent years, an increasing number of therapies have increased the treatment options available to patients. Early treatment is beneficial in improving the prognosis, but children with MPSs are often delayed in their diagnosis. Therefore, there is an urgent need to develop a method for early screening and diagnosis of the disease. Tandem mass spectrometry (MS/MS) is an analytical method that can detect multiple substrates or enzymes simultaneously. GAGs are reliable markers of MPSs. MS/MS can be used to screen children at an early stage of the disease, to improve prognosis by treating them before symptoms appear, to evaluate the effectiveness of treatment, and for metabolomic analysis or to find suitable biomarkers. In the future, MS/MS could be used to further identify suitable biomarkers for MPSs for early diagnosis and to detect efficacy.

Gene variants and clinical characteristics of children with sitosterolemia.

OBJECTIVE: To enhance the detection, management and monitoring of Chinese children afflicted with sitosterolemia by examining the physical characteristics and genetic makeup of pediatric patients. METHODS: In this group, 26 children were diagnosed with sitosterolemia, 24 of whom underwent genetic analysis. Patient family medical history, physical symptoms, tests for liver function, lipid levels, standard blood tests, phytosterol levels, cardiac/carotid artery ultrasounds, fundus examinations, and treatment were collected. RESULTS: The majority (19, 73.1%) of the 26 patients exhibited xanthomas as the most prevalent manifestation. The second most common symptoms were joint pain (7, 26.9%) and stunted growth (4, 15.4%). Among the 24 (92.3%) patients whose genetics were analyzed, 16 (66.7%) harbored ABCG5 variants (type 2 sitosterolemia), and nearly one-third (8, 33.3%) harbored ABCG8 variants (type 1 sitosterolemia). Additionally, the most common pathogenic ABCG5 variant was c.1166G > A (p.Arg389His), which was found in 10 patients (66.7%). Further analysis did not indicate any significant differences in pathological traits among those carrying ABCG5 and ABCG8 variations (P > 0.05). Interestingly, there was a greater abundance of nonsense variations in ABCG5 than in ABCG8 (P = 0.09), and a greater frequency of splicing variations in ABCG8 than ABCG5 (P = 0.01). Following a change in diet or a combination of ezetimibe, the levels of cholesterol and low-density lipoprotein were markedly decreased compared to the levels reported before treatment. CONCLUSION: Sitosterolemia should be considered for individuals presenting with xanthomas and increased cholesterol levels. Phytosterol testing and genetic analysis are important for early detection. Managing one's diet and taking ezetimibe can well control blood lipids.

Using sno-lncRNAs as potential markers for Prader-Willi syndrome diagnosis.

The genetic disorder Prader-Willi syndrome (PWS) is mainly caused by the loss of multiple paternally expressed genes in chromosome 15q11-q13 (the PWS region). Early diagnosis of PWS is essential for timely treatment, leading to effectively easing some clinical symptoms. Molecular approaches for PWS diagnosis at the DNA level are available, but the diagnosis of PWS at the RNA level has been limited. Here, we show that a cluster of paternally transcribed snoRNA-ended long noncoding RNAs (sno-lncRNAs, sno-lncRNA1-5) derived from the SNORD116 locus in the PWS region can serve as diagnostic markers. In particular, quantification analysis has revealed that 6,000 copies of sno-lncRNA3 are present in 1 µL whole blood samples from non-PWS individuals. sno-lncRNA3 is absent in all examined whole blood samples of 8 PWS individuals compared to 42 non-PWS individuals and dried blood samples of 35 PWS individuals compared to 24 non-PWS individuals. Further developing a new CRISPR-MhdCas13c system for RNA detection with a sensitivity of 10 molecules per µL has ensured sno-lncRNA3 detection in non-PWS, but not PWS individuals. Together, we suggest that the absence of sno-lncRNA3 represents a potential marker for PWS diagnosis that can be detected by both RT-qPCR and CRISPR-MhdCas13c systems with only microlitre amount of blood samples. Such an RNA-based sensitive and convenient approach may facilitate the early detection of PWS.

Effects of early recombinant human growth hormone treatment in young Chinese children with Prader-Willi syndrome.

BACKGROUND: Prader-Willi syndrome (PWS) is a rare and multisystemic genetic disorder that is characterized by severe hypotonia, hyperphagia, short stature, and global developmental delay. Although early recombinant human growth hormone (rhGH) treatment has been proven to rescue some symptoms and bring additional benefits to PWS patients, studies in patients under 2 years old are scarce. Thus, this study aims to investigate the effectiveness and safety of rhGH treatment for young children. METHODS: A total of 96 genetically confirmed Chinese PWS infants or toddlers (47 males) followed between 2013 and 2022 were retrospectively analyzed. Sixty-five infants (early treatment group) started rhGH treatment during their first year, and 31 toddlers (later treatment group) started at the age of 1-2 years. Auxological parameters, carbohydrate metabolism parameters, thyroid function, liver function, insulin-like growth factor-1 (IGF-1), and radiographs were acquired before the initiation of the treatment and every 3-6 months thereafter. Height/length, weight, and weight for height were expressed as standard deviation scores (SDSs) according to WHO child growth standards. RESULTS: The mean SDS of length/height in the early treatment group was significantly higher than that in the later treatment group throughout the observation period (all P < 0.001). The change in the length SDS between the two groups at 1 year old and 4 years old was 1.50 (95% CI, 0.88-2.13) and 0.63 (95% CI, 0.16-1.10), respectively. Compared to the later treatment group, the weight SDS in the early treatment group increased by 0.94 (95% CI, 0.37-1.52) at 1 year old and 0.84 (95% CI, 0.28-1.39) at 2 years old. No statistical significance was found after 2.5 years of age. No significant differences were observed in IGF-1, incidence of liver dysfunction, hypothyroidism or spinal deformity between the two groups. CONCLUSIONS: rhGH treatment improved growth and body composition in infants and toddlers. Furthermore, an early start of rhGH treatment is expected to have more efficacy than the later treatment group without an increase in adverse effects.

Clinical spectrum transition and prediction model of nonalcoholic fatty liver disease in children with obesity.

Objective: This study aims to outline the clinical characteristics of pediatric NAFLD, as well as establish and validate a prediction model for the disease. Materials and methods: The retrospective study enrolled 3216 children with obesity from January 2003 to May 2021. They were divided into obese without NAFLD, nonalcoholic fatty liver (NAFL), and nonalcoholic steatohepatitis (NASH) groups. Clinical data were retrieved, and gender and chronologic characteristics were compared between groups. Data from the training set (3036) were assessed using univariate analyses and stepwise multivariate logistic regression, by which a nomogram was developed to estimate the probability of NAFLD. Another 180 cases received additional liver hydrogen proton magnetic resonance spectroscopy (1H-MRS) as a validation set. Results: The prevalence of NAFLD was higher in males than in females and has increased over the last 19 years. In total, 1915 cases were NAFLD, and the peak onset age was 10-12 years old. Hyperuricemia ranked first in childhood NAFLD comorbidities, followed by dyslipidemia, hypertension, metabolic syndrome (MetS), and dysglycemia. The AUROC of the eight-parameter nomogram, including waist-to-height ratio (WHtR), hip circumference (HC), triglyceride glucose-waist circumference (TyG-WC), alanine aminotransferase (ALT), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1(ApoA1), insulin sensitivity index [ISI (composite)], and gender, for predicting NAFLD was 0.913 (sensitivity 80.70%, specificity 90.10%). Calibration curves demonstrated a great calibration ability of the model. Conclusion and relevance: NAFLD is the most common complication in children with obesity. The nomogram based on anthropometric and laboratory indicators performed well in predicting NAFLD. This can be used as a quick screening tool to assess pediatric NAFLD in children with obesity.

Dysregulated adipose tissue expansion and impaired adipogenesis in Prader-Willi syndrome children before obesity-onset.

OBJECTIVE: Prader-Willi syndrome (PWS) is a rare genetic imprinting disorder resulting from the expression loss of genes on the paternally inherited chromosome 15q11-13. Early-onset life-thriving obesity and hyperphagia represent the clinical hallmarks of PWS. The noncoding RNA gene SNORD116 within the minimal PWS genetic lesion plays a critical role in the pathogenesis of the syndrome. Despite advancements in understanding the genetic basis for PWS, the pathophysiology of obesity development in PWS remains largely uncharacterized. Here, we aimed to investigate the signatures of adipose tissue development and expansion pathways and associated adipose biology in PWS children without obesity-onset at an early stage, mainly from the perspective of the adipogenesis process, and further elucidate the underlying molecular mechanisms. METHODS: We collected inguinal (subcutaneous) white adipose tissues (ingWATs) from phase 1 PWS and healthy children with normal weight aged from 6 M to 2 Y. Adipose morphology and histological characteristics were assessed. Primary adipose stromal vascular fractions (SVFs) were isolated, cultured in vitro, and used to determine the capacity and function of white and beige adipogenic differentiation. High-throughput RNA-sequencing (RNA-seq) was performed in adipose-derived mesenchymal stem cells (AdMSCs) to analyze transcriptome signatures in PWS subjects. Transient repression of SNORD116 was conducted to evaluate its functional relevance in adipogenesis. The changes in alternative pre-mRNA splicing were investigated in PWS and SNORD116 deficient cells. RESULTS: In phase 1 PWS children, impaired white adipose tissue (WAT) development and unusual fat expansion occurred long before obesity onset, which was characterized by the massive enlargement of adipocytes accompanied by increased apoptosis. White and beige adipogenesis programs were impaired and differentiated adipocyte functions were disturbed in PWS-derived SVFs, despite increased proliferation capacity, which were consistent with the results of RNA-seq analysis of PWS AdMSCs. We also experimentally validated disrupted beige adipogenesis in adipocytes with transient SNORD116 downregulation. The transcript and protein levels of PPARγ, the adipogenesis master regulator, were significantly lower in PWS than in control AdMSCs as well as in SNORD116 deficient AdMSCs/adipocytes than in scramble (Scr) cells, resulting in the inhibited adipogenic program. Additionally, through RNA-seq, we observed aberrant transcriptome-wide alterations in alternative RNA splicing patterns in PWS cells mediated by SNORD116 loss and specifically identified a changed PRDM16 gene splicing profile in vitro. CONCLUSIONS: Imbalance in the WAT expansion pathway and developmental disruption are primary defects in PWS displaying aberrant adipocyte hypertrophy and impaired adipogenesis process, in which SNORD116 deficiency plays a part. Our findings suggest that dysregulated adiposity specificity existing at an early phase is a potential pathological mechanism exacerbating hyperphagic obesity onset in PWS. This mechanistic evidence on adipose biology in young PWS patients expands knowledge regarding the pathogenesis of PWS obesity and may aid in developing a new therapeutic strategy targeting disturbed adipogenesis and driving AT plasticity to combat abnormal adiposity and associated metabolic disorders for PWS patients.

Case Report: Mucolipidosis II and III Alpha/Beta Caused by Pathogenic Variants in the GNPTAB Gene (Mucolipidosis).

Objective: This study aimed to improve the cognition of mucolipidosis (ML) II and III alpha/beta by analyzing the clinical manifestations of two patients. Methods: The clinical, biochemical, and molecular data of two clinical cases associated with ML II and III alpha/beta were analyzed and compared with other case reports of ML II and III alpha/beta. Results: The first patient was a 14-month-old girl who was hospitalized because of abnormal postnatal coarse facial features. The child had no abnormal birth history, but developed multiple abnormalities such as psychomotor retardation, abnormal facial features, bilateral limb muscle hypotonia, and genital abnormalities. The X-ray of the spine revealed multiple bone malformations. Brain magnetic resonance imaging (MRI) showed delayed myelination. Genetic testing showed the presence of two compound heterozygous pathogenic variants (c.1364C>T and c.1284+1G>T) in the GNPTAB gene. The second patient was an 18-month-old boy who was hospitalized for recurrent respiratory tract infections. The patient was a high-risk preterm infant with postnatal psychomotor retardation, language development retardation, intellectual disability, and coarse facial features. X-ray showed multiple bone malformations. Craniocerebral ultrasound showed bilateral ventricle widening. Genetic testing showed the presence of two compound heterozygous pathogenic variants (c.1284+1G>T and c.483delT) in the same gene. Conclusions: ML II and III alpha/beta are rare autosomal-recessive lysosomal storage diseases that are attributed to GNPTAB variants that cause N-acetylglucosamine-1-phosphotransferase deficiency, finally leading to multiple clinical signs and symptoms. A proper ML II and/or III alpha/beta diagnosis requires a combined analysis of a patient's clinical manifestations, imaging examination, enzymatic analysis, and genetic testing results. Ultimately, genetic counseling is essential for this disease.

Diabetes Education in Children and Adolescents with Type 1 Diabetes in China.

Background: The prevalence of Type 1 Diabetes is increasing in pediatrics and diabetes education plays one of the most important role in the management of diabetes, especially in children. However, the related evidence concerned diabetes education is rare in children and adolescents. Therefore, we aimed to investigate the status of diabetes education in hospital, which could help us know the reality of diabetes education. Methods: We choose a nurse who is mainly responsible for diabetes education and management in each hospital to fill out the questionnaire. Overall, 98 nurses were enrolled from tertiary children's specialized hospitals and pediatric wards of general tertiary hospitals from Jan 2018 to Dec 2019. Results: Of 98 nurses enrolled, 61 (63.3%) nurses from 98 hospitals responded, 39 (63.9%) of them received specialized training in diabetes. There were no differences in education characteristics among regions of China. There were 26(42.6%) hospitals have a full-time nurse for diabetes education or nurses with endocrinology training increased with the number of cases/year (P=0.02 and P=0.009). The use of game-based education, knowledge assessment at discharge did not vary among hospital volumes, and the presence of a psychiatrist (P=0.41, P=0.65, and P=0.85, respectively). Diet management education is the most common (23.0%) difficulty in children diabetes education. Conclusion: The level of diabetes education in children and adolescents varied among hospitals, but not among regions in China. There was a lack of resources provided for children and adolescents diabetes education in terms of training and specialized services.

Prevalence and phenotypic features of diabetes due to recessive, non-syndromic WFS1 mutations.

OBJECTIVE: Recessive WFS1 mutations are known to cause Wolfram syndrome, a very rare systemic disorder. However, they were also found in non-syndromic diabetes in Han Chinese misdiagnosed with type 1 diabetes (T1D), a molecular cause that appears to be considerably more common than the fully expressed syndrome. We aimed to better define the incidence and clinical features of non-syndromic diabetes due to recessive WFS1 mutation. DESIGN: We analyzed the genotype and phenotype of 320 consecutive incident Chinese pediatric diabetic patients diagnosed from 2016 to 2019 to search for non-syndromic diabetic cases due to recessive WFS1 mutation. METHODS: A cohort of 105 pancreatic autoantibody-negative patients were recruited for exome sequencing. All patients tested positive for pathogenic diallelic WFS1 mutations were examined for phenotypic features (fundoscopy, audiogram, and urine density). RESULTS: We found three cases of non-syndromic diabetes due to recessive WFS1 mutations (incidence = 0.94% (95% CI: 0.25-2.7%)). All three cases only had mild diabetes when diagnosed. All patients had well-conserved fasting C-peptide when diagnosed but one of them progressed to T1D-like insulin deficiency. In addition, we found a fourth case with previously undetected features of Wolfram syndrome. CONCLUSIONS: Non-syndromic diabetes due to WFS1 mutation may be common among Chinese pediatric patients with diabetes. It is important to differentiate it from other maturity-onset diabetes in the young subtypes with similar phenotype by molecular diagnosis because of different prognosis and, potentially, therapy.

Abdominal Adiposity and Total Body Fat as Predictors of Cardiometabolic Health in Children and Adolescents With Obesity.

Objective: We aimed to assess the role of adipose tissue distribution in cardiometabolic risk (in particular insulin sensitivity) in a population of children and adolescents with obesity. Methods: In this cross-sectional study, participants were 479 children and adolescents with obesity (322 boys and 157 girls) aged 3 to 18 years attending the Children's Hospital at Zhejiang University School of Medicine (Hangzhou, China). Clinical assessments included anthropometry, body composition (DXA scans), carotid artery ultrasounds, and OGTT. Insulin sensitivity was assessed using the Matsuda index. Participants were stratified into groups by sex and pubertal stage. Key predictors were DXA-derived android-to-gynoid-fat ratio (A/G) and total body fat percentage (TBF%). Results: Irrespective of sex and pubertal stage, there was a strong association between increasing A/G (i.e., greater abdominal adiposity) and lower insulin sensitivity. In multivariable models, every 0.1 increase in A/G was associated with a reduction in insulin sensitivity in prepubertal boys [-29% (95% CI -36%, -20%); p < 0.0001], pubertal boys [-13% (95% CI -21%, -6%); p = 0.001], and pubertal girls [-16% (95% CI -24%, -6%); p = 0.002]. In contrast, TBF% was not associated with insulin sensitivity when A/G was adjusted for, irrespective of pubertal stage or sex. In addition, every 0.1 increase in A/G was associated with increased likelihood of dyslipidemia in prepubertal boys [adjusted odds ratio (aOR) 1.62 (95% CI 1.05, 2.49)], impaired glucose tolerance in pubertal boys [aOR 1.64 (95% CI 1.07, 2.51)] and pubertal girls [aOR 1.81 (95% CI 1.10, 2.98)], and odds of NAFLD in both prepubertal [aOR 2.57 (95% CI 1.56, 4.21)] and pubertal [aOR 1.69 (95% CI 1.18, 2.40)] boys. In contrast, higher TBF% was only associated with higher fasting insulin and ALT in pubertal boys, being also predictive of NAFLD in this group [aOR 1.15 per percentage point (95% CI 1.06, 1.26)], but was not associated with the likelihood of other cardiometabolic outcomes assessed in any group. Conclusions: A/G is a much stronger independent predictor of cardiometabolic risk factors in children and adolescents with obesity in China, particularly glucose metabolism.

Gitelman syndrome combined with growth hormone deficiency: Three cases report.

RATIONALE: Gitelman syndrome (GS) is a rare autosomal recessive hereditary salt-losing tubulopathy caused by loss-of-function mutations in the SLC12A3 gene. It is usually characterized by hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. There are only a few reports on GS combined with growth hormone deficiency (GHD). PATIENT CONCERNS: Three patients presented with weakness, spasm, and growth retardation, respectively. DIAGNOSES: GS was diagnosed based on the clinical symptoms, laboratory test results, and genetic analysis. GH stimulation tests were performed when the magnesium level returned to normal under magnesium oxide (MgO) therapy. INTERVENTIONS: Initially, all patients received oral replacement of MgO and potassium chloride, and 2 of them received simultaneous spironolactone therapy. Recombinant human growth hormone (rhGH) therapy was initiated after they were diagnosed with GHD. OUTCOMES: All 3 patients exhibited satisfactory growth velocity and normal serum magnesium level, although the potassium level was still slightly lower than normal. LESSONS: We suggest that all GS patients should undergo genetic evaluation, especially regarding SLC12A3 gene mutation. GHD should be considered if these patients have short stature. rhGH therapy is useful for stimulating the patients' growth, and it may increase the serum magnesium level.

[A proposal for the cutoff point of waist-to-height for the diagnosis of metabolic syndrome in children and adolescents in six areas of China].

OBJECTIVE: This study aimed to determine the optimal cutoff point of Waist-to-height (WHtR) for the diagnosis of metabolic syndrome (MS) in children and adolescents in six areas of China. METHODS: Ninety thousand two hundred and eighty four children aged 6 to 15 years old from 6 areas, including Beijing, Tianjin, Zhejiang, Shanghai, Chongqing and Nanning in China, were surveyed in a random cluster sample. Receiver operating characteristic (ROC) curve analysis was employed to determine the optimal cutoff values of WHtR for detecting the children and adolescents with two or more risk factors of MS. RESULTS: The optimal WHtR cutoff values derived from the ROC analysis was 85(th) and 80(th) percentiles in males and females, with 6-15 years of age, respectively. The sensitivity and specificity under these cutoff values were 35.78% and 85.41% in males and 49.21% and 79.87% in females, for 6-9 years of age, while the sensitivity and specificity were 49.60% and 85.90% in males and 47.01% and 80.07% in females for 10-15 years of age. The areas under the ROC curves (AUCs) for WHtR 85(th) percentile were 0.61 and 0.64 in males and females for 6-9 years of age, and 0.68 and 0.63 in males and females for 10-15 years of age. The AUCs for WHtR 85(th) percentile in both genders were significantly larger than that for WHtR 90(th) percentile for 10-15 years of age. CONCLUSION: Our findings indicated that the 85(th) percentile of WHtR (0.48 in both genders for 6-9 years of age, 0.48 in males and 0.46 in females for 10-15 years of age) might be an appropriate cutoff to predict the children and adolescents with two or more risk factors.

WT1 mutation as a cause of 46 XY DSD and Wilm's tumour: a case report and literature review.

AIM: The Wilms' Tumour gene is thought to have tumour suppressor activity and to play an important role in nephrogenesis, genitourinary development, haematopoiesis and sex determination. WT1 mutations will impair gonadal and urinary tract development and have been demonstrated to cause syndromes of WAGR, Denys-Drash and Fraiser. METHODS: To elucidate the role of constitutional mutations of WT1, in the expression of the different clinical feature, we describe a 14-year-9-month nonmosaic XY sex-reversed woman with pure gonadal dysgenesis (46, XY karyotype, completely female external genitalia, normal Mullerian ducts, absence of Wolffian ducts, streak gonads) who had right kidney removed at 7 months of age because of Wilms' tumour and was diagnosed as secondary thrombocytopenia (Plt 60-80 × 10(9) /L) since she was 4 years old. We sequenced the genomic DNA of all the 10 exons of the WT1 in which mutations may occur in proposita. RESULTS: A new de novo insertion mutation in the first exon was found. A 'GCCGCCTCACTCC' is inserted between codon 138 and 139, resulting in the creation of a stop codon and a truncated protein. CONCLUSION: The present data provide further evidence to support the role of WT1 in diverse cellular functions.

[A 10-year review of childhood type 1 diabetes mellitus and the clinical value of interleukin-10 in diabetic ketoacidosis].

OBJECTIVE: To review the incident status of childhood type 1 diabetes mellitus hospitalized in the Children's Hospital of Zhejiang University School of Medicine from 1999 to 2009 and to explore the clinical value of IL-10 in diabetic ketoacidosis. METHODS: The clinical data of 263 children with type 1 diabetes mellitus hospitalized in the Children's Hospital of Zhejiang University School of Medicine from January 1999 to February 2009 were retrospectively reviewed. Serum lipid levels were measured in 48 children with type 1 diabetes mellitus and in 24 healthy children. The diabetic children were classified into two subgroups, with or without ketoacidosis. Serum lipid and cytokines levels were compared. RESULTS: Childhood type 1 diabetes mellitus was common in females (56.3%). The peak incident age of the disease was between 6 and 11.9 years. Diabetic ketoacidosis was as the presenting symptom for the first visit in 86 cases (32.7%). The levels of serum lipid, blood glucose and HbA1c in diabetic children with ketoacidosis were significantly higher than those without ketoacidosis (P<0.05). Logistic analysis demonstrated that the increased levels of blood glucose, serum lipid and HbA1c were risk factors for diabetic ketoacidosis. The level of serum IL-10 in diabetic children with ketoacidosis was significantly higher than that in patients without ketoacidosis (P<0.01), while there were no differences in serum levels IL-2, IL4, IL-6, TNF-α and IFN-γ between them. Serum levels IL-2, IL-4, IL-6, IL-10, TNF-α and IFN-γ in diabetic children were significantly higher than those in healthy children (P<0.01). CONCLUSIONS: Ketoacidosis is a common acute complication of type 1 diabetes mellitus. The disorders of glucose and lipid metabolism are the risk factors for ketoacidosis in diabetic children. IL-10 may be a sensitive index of diabetic ketoacidosis in children with type 1 diabetes mellitus.