Kawasaki disease (KD) is an acute febrile illness that is the predominant cause of pediatric acquired heart disease in infants and young children. Because the diagnosis of KD depends on clinical manifestations, incomplete cases are difficult to diagnose, especially in infants younger than 1 year. Incomplete clinical manifestations in infants are related with the development of KD-associated coronary artery abnormalities. Because the diagnosis of infantile KD is difficult and complications are numerous, early suspicion and evaluation are necessary.

Purpose: Sodium is an essential nutritional electrolyte that affects growth. A low serum sodium concentration in healthy premature infants beyond 2 weeks of life is called lateonset hyponatremia (LOH). Here, we investigated the association between LOH severity and growth outcomes in premature infants. Methods: Medical records of premature infants born at ≤32 weeks of gestation were reviewed. LOH was defined as a serum sodium level <135 mEq/L regardless of sodium replacement after 14 days of life. Cases were divided into two groups, <130 mEq/L (severe) and ≥130 mEq/L (mild). Characteristics and growth parameters were compared between the two groups. Results: A total of 102 premature infants with LOH were included. Gestational age ([GA] 27.7 vs. 29.5 weeks, p<0.001) and birth weight (1.04 vs. 1.34 kg, p<0.001) were significantly lower in the severe group. GA was a risk factor of severe LOH (odds ratio [OR], 1.328, p=0.022), and severe LOH affected the development of bronchopulmonary dysplasia (OR, 2.950, p=0.039) and led to a poor developmental outcome (OR, 9.339, p=0.049). Growth parameters at birth were lower in the severe group, and a lower GA and sepsis negatively affected changes in growth for 3 years after adjustment for time. However, severe LOH was not related to growth changes in premature infants. Conclusion: Severe LOH influenced the development of bronchopulmonary dysplasia and developmental outcomes. However, LOH severity did not affect the growth of premature infants beyond the neonatal period.

PurposeNeonatal late-onset hypocalcemia is defined as hypocalcemia developed after postnatal 3 days and associated with hypoparathyroidism, high phosphate diets and vitamin D deficiency. We experienced the increment of neonatal late onset hypocalcemia over 1 year. We tried to evaluate the relationship between late onset hypocalcemia and maternal hypovitaminosis D.MethodsThe medical records in the neonates with late-onset hypocalcemia during January 2007 to July 2008 were retrospectively reviewed. Among those patients, 17 paired sera of mothers and neonates had collected. The levels of 25-OH vitamin D (25OHD) and intact parathyroid hormone (iPTH) were measured and were compared with neonate and the mother.ResultsThe mean gestational age was 38+1 weeks, and the mean body weight was 2,980 g. The onset time of hypocalcemia was 5.9 days of age. Most of them (88.2%) were feeding with formula and no one was only breast milk feeding. Of the 17 patients, 13 were born in spring or in winter. The median levels of calcium, phosphorus, alkaline phosphatase, iPTH and 25OHD were 7.0 mg/dL, 8.6 mg/dL, 191.0 U/L, 57.2 pg/mL and 24.0 ng/mL in neonates. The levels of 25OHD of 6 neonates were <20 ng/mL. A total of 16 mothers were considered vitamin D-deficient (<20 ng/mL), and vitamin D insufficient (20<25OHD<30 ng/mL).ConclusionNeonatal late-onset hypocalcemia in our study seems to be influenced by maternal vitamin D deficiency and insufficiency. Sun tanning and vitamin D supplements from winter to spring would be helpful to prevent maternal vitamin D deficiency, one of the causes of neonatal late-onset hypocalcemia.

It has been demonstrated that vitamin C exhibits anti-cancer activity in various tumor cell lines; however, its specific mechanism of action remains unknown. Although the diagnosis and therapy of cancer patients have markedly improved in recent years, safer and more cost-effective treatments are still required. Therefore, the present study examined the effect of vitamin C on the induction of cell death in gastric cancer and its underlying mechanism of action. It was observed that the cytotoxicity of vitamin C on the human gastric cancer cell line AGS is dependent on the apoptotic pathway, including caspase cascades, but not on the necroptotic pathway. It was demonstrated that the vitamin C-induced calcium influx and ROS generation have critical roles in the induction of apoptosis. Furthermore, vitamin C treatment depleted adenosine triphosphate (ATP) production in AGS cells, and the autophagy pathway may be involved in this process. Taken together, the current study suggests that a high dose of vitamin C may induce gastric cancer cell apoptosis through the dysfunction of mitochondria, including calcium influx, reactive oxygen species generation and ATP depletion.