Follow-up of parenchymal changes in the thyroid gland with diffuse autoimmune thyroiditis in children prior to the development of papillary thyroid carcinoma.

PURPOSE: To present the outcomes of ultrasound (US) follow-ups in children with autoimmune thyroid disease who did not have a thyroid nodule on admission but developed papillary thyroid carcinoma (PTC) and to characterize the parenchymal changes in the thyroid gland prior to the development of PTC. METHODS: A retrospective thyroid US scan review of 327 patients diagnosed with AIT was performed. Forty patients (40/327, 12.2%) presented nodular AIT variant with a normoechogenic background. Eleven patients (11/327, 3.4%, 11/40, 27.5%) presenting this variant were diagnosed with PTC (nine females-mean age 15.3 years; two males aged 11 and 13 years). In five of 11 patients, the suspicious nodule that was later confirmed to be PTC was detected on the initial US at presentation. For the remaining six females (6/11) who developed PTC during the follow-up, we retrospectively analysed their US thyroid scans and these patients were selected for analysis in this study. RESULTS: On admission, the US evaluation revealed an enlarged normoechogenic thyroid gland in three patients and a hypoechogenic thyroid gland with fibrosis as indicated by irregular, chaotic hyperechogenic layers in three patients. No thyroid nodules were identified. Ultrasound monitoring revealed increasing echogenicity of the thyroid parenchyma during the follow-up. PTC developed in a mean time of 4.6 years (1 9/12-7 4/12 years) since referral to the outpatient thyroid clinic and 2.9 years (6/12-6 9/12) since the last nodule-free US thyroid scan. CONCLUSIONS: Sonographic follow-up assessments warrant further exploration as a strategy to determine PTC susceptibility in the paediatric population.

Associations between bone, fat tissue and metabolic control in children and adolescents with type 1 diabetes mellitus.

AIMS: To investigate the relationship between bone-derived osteocalcin (OC), osteoprotegerin (OPG), Receptor Activator of Nuclear Factor NF-ĸB ligand (RANKL), and fat tissue-derived leptin and adiponectin with a clinical outcome of type 1 diabetes mellitus (T1DM) in children and adolescents. METHODS: 78 patients (43 girls and 35 boys), aged 11.5±4.3 years with T1DM and 11 age- and BMI-matched controls were included into the study. Patients were divided into 3 groups according to HbA1c level, I - below 7% [53 mmol/mol], II - 7-9% [53-75 mmol/mol] and III - above 9% [75 mmol/mol]. Blood samples for biochemical measurements were drawn at 8.00 AM, when the patients were in a fasting state. HbA1c was measured by the standardized IFCC method. OC, OPG, RANKL, leptin and adiponectin were measured by ELISA. ANOVA, and multiple regression analysis were used for statistical analysis. RESULTS: Significant differences in leptin and osteocalcin levels between groups with different HbA1c values were observed (p=0.03, p=0.04). Multiple regression analysis adjusted for age showed that serum OC and leptin negatively correlated with HbA1c levels (r=-0.22, p=0.004 and r=-0.27, p=0.0001, respectively). In contrast, serum OPG correlated positively with HbA1c (r=0.26, p=0.02) as well as with adiponectin (r=0.26, p=0.02) and RANKL (r=0.27, p=0.02) levels. The correlation of OC with HbA1c was the strongest in group I - patients with good metabolic control of DM (r=-0.43, p=0.03). In that group, in multiple regression analysis adjusted for age and BMI leptin correlated positively with daily dose of insulin (r=0.52, r=0.009). In group II and III in multiple regression analysis adjusted for age and BMI OC correlated negatively with leptin (r=-0.37, p=0.01). CONCLUSIONS: Our data suggest significant relationships between bone, fat tissue and glucose metabolism in pediatric patients with T1DM. The results can confirm that poor metabolic control is associated with reduced bone formation. On the other hand fat and bone tissue can influence glucose metabolism, potentiality in insulin-dependent manner. From these data leptin or OC may be potentially used as additional therapeutic agents for T1DM.

A role of hydrogen peroxide producing commensal bacteria present in colon of adolescents with inflammatory bowel disease in perpetuation of the inflammatory process.

Bacteria in the gut play a central role in the initiation and progress of inflammatory bowel disease (IBD). This study was prepared to elucidate the role in the inflammatory process of the bacterial species which are able to produce hydrogen peroxide, present in samples taken from colon lesions in adolescents with inflammatory bowel disease. Fifty eight adolescents were enrolled into the study from January 2004 to October 2006 in Cracow, Poland. Biopsies and stool samples were collected. Bacteriological examinations and measurements of hydrogen peroxide production by enterococci, streptococci and lactobacilli were performed. For the first time it has been shown here that HP producing bacteria may contribute to increased amounts of hydrogen peroxide in the inflamed mucosa of Crohn's disease and ulcerative colitis patients. Moreover, we have been able to demonstrate an increase of total populations of aerobic bacteria but not anaerobes in the studied samples of mucosa of adolescents with inflammatory bowel disease which is an indirect evidence of higher oxygen tension present in inflamed tissues in IBD. We have also been able to demonstrate the direct relationship between presence of blood in stools of IBD adolescents and increased populations of Enterobacteriaceae but not streptococci in samples of colon mucosa. It is, therefore, possible that different products of Enterobacteriaceae and especially their lipopolysaccharides may also contribute to perpetuation of the chronic colon inflammation.

Interleukin-6 (IL-6) and IGF-IGFBP system in children and adolescents with type 1 diabetes mellitus.

BACKGROUND: Some studies suggest that IL-6 is connected with glucose metabolism and insulin action, so like IGF-IGFBPs system it could play the role in diabetes etiopathogenesis. AIM: The aim of the study was therefore to test the hypothesis that in children and adolescents IL-6 is of importance for the etiopathogenesis of diabetes mellitus type 1 and that IL-6 is connected with carbohydrate metabolism and IGF-IGFBPs action. METHODS: There were 49 patients with type 1 diabetes: 10 persons at onset diabetes and 39 with disease lasted at least 1 year and 33 age-matched healthy children included into the study. Serum IGF-I concentrations were measured by RIA; IGFBP-1 and IGFBP-2 by IRMA and IL-6 concentrations using quantitative ELISA immunoassays. HbA1c was measured by HPLC method. Multiple regression, ANOVA, and Student's t-test were used for statistical analysis. RESULTS: IL-6 and IGF-I, IGFBP-1 and IGFBP-2 levels did not differ statistically significant between diabetic patients and controls. IL-6 concentrations were statistically higher at onset diabetes than in diabetic patients with long-term disease. IL-6 did not correlate with IGF-I and its binding proteins - 1 and - 2 in examined groups. At onset of disease IL-6 correlated with insulin requirement. There were not found correlations between IL-6 and HbA1c in diabetic groups. IGF-I positively correlated with age and growth in both groups and with IGFBP-2 in diabetic patients. IGFBP-2 correlated negatively with BMI in all examined groups. CONCLUSIONS: IL-6 might play a significant role in type 1 diabetes mellitus etiopathogenesis. It seems that IL-6 does not regulate IGF-IGFBP system in diabetic children and adolescents or IL-6 maybe cooperate with IGF-I, but their significant dependence on insulin action influences their mutual relationships.