We investigated the postnatal pattern of changes in adrenal size in very low-birth-weight (VLBW) infants and its relation to late-onset glucocorticoid-responsive circulatory collapse (LGCC) that may be associated with adrenal insufficiency. In 36 VLBW infants born at <33 weeks' gestation, ultrasound examinations of postnatal changes in adrenal size during the first 3 weeks of life were performed. VLBW infants were classified into three groups: group A (n = 6), the actual adrenal area was greater than or equal to the predicted value at birth and unchanged at 3 weeks; group B (n = 24), the actual adrenal area was greater than or equal to the predicted value and decreased at 3 weeks; and group C (n = 6), the actual adrenal area was less than the predicted value and unchanged at 3 weeks. Five infants developed LGCC, and all five were in group A. These observations suggest that the life of the adrenal fetal zone might be extended beyond 3 weeks after birth in some VLBW infants and that prolonged fetal zone activity might correlate with LGCC. On the other hand, adrenal maturation might have already occurred at birth in some VLBW infants. Sonographic evaluation of adrenal size may enable prediction of subsequent LGCC in VLBW infants.

Hemolytic anemia with abundant Heinz bodies developed in an extremely low birth weight infant. The infant was born at 25 weeks' gestation with a birth weight of 741 g. The disord er manifested at 28 days of age after the acute period. Results of a routine weekly blood examination showed an unexpected sudden fall in the hemoglobin level and an increased total bilir ubin level. Peripheral blood smear revealed that a high percentage of erythrocytes contained Heinz bodies. With repeated blood transfusions and aggressive phototherapy this condition resolved within a week. The patient had not been exposed to known toxins with oxidizing agents. Glucose-6-phosphate dehydrogenase levels were normal, and an unstable hemoglobin was not present. Although the cause and underlying mechanisms of this phenomenon are unknown, the immature antioxidant function of the erythrocyte membrane against oxygen radicals in an extremely premature infant might be a factor in the etiology.

We investigated time-related predictors of death or neurological sequelae in extremely preterm infants (EPI) born at 22 to 24 weeks' gestation by categorizing clinical patterns according to their survival time and morbidity. Data on 113 infants born at 22 to 24 weeks' gestation from January 1991 through April 2006 were analyzed by a case-control approach. Cesarean section, Apgar score or= 24 hours, pulmonary hemorrhage and intraventricular hemorrhage (IVH) were significantly associated with death by day 6. Among those surviving >or= 7 days, sepsis and severe IVH were significantly associated with death. Assessment of survivors at a minimum follow-up period of 2 years revealed that protracted mechanical ventilation was significantly associated with a poor neurological outcome. There are various characteristic key events in relation to the outcome at different ages of life in EPI born at 22 to 24 weeks' gestation. Clinicians and parents should discuss management options for the infant on the basis of these findings.

Pediatrics InternationalVolume 50, Issue 4 p. 603-604 Urinary retention in a boy with terminal deletion of chromosome 10q at band 26.1 Osamu Motoyama, Corresponding Author Osamu Motoyama 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanOsamu Motoyama, MD, Department of Pediatrics, Toho University Medical Center, Sakura Hospital, 564-1 Shimoshizu, Sakura-shi, Chiba 285-8741, Japan. Email: [email protected]Search for more papers by this author 1 Mika Tokuyama, Mika Tokuyama 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanSearch for more papers by this author 2 Naoki Uga, Naoki Uga 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanSearch for more papers by this author 3 Kikuo Iitaka, Kikuo Iitaka 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanSearch for more papers by this author 4 Osamu Motoyama, Corresponding Author Osamu Motoyama 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanOsamu Motoyama, MD, Department of Pediatrics, Toho University Medical Center, Sakura Hospital, 564-1 Shimoshizu, Sakura-shi, Chiba 285-8741, Japan. Email: [email protected]Search for more papers by this author 1 Mika Tokuyama, Mika Tokuyama 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanSearch for more papers by this author 2 Naoki Uga, Naoki Uga 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanSearch for more papers by this author 3 Kikuo Iitaka, Kikuo Iitaka 1Department of Pediatrics, Toho University Medical Center, Sakura Hospital, Chiba, Departments of 2Pediatrics and 3Neonatology, Toho University Medical Center, Omori Hospital, Tokyo and 4Department of Pediatrics, Yamato City Hospital, Kanagawa, JapanSearch for more papers by this author 4 First published: 25 August 2008 https://doi.org/10.1111/j.1442-200X.2008.02683.xCitations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Leonard NJ, Harley FL, Lin CC. Terminal deletion of chromosome 10q at band 26.1: Follow-up in an adolescent male with high-output renal failure from congenital obstructive uropathy. Am. J. Med. Genet. 1999; 86: 115– 17. 2 Ogata T, Muroya K, Sasagawa I et al. Genetic evidence for a novel gene(s) involved in urogenital development on 10q26. Kidney Int. 2000; 58: 2281– 90. 3 Gorinati M, Zamboni G, Padoin N, Dodero A, Caufin D, Memo L. Terminal deletion of long arm of chromosome 10: Case report and review of the literature. Am. J. Med. Genet. 1989; 33: 502– 4. 4 International Reflux Study Committee. Medical versus surgical treatment of primary vesicoureteral reflux: A prospective international reflux study in children. J. Urol. 1981; 125: 277– 83. 5 Kogasaka R, Morohoshi T, Sawada Y, Fujiwara M. Terminal deletion of chromosome 10q and its clinical features. Acta Paediatr. Jpn. 1990; 32: 83– 7. 6 Bauer SB. Neuropathology of the lower urinary tract. In: PP Kelalis, LR King, AB Belman (eds). Clinical Pediatric Urology, 3rd edn. WB Saunders, Philadelphia, 1992; 399– 440. 7 Wright FS. Disorders of micturition and defecation. In: KF Swaiman, FS Wright (eds). The Practice of Pediatric Neurology, 2nd edn. CV Mosby, St Louis, 1982; 318– 26. 8 Shapiro SD, Hansen KL, Pasztor LM et al. Deletions of the long arm of chromosome 10. Am. J. Med. Genet. 1985; 20: 181– 96. Citing Literature Volume50, Issue4August 2008Pages 603-604 ReferencesRelatedInformation

Background: Spontaneous isolated gastrointestinal perforation (SIP) in very low-birthweight infants has been reported as a different disease entity from necrotizing enterocolitis (NEC). The objective of this study was to investigate the incidence and risk factors of NEC and SIP.Methods: The authors reviewed the medical records of very low-birthweight infants who were admitted to Toho University Perinatal Center, Tokyo, Japan, between 1 January 1991 and 31 December 2002. The diagnosis of NEC was made with the finding of bloody gastric fluid or stool, abdominal distention, and abnormal abdominal X-ray findings such as pneumatosis intestinalis or fixed dilated intestinal loops. SIP was defined at laparotomy as the presence of an isolated gastrointestinal perforation surrounded by normal appearing bowel.Results: A total of 556 very low-birthweight infants were included in this study. Of those, 15 infants were excluded because of major anomalies. Out of 541 infants, 14 were diagnosed to have NEC or gastrointestinal perforation. In total, 13 infants had gastrointestinal perforation and 10 were confirmed as SIP. Two SIP suggestive cases were included in SIP cases. There was only one case of NEC (0.2%) during 12 years in the authors' institute. Eight SIP cases had antenatal nonsteroidal anti-inflammatory drugs (NSAID). The treatment with antenatal NSAID was significantly associated with the incidence of SIP (p < 0.001).Conclusions: The authors experienced only one proven case of NEC (0.2%), 12 cases of SIP (2.2%) among 556 very low-birthweight infants admitted during 12 years. Antenenatal NSAID were strongly associated with SIP.

Background: Various cytokines are reportedly associated with many neonatal diseases. Asphyxia is considered to result in ischemia-reperfusion injuries and induces abnormal inflammatory responses involving excessive cytokine production. Objectives: To evaluate alteration in sera levels of various cytokines/chemokines in case of perinatal asphyxia at birth. Methods: In orderto determine the concentrations of various cytokines/chemokines in sera, we used a highly sensitive fluorescence microsphere method. We measured the concentration of 8 types of cytokines/chemokines in sera obtained from 17 cases of asphyxia, 10 normal neonates, and 6 healthy adults. Results: The concentrations of IL-6, IL-8, and IL-10 in the sera of asphyxiated neonates were higher than those in the normal neonates. Irrespective of the presence or absence of asphyxia, sera concentrations of IL-2, IL-4, IFN-γ, and TNF-α were higher in the neonates than those in the adults. The concentration of IFN-γ in the asphyxiated neonates was lower than that in the normal neonates. Sera levels of IL-10 were higher in the asphyxiated cases than those in the normal neonates. The sera levels of IL-6, IL-8, and IL-10 in asphyxiated neonates with either a poor outcome or death were higher than those without poor outcomes. Conclusions: The concentrations of various types of cytokines/chemokines were different in neonatal sera and some of them increased drastically during asphyxia. The concentration of an anti-inflammatory cytokine IL-10 was elevated in asphyxiated neonates immediately after birth, thereby suggesting that IL-10 might be associated with neuroprotective functions.

Pediatrics InternationalVolume 24, Issue 3 p. 412-413 Neonatal Hyperreninemic Hypertension: Effects of Oral Angiotensin Converting Enzyme Inhibitor (Captopril) on Blood Pressure and Renin-Angiotensin Systems. Ryo Sumazaki, Ryo Sumazaki Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorNaoki Uga, Naoki Uga Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorMasahiro Fujita, Masahiro Fujita Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorKeijiro Yabuta, Keijiro Yabuta Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorToshiro Fujita, Toshiro Fujita Department of Internal Medicine, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this author Ryo Sumazaki, Ryo Sumazaki Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorNaoki Uga, Naoki Uga Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorMasahiro Fujita, Masahiro Fujita Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorKeijiro Yabuta, Keijiro Yabuta Department of Pediatrics, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this authorToshiro Fujita, Toshiro Fujita Department of Internal Medicine, Institute of Clinical Medicine, The University of TsukubaSearch for more papers by this author First published: September 1980 https://doi.org/10.1111/j.1442-200X.1980.tb00562.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume24, Issue3September 1980Pages 412-413 RelatedInformation