A recent survey found that approximately 4% of very low birth weight infants in Japan were treated with glucocorticoids postnatally for circulatory collapse thought to be caused by late-onset adrenal insufficiency. We identified 11 preterm infants with clinical signs compatible with this diagnosis (hypotension, oliguria, hyponatremia, lung edema, and increased demand for oxygen treatment) and matched them for gestational age with 11 infants without such signs. Blood samples were obtained for cortisol and its precursors from the patient group before the administration of hydrocortisone, and from the control group during the same postnatal week. All samples were analyzed using a gas chromatography-mass spectrometry system. Cortisol concentrations did not differ between the two groups (6.6 Ϯ 4.5 vs 3.4 Ϯ 2.7 g/dL); however, the total concentration of precursors in the pathway to cortisol production was significantly higher in the patient group (72.2 Ϯ 50.3 vs 25.0 Ϯ 28.5 g/dL; p Ͻ 0.05). We conclude that the clinical picture of late-onset adrenal insufficiency in preterm infants is not a result of an absolute deficiency of cortisol production, but may be a result of a limited ability to synthesize sufficient cortisol for the degree of clinical stress. A ccording to a recent nationwide survey in Japan, about 4% of very low birth weight (VLBW) infants are treated with postnatal steroids because of adrenal insufficiency of prematurity (AOP). This condition was defined in the survey as postnatal steroid usage during a hospital stay for treatment of late-onset circulatory collapse in premature infants (1). Reports on glucocorticoid-responsive hypotension among VLBW infants in the early postnatal period suggest that the hypothalamus-pituitary-adrenal system does not function sufficiently in the immediate postnatal period (2-7), and, as a result, the serum cortisol level is relatively low during the first week of life (8 -13). However, it has been suggested that this adrenal insufficiency in preterm infants is transient and that adrenal function tends to return to normal by the end of the second week of life (14). Two randomized control trials have demonstrated the benefit of glucocorticoids for preventing and treating refractory hypotension during the first week of life in VLBW infants (15,16). Therefore, glucocorticoid-responsive hypotension was not considered a common phenomenon beyond the first week of life in this population. However, VLBW infants sometimes develop late-onset glucocorticoid-responsive circulatory collapse.The purpose of the current study differs from previous reports on the above pathophysiological etiologies, because we focused specifically on late-onset circulatory instability, which is usually prominent after the first week of life in preterm infants. AOP was defined as postnatal steroid treatment for late-onset (after the first week of life) adrenal insufficiency in premature infants. To elucidate the pathogenesis of this disorder, a comparison of steroid hormone concentrations between ...

The proposed set of ICD-10 codes encompasses the codes used in different countries for most SUDI cases. Use of these codes will allow for better international comparisons and tracking of trends over time.

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These catecholaminergic changes may be caused by chronic hypoxia or ischemia, and also may underlie alterations in respiratory and cardiovascular control in sleep.

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Nebulized HS therapy did not significantly reduce LOS among infants with bronchiolitis due to RSV.

Background: Coronary artery abnormalities (CAAs) still occur in patients with Kawasaki disease receiving intensified treatment with corticosteroids. We aimed to determine the risk factors of CAA development and resistance to intensified treatment in Post RAISE (Prospective Observational Study on Stratified Treatment With Immunoglobulin Plus Steroid Efficacy for Kawasaki Disease)—the largest prospective cohort of Kawasaki disease patients to date. Methods: In Post RAISE, 2648 consecutive patients with Kawasaki disease were enrolled. The present study analyzed 724 patients predicted to be intravenous immunoglobulin (IVIG) nonresponders (Kobayashi score ≥5) who received intensified treatment consisting of IVIG plus prednisolone. The association between the baseline characteristics and CAA at 1 month after disease onset was examined. The association between the baseline characteristics and treatment resistance was also investigated. Results: Maximum Z score at baseline ≥2.5 (odds ratio, 3.4 [95% CI, 1.5–7.8]), age at fever onset <1 year (odds ratio, 3.4 [95% CI, 1.6–7.4]), and nonresponsiveness to IVIG plus prednisolone treatment (odds ratio, 6.8 [95% CI, 3.3–14.0]) were independent predictors of CAA development. Nonresponsiveness to IVIG plus prednisolone was significantly associated with 8 baseline variables. Baseline total bilirubin (odds ratio, 1.4 [95% CI, 1.2–1.7]) was the only significant independent predictor other than the variables included in the Kobayashi score, enabling treatment resistance to be identified at diagnosis. The area under the ROC curve was 0.74 (95% CI, 0.69–0.79). At a cutoff point of 1.0, the sensitivity and specificity for predicting treatment resistance were 71% and 65%, respectively. Conclusions: In Post RAISE, younger age at fever onset, a larger maximum Z score at baseline, and nonresponsiveness to IVIG plus prednisolone were risk factors significantly associated with CAA development. Nonresponders were able to be identified at diagnosis based on the total bilirubin value. To prevent CAA, more intensified or adjunctive therapies using other agents, such as pulsed methylprednisolone, ciclosporin, infliximab, and Anakinra, should be considered for patients with these risk factors. Registration: URL: https://www.umin.ac.jp/ctr/ ; Unique identifier: UMIN000007133.

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