Thyroid imaging study in children with suspected thyroid dysgenesis.

PURPOSE: Thyroid dysgenesis is one of the most common causes of permanent congenital hypothyroidism. Thyroid ultrasonography or scan is used to detect thyroid dysgenesis. We analyzed the sensitivity and specificity of thyroid ultrasonography and scan in diagnosing thyroid dysgenesis to determine the clinical utility of each thyroid imaging method. METHODS: Sixty-one patients younger than 7 years of age were investigated via thyroid scan. Nineteen patients who were initially interpreted as having thyroid dysgenesis, such as ectopia, hemiagenesis, or aplasia, by thyroid scan were included in the study. Clinical characteristics and findings of a thyroid imaging study were reviewed. RESULTS: Initially, thyroid scan results were interpreted as ectopia (n=9), hemiagenesis (n=1), and nonvisualization (n=9). In contrast, the results of thyroid ultrasonography were normal thyroid gland (n=5), ectopia (n=6), and hypoplasia (n=8). After reviewing the results of both studies, final imaging diagnoses were as follows: normal thyroid gland (n=5), hemiagenesis (n=1), ectopia (n=9) including 2 dual ectopy, hypoplasia (n=3), and aplasia (n=1). Thyroid ultrasonography showed higher sensitivity and specificity in detecting presence of normal thyroid gland. Thyroid scan was better to detect ectopia. Among 8 patients who were initially interpreted as having hypoplasia by ultrasonography, 4 were confirmed as ectopia and one as aplasia. CONCLUSION: This study showed that thyroid ultrasonography is useful as the first-line imaging study to detect normal-sized eutopic thyroid gland. Thyroid scan should be performed to investigate the presence of ectopia if hypoplasia or aplasia is suspected by ultrasonography.

Serum Hepcidin to Prohepcidin Ratio in Children with Iron Deficiency Anemia.

BACKGROUND: Hepcidin is produced in hepatocytes as a precursor form that needs to be converted to a mature hepcidin to be active. In iron deficiency anemia (IDA), the synthesis of hepcidin is inhibited; however, it is not clear how the maturation of hepcidin precursor is affected. To assess the relative maturity of serum hepcidin in the setting of IDA, we compared the ratio of mature hepcidin to prohepcidin in children with different iron statuses. METHODS: A total of 51 children (age: 0.6~18.2 yr) with normal renal function and C-reactive protein levels were enrolled. Based on hemoglobin levels and iron status, the subjects were classified as control (n=29), iron deficiency without anemia (n=6), and IDA (n=16). Serum concentrations of hepcidin and prohepcidin were measured by enzyme-linked immunosorbent assays. RESULTS: Hepcidin was positively correlated with hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, iron, transferrin saturation, and ferritin, and negatively correlated with total iron binding capacity and transferrin. IDA patients had lower levels of prohepcidin [4.7(1.9~21.7) vs 34.6(11.0~140.4) ng/mL, p<0.001] and hepcidin [9.6(3.3~39.5) vs 75.2(19.9~256.4) ng/mL, p<0.001] than control subjects. Hepcidin was strongly correlated with prohepcidin (r=0.991, p<0.001). As compared with control subjects, the hepcidin to prohepcidin ratio was lower in those with IDA (1.89±0.24 vs 2.11±0.18, p=0.009) or low serum ferritin. CONCLUSION: These findings suggest that inhibited maturation, as well as inhibited synthesis, may contribute to low hepcidin level in IDA.

MicroRNA-205 directly regulates the tumor suppressor, interleukin-24, in human KB oral cancer cells.

MicroRNA (miRNA) is a form of small noncoding RNA that regulates the expression of genes either by inhibiting mRNA translation or by inducing its degradation. Small microRNA play important roles in regulating a large number of cellular processes, including development, proliferation and apoptosis. This study examined the biological functions of miR-205 as a tumor suppressor in KB oral cancer cells. The results showed that miR-205 expression was significantly lower in KB oral cancer cells than in human normal oral keratinocytes. Furthermore, the miR-205 over-expressed in KB oral cancer cells increased the cell cytotoxicity and induced apoptosis through the activation of caspase-3/-7. The transfection of miR-205 into KB oral cancer cells strongly induced IL-24, a well known cytokine that acts as a tumor suppressor in a range of tumor tissues. In addition, miR-205 targeted the IL-24 promoter directly to induce gene expression. Overall, miR-205 has significant therapeutic potential to turn on silenced tumor suppressor genes by targeting them with miRNA.

Identifying the polymorphisms in the thymic stromal lymphopoietin receptor (TSLPR) and their association with asthma.

The present study aimed to investigate whether the polymorphisms in the TSLPR gene are associated with atopic and asthmatic disease in the Korean population. We identified eleven single nucleotide polymorphisms (SNPs) and two variation sites in the TSLPR gene, including the promoter region. The genotype and allele frequencies of g.33G>C of the TSLPR gene in asthma patients were significantly different from the respective frequencies of the control group (P =0.006 and 0.003, respectively). Our additional analysis showed that the genotype and allele frequencies of the g.33G>C and g.19646A>G of the TSLPR gene were significantly associated in the atopic asthma patients rather than in the non-atopic asthma patients (genotype frequencies; P =0.0001 and 0.0003 respectively, allele frequencies; P =0.0005 and 0.0001 in that order). Our results suggest that the SNPs of the TSLPR gene could be associated with the susceptibility to atopic asthma in the Korean population.