锌缺乏与儿童感染性疾病

锌与儿童生长和健康的关系,早已受到关注。但由于锌缺乏没有特定和明确的症状与体征,临床上也没有简便、可靠的判断人体锌营养状况的生物指标;因此对儿童锌缺乏的程度和危害性认识仍然不足。最近,发展中国家的一系列研究相继证实锌缺乏与小儿腹泻、肺炎等感染性疾病之间存在高度相关性,因而再次引起人们对儿童,尤其是发展中国家儿童锌缺乏的关注。据估计,控制儿童锌缺乏有可能在全世界范围内减少5岁以下儿童死亡率5个百分点。     

儿童感染性疾病的病原学诊断

感染性疾病严重威胁儿童的生命与健康,病原学诊断是儿童感染性疾病防治工作中的关键环节。本文在分类介绍病原学诊断常用技术的基础上,着重对近年来免疫学、分子生物学、细胞学等方面的一些新技术进行评价和展望。同时也对下呼吸道感染、中枢神经系统感染、败血症等儿科常见感染性疾病的病原学诊断现状作一分析。     

锌与腹泻

营养不良在幼儿持续性腹泻的病因、治疗和预后方面是主要的因素。除了热量摄入不足以外,几种特殊的营养素的缺乏与之有关。锌在某些社区是受到特别关注的微量元素。锌缺乏在其它方面正常的儿童中已得到证实。锌缺乏的危险随粪便中有大量锌丢失的腹泻而增加,这种锌丢失导致恶性循环。     

小儿感染性疾病致病机制及其中医药防治培训会议

为了推动我国儿童感染性疾病事业的发展,促进学术交流,会议主要针对儿科各专业、中医儿科、儿保科、病毒研究人员开展儿童感染性疾病的致病机制以及运用中医药对其防治方面培训,使其掌握儿童常见感染性疾病的致病机制、病原的实验室检测与诊断以及临床有效的防治方法。此次会议便于学员更好掌握国内外感染性疾病的最新进展,学习交流感染性疾病防治的中西医新技术,新知识,新理念。将中西医结合治疗儿童感染性疾病有效的方法通过优化方案加以推广,     

β内酰胺类-β内酰胺酶抑制剂复方制剂儿科临床应用专家共识

内酰胺类-β内酰胺酶抑制剂复方制剂是治疗儿童感染性疾病的常用药物。虽然已有针对成人的β内酰胺类复方制剂应用的共识，但由于儿童不同于成人的生理特点，亟需一个专门针对儿童的β内酰胺类复方制剂应用的指导文件。该共识从β内酰胺类复方制剂的药物学特点、儿童药代动力学特点、儿童药效学特点、在常见儿童感染性疾病中的作用及药物管理等方面，对该类药物在儿童中的应用给出了全面建议，以规范儿科临床的合理使用。     

重视儿科感染性疾病关注疫苗与抗生素的合理应用

上一世纪 ,随着社会的发展、人们生活水平的提高和科技的进步 ,尤其是疫苗与抗生素的研究、开发和广泛应用 ,使威胁世界儿童健康的最大的感染性疾病 (包括传染病 )得到有效控制。人们普遍认为 ,目前疾病谱已经发生变化 ,先天性遗传性疾病、肿瘤、意外伤害和一些慢性疾病逐渐成为主要的儿童疾病 ,感染性疾病已经变得不重要了。因此 ,我国儿科感染性疾病的专科队伍逐渐萎缩 ,不少儿童医院取消了传染科 ,诊断上不重视病原学研究 ,治疗上滥用抗生素等抗感染药物 ,预防方面忽视疫苗的研制与应用。儿科工作者对感染性疾病放松了警惕。儿童感染性疾…     

锌与儿童呼吸道感染

锌是人体重要的微量元素,锌缺乏将导致一系列代谢紊乱和病理变化.我国儿童普遍存在锌缺乏的问题.近年来,补锌对儿童呼吸道感染的防治作用得到广泛关注.该文就补锌对儿童上呼吸道感染和下呼吸道感染的发病率、病死率及病程长短的影响,以及锌在呼吸道疾病的可能作用机制等方面进行综述.     

小剂量补充锌剂对学龄前儿童血清锌水平及细胞免疫功能的影响

为观察补充锌剂对学龄前儿童体内锌水平以及细胞免疫功能的影响 ,对143名学龄前儿童进行了为期6个月的对照观察 ,其中补锌组88名 ,对照组55名。每天补充10mg元素锌。6个月后 ,补锌组儿童的血清锌浓度从12.8μmol/L±1.87μmol/L提高到15.4μmol/L±1.68μmol/L(P<0.01) ;并明显高于对照组14.4μmol/L±1.20μmol/L(P<0.01) ;此外 ,对其中血清锌浓度低下的40名儿童 ,补锌组25名 ,对照组15名 ,用流式细胞技术分析补充锌剂前后T细胞亚群的变化 ,结果显示补锌组儿童的CD4 +细胞从37.3 %±4.54%上升到39.6 %±3.36 %(P<0.01),CD8 +细胞从26.7 %±5.07 %上升到28.2 %±4.66 %(P<0.01)。表明小剂量补充锌剂能改善儿童的锌营养状况及免疫功能 ,可能有助于减少感染性疾病的发生     

必须重视儿科感染性疾病

20世纪,随着社会的发展、人们生活水平的提高和科技的进步,尤其是疫苗与抗生素的研究、开发和广泛应用,威胁世界儿童健康最大的感染性疾病(包括传染病)得到有效控制。人们普遍认为,目前疾病谱已经发生变化,先天性遗传性疾病,肿瘤、意外伤害和一些慢性疾病逐渐成为主要的儿童疾病,感染性疾病已经变得不重要了。因此,目前我国儿科感染性疾病专科的队伍逐渐萎缩,不少儿童医院取消传染科;诊断上不重视病原学研究,治疗上滥用抗生素等抗感染药物。儿科工作者对感染性疾病放松了警惕。 儿童感染性疾病真的不重要了?答案是否定的。世界:卫生组织在1999年发出警告:“感染性疾病仍是全球健康事业的主要危害”。尤其对儿童,它仍是最大杀手。每年全球有1千3百万小儿死于感染性疾病,占儿童死亡的63％,其它大部份发生在发展中国     

小儿感染性疾病红细胞内锌原卟淋测定及其临床意义

为了解小儿感染性疾病红细胞内锌原卟啉 (ZPP)值及其临床意义。方法 :对 6 1例小儿感染性疾病进行ZPP及血红蛋白 (Hb)、红细胞计数 (RBC)及平均红细胞体积 (MCV)的测定 ,以健康体检儿童作为对照。结果 :感染组儿童ZPP值明显高于对照组 (P <0 0 5 ) ,Hb、MCV值明显低于对照组 (P <0 0 5 ) ,RBC值无明显差异 (P<0 0 5 )。不同性别之间ZPP、Hb、RBC、MCV值无统计学差异 (P <0 0 5 )。肺炎、肺结核、肠炎的ZPP值较上呼吸道感染及皮肤感染患儿高 ,败血症患儿ZPP值最高 ,Hb、RBC、MCV值较低 ,但无统计学差异 (P <0 0 5 )。结论 :小儿感染性疾病存在铁代谢紊乱。应用ZPP筛查铁缺乏症时 ,应避免感染因素的干扰 ,ZPP也可作为儿童感染及感染严重程度的观察指标。     

Zinc and diarrhea

Malnutrition is a major factor in the etiology, management and prognosis of persistent diarrhea in young children. Apart from inadequate energy intake, deficiencies of several specific nutrients have been implicated. Zinc is a micronutrient that appears to be of special interest, at least in some communities. Zinc deficiency has been documented in otherwise normal children. The risk of deficiency, however, is enhanced by diarrhea which is associated with variable but sometimes gross increases in zinc losses in the feces. These losses could contribute to a vicious circle, as there is now evidence that mild as well as severe zinc deficiency states can contribute to the duration and severity of diarrheal disease. During rehabilitation, impaired zinc nutriture could be responsible for slow growth, especially if the rehabilitation diet is high in phytate, a recognized inhibitor of zinc absorption. Research should be directed to a better understanding of zinc metabolism and homeostasis during diarrhea disease, to the consequences of zinc deficiency and to the benefits to be derived from zinc supplementation programs.     

Zinc, Pregnancy and Parturition

ABSTRACT. The role of zinc in the nutrition of pregnant women and its relations to prenatal growth and parturition are reviewed. Zinc deficiency (ZD) affects fetal growth and development both in experimental animals and in man. The teratogenicity of zinc deficiency was widely demonstrated in animals and is also evident in humans. Alcohol intoxication potentiates the effects of ZD in animals. Plasma zinc levels decrease during pregnancy and apparently an adequate and continuous intake of zinc is required for a normal embryonic development. The zinc content of amniotic fluid seems to be related with fetal growth but its value as an indicator of embryonic development is controversial. Zinc deficiency also affects adversely parturition. Mild zinc deficiency may affect a large number of pregnant women, being potentially harmful to the mother and the fetus. This situation requires the screening of high-risk groups, the definition of adequate dietary intakes for each population, and the supplementation with zinc when deficits are detected.     

Zinc deficiency in children with sickle cell disease

Zinc status was studied in 47 children with homozygous sickle cell disease (SCD). Decreased hair and plasma zinc was demonstrated in these children and hyperzincuria was found in the older patients. This study indicates that zinc deficiency in patients with SCD is probably due to hyperzincuria.     

Zinc nutrition and growth retardation

Human growth retardation from zinc deficiency was first reported over 40 years ago. More recently marginal zinc deficiency was shown to occur during pregnancy and infancy, and to be prevalent in children throughout the world. Zinc with or without macronutrients and other micronutrient deficits may also occur in patients with gastrointestinal disease. Particular attention must be given to the suboptimal intake of zinc which results in growth retardation. The single most important cause of nutritional growth retardation (NGR) worldwide is poverty related malnutrition involving multiple macro-and-micro nutrient deficits. NGR is an underappreciated entity in pediatric endocrine clinics since these patients do not manifest clinical evidence of malnutrition or overt nutrient deficits. A deceleration in body weight progression and decreased growth rates are the only clinical manifestations of the altered nutrient status. The growth deceleration occurs as an adaptive response to suboptimal nutrition to maintain equilibrium between genetic growth potential and nutritional intake. However the potential effects of suboptimal zinc intake in patients with NGR may be difficult to assess as there are no good clinical markers pertaining to this mineral. Zinc is known to be an essential micronutrient involved in growth, though the mechanism(s) by which zinc deficiency impairs growth has not been elucidated. Several hundred zinc-containing nucleoproteins are involved in gene expression of multiple proteins, many of them are important for growth. Zinc deficiency reduces IGF-I production, and may decrease cellular IGF-responsiveness. This may explain why the zinc status of GH deficient children significantly affects their response to GH treatment. In experimental models mild restriction of energy appeared to be more important in regard to growth retardation than suboptimal zinc intake, and the simultaneous restriction of energy and zinc did not augment the growth deterioration of chronic suboptimal nutrition. The USDA food guide is a simple guideline which should serve the needs of pediatric endocrinologists when evaluating the quality of the dietary intake of a short child and to provide guidelines for food intake to the patients.     

Effects of oyster extract on the reproductive function of zinc-deficient mice: bioavailability of zinc contained in oyster extract

ABSTRACT Zinc is a vital nutrient in the normal reproductive function and embryonic development of mammals, and it is well known that oyster extract contains significant amounts of zinc. The effects of oyster extract on reproductive function, such as embryonic development, serum levels of zinc and sperm maturation were examined in zinc‐deficient mice. Zinc deficiency in dams during pregnancy induced a decrease in the successful pregnancy rate, maternal weight gain, the number of live fetuses and fetal body weight. Zinc deficiency for 12 weeks in male mice induced a decrease in body weight, testis weight and sperm count in the epididymis. However, reproductive failure, embryonic defects and decreased sperm motility in zinc‐deficient mice were improved by supplementation with oyster extract. Some nutrients contained in oyster extract, such as taurine and glycogen, may be related to the recovery of reproductive function. There were significantly lower serum concentrations of zinc in dams fed a zinc‐deficient diet However, the serum zinc concentration was normal in the oyster extract‐supplemented group. No difference in the concentration of serum zinc was observed between the oyster extract‐ and zinc carbonate‐supplemented groups. From these findings, it is suggested that oyster extract is a useful supplement that can prevent reproductive defects from zinc deficiency, and the bioavailability of zinc may be identical to zinc carbonate.     

Zinc in child health and disease

Zinc deficiency is common in children from developing countries due to lack of intake of animal foods, high dietary phytate content, inadequate food intake and increased fecal losses during diarrhea. Zinc has a fundamental role in cellular metabolism, with profound effects on the immune system and the intestinal mucosa. Zinc supplementation has shown significant benefits in prevention and treatment of diarrhea and pneumonia. Routine zinc supplementation given to low birth weight babies for a year has resulted in substantial reduction in mortality. Zinc deficiency may have adverse effects on physical growth and neurodevelopment. WHO Task Force, 2001, and the National task Force of IAP has recommended use of zinc in the treatment of diarrhea. It is also recommended as part of standard case management in persistent diarrhea and in those with severe malnutrition. Further evidence is required for qualifying its use in treatment of other infective diseases like pneumonia and malaria. Improved dietary quality & intake, food fortification and cultivation of zinc dense plants are some ways of mitigating zinc deficiency.     

Acquired zinc deficiency in a breast-fed premature infant]

Symptomatic zinc deficiency can occur in exclusively breast-fed infants. We report a case in a preterm infant. CASE REPORT: A 3-months-old exclusively breast-fed premature infant presented with peri-orificial and acral eczematoid lesions. Laboratory investigations revealed lowered zinc levels in the infant's serum and in her mother's milk. A rapid healing occurred after oral zinc supplementation. DISCUSSION: Zinc deficiency in breast-fed infants is a rare disease caused by a low level of zinc in mother's milk. The clinical features resemble those of acrodermatitis enteropathica. Oral zinc supplementation is required until weaning.     

Symptomatic zinc deficiency in a premature infant

ABSTRACT. A 3-month-old premature breast fed infant developed symptomatic zinc deficiency manifested by rash identical to that of acrodermatitis enteropathica, diarrhoea, irritability and poor weight gain. Deficient maternal breast milk zinc secretion was demonstrated. This was not related to maternal dietary zinc deficiency and was associated with normal maternal plasma zinc levels. No change in maternal plasma or breast milk zinc occurred with maternal zinc supplementation, suggesting that the aetiology of the low breast milk zinc was a primary defect in mammary gland zinc secretion. A rapid clinical response and return of plasma zinc to normal occurred with oral zinc treatment. Zinc therapy was ceased at 9 months of age without recurrence of symptoms or hypozincaemia. Four similar infants have been reported previously suggesting a common pathogenesis.     

Oral plasma zinc tolerance test in patients with protein energy malnutrition.

Zinc absorption was measured in 37 children with malnutrition using the oral zinc tolerance test (22.5 mg elementary zinc) and the results compared with those of a group of healthy control subjects. The increase in plasma zinc was significantly lower in patients with marasmic kwashiorkor than in the control group. The zinc tolerance test was, however, normal in marasmic patients. We conclude that zinc deficiency occurs in some types of protein energy malnutrition, and that malabsorption may aggravate zinc deficiency. It is reasonable to give higher doses of zinc than are usually recommended during oral zinc supplementation in patients with protein energy malnutrition.