Influence of clinical status on the association between plasma total and unbound bilirubin and death or adverse neurodevelopmental outcomes in extremely low birth weight infants

Objectives: To assess the influence of clinical status on the association between total plasma bilirubin and unbound bilirubin on death or adverse neurodevelopmental outcomes at 18–22 months corrected age in extremely low birth weight infants. Method: Total plasma bilirubin and unbound bilirubin were measured in 1101 extremely low birth weight infants at 5 ± 1 days of age. Clinical criteria were used to classify infants as clinically stable or unstable. Survivors were examined at 18–22 months corrected age by certified examiners. Outcome variables were death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death prior to follow‐up. For all outcomes, the interaction between bilirubin variables and clinical status was assessed in logistic regression analyses adjusted for multiple risk factors. Results: Regardless of clinical status, an increasing level of unbound bilirubin was associated with higher rates of death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss and death before follow‐up. Total plasma bilirubin values were directly associated with death or neurodevelopmental impairment, death or cerebral palsy, death or hearing loss, and death before follow‐up in unstable infants, but not in stable infants. An inverse association between total plasma bilirubin and death or cerebral palsy was found in stable infants. Conclusions: In extremely low birth weight infants, clinical status at 5 days of age affects the association between total plasma bilirubin and death or adverse neurodevelopmental outcomes at 18–22 months of corrected age. An increasing level of UB is associated a higher risk of death or adverse neurodevelopmental outcomes regardless of clinical status. Increasing levels of total plasma bilirubin are directly associated with increasing risk of death or adverse neurodevelopmental outcomes in unstable, but not in stable infants.     

Granulocyte colony-stimulating factor crosses the placenta and stimulates fetal rat granulopoiesis

We studied the effect of recombinant human granulocyte colony- stimulating factor (rhG-CSF) administration to pregnant rats upon fetal and neonatal myelopoiesis. Pregnant rats were treated with rhG-CSF twice daily for 2, 4, and 6 days before parturition. rhG-CSF crossed the placenta and reached peak fetal serum concentrations 4 hours after administration. Peak fetal serum levels were 1,000-fold lower than levels detected in the dam. Hematopoietic effects of rhG-CSF were assessed by cytologic analysis of the newborn blood, spleen, bone marrow, thymus, and liver. White blood cell counts were increased twofold to fourfold in newborns. This increase was due to circulating numbers of polymorphonuclear cells (PMN). rhG-CSF induced a myeloid hyperplasia in the newborn marrow consisting of immature and mature myeloid cells in the day-2 and day-4 treated pups. Bone marrow of pups treated for 6 days contained mostly hyper-segmented PMN with little or no increase in myeloid precursors. An increase in the number of postmitotic (PMN, bands, and metamyelocytes) and mitotic (promyeloblasts, myeloblasts, and metamyeloblasts) myeloid cells in the spleen of neonates was observed. No change was detected in splenic lymphocytes or monocytes. No effect of rhG-CSF was noted in the newborn liver or thymus. These results demonstrate that maternally administered rhG-CSF crosses the placenta and specifically induces bone marrow and spleen myelopoiesis in the fetus and neonate. The significant myelopoietic effects of rhG-CSF at low concentrations in the fetus suggest an exquisite degree of developmental sensitivity to this cytokine and may provide enhanced defense mechanisms to the neonate.     

Abnormal Pancreatic Electrolyte Secretion in Cystic Fibrosis

ABSTRACT. We performed pancreatic function tests on sixty-five cystic fibrosis (CF), and eleven control children. The technique used continuous IV infusion of cholecystokinin and secretin, with duodenal juice collection over a 90 min period, and was made quantitative by continuous duodenal infusion and distal collection of an unabsorbable marker (bromosulphthalein). Some CF patients had near normal pancreatic enzyme outputs, some had impaired but measurable levels, but most (79 %) had almost absent trypsin secretion. CF children with better pancreatic function, were younger and more likely to be male. All controls showed a large increase in bicarbonate concentration and secretion rate per kilogram body weight during the test, but most children with CF (96.5 %) did not. Because two of our CF patients had water and bicarbonate secretion within the control range, this finding does not exclude the diagnosis of CF. Sodium, potassium and chloride ion secretion in CF patients was lower than controls but overlap occurred. We found a linear correlation between acinar and tubular secretion in CF patients which indicates that there is probably not a primary genetic defect in pancreatic bicarbonate secretion in CF.     

A Survey of Stress at Work

A survey was carried out among members of the Society of OccupationalMedicine on their assessment of stress-related illness in industry.It was found that medical officers in organizations estimatedthat over 45 per cent of their managers suffered from some formof psychosocial stress (e.g anxiety, psychosomatic illness,depression), ‘to some or a ereat extent’. Professor C. L. Cooper, University of Manchester Institute of Science and Technology, P.O. Box 88, Manchester M60 1QD.     

POLYMORPHONUCLEAR LEUCOCYTE FUNCTION IN RHEUMATOID ARTHRITIS

Controversy exists over the function of polymorphonuclear leucocytes(PMN) in rheumatoid arthritis (RA). We found no difference inthe phagocytic and migratory ability of PMN from 45 patientswith RA, when compared with PMN from 19 RA patients who hada history of recurrent infection, and 40 normal healthy age-and sex-matched controls. We conclude that the increased incidenceof bacterial infection reported in RA is not the consequenceof an intrinsic defect in PMN function. KEY WORDS: Polymorphonuclear leucocytes, Rheumatoid arthritis     

自体骨粉移植修复下颌骨部分缺损的组织学检测

目的:通过动物实验进行组织学光镜及扫描电镜检测,观察自体骨粉移植修复下颌骨缺损的愈合过程。方法:实验于2005-05/11在南方医科大学动物实验中心完成,选用12只健康雄性大耳白兔。实验分为两组:一侧为自体骨粉移植组,另一侧为空白对照组,均采用自体左右对照。①缺损模型建立:于双侧下颌骨体部下缘用磨削机器各造成1.0×1.0cm的全层骨缺损。②自体骨粉移植:将所有自体骨粉回填一侧缺损处作为自体骨粉移植组,另一侧缺损旷置作为空白对照组。③分别于术后2,4及8周各处死4只动物,获取整块下颌骨标本作组织学光镜及扫描电镜检测,光镜切片应用苏木精-伊红染色,扫描电镜只观察自体骨粉移植组标本。结果:12只大耳白兔均进入结果分析,无脱失。①两组标本组织学观察结果:自体骨粉移植组术后2周时形成薄层骨痂;4周时为新生的骨小梁,但排列紊乱;8周时骨小梁形成的编织骨已逐渐向板层骨过渡。空白对照组术后8周时骨小梁分布仍稀疏。②自体骨粉移植组标本超微结构观察结果:术后4周骨基质钙化程度提高,大量成骨细胞位于骨陷窝内。缺损间隙逐渐变窄形成多孔较疏松的新骨组织,新生骨小梁形成,新骨超微结构呈“蜂窝状”。8周时骨小梁钙化程度继续升高,形成的板状骨排列出现一定方向性,新生骨组织由多孔疏松的结构向致密性结构转化,新原骨组织基本上融为一体产生骨性结合,髓腔相通。结论:自体骨粉移植修复下颌骨成骨可靠,愈合加快,愈合方式以骨传导爬行替代为主,且应用方法简便。