早产儿代谢性骨病

早产儿代谢性骨病是由于体内钙磷代谢紊乱等因素导致的骨矿物质含量的异常,临床表现为类似佝偻病的症状甚至骨折等.早产儿代谢性骨病的病因包括钙、磷、维生素D和相关蛋白摄入不足或代谢异常等.早产是代谢性骨病的最重要的危险因素,代谢性骨病的风险与胎龄及出生体质量均呈负相关.其诊断主要依靠临床表现、影像学表现、生化指标以及骨密度测定.通过合理的营养支持、适度锻炼等可以预防和治疗代谢性骨病.     

早产儿代谢性骨病研究进展

早产儿代谢性骨病为新生儿期重要的慢性疾病,因早产儿钙、磷、维生素D等代谢异常等导致的骨矿物质含量下降,骨小梁数量减少、骨皮质变薄等,严重时可有佝偻病样表现,甚至出现骨折。早产儿的低胎龄和低出生体质量为代谢性骨病的重要危险因素,诊断依靠临床表现、实验室、影像学、超声学等检查。治疗需加强被动运动,补充钙、磷、维生素D,加强预防等。早发现、早诊断、早治疗,可减少代谢性骨病后遗症的发生率,减轻对早产儿的远期影响。     

早产儿代谢性骨病4例

早产儿出生后由于消化道功能极不成熟，发生坏死性小肠结肠炎的风险很高，常常不能顺利地开始胃肠道喂养，而需要较长时间的胃肠外营养支持。胃肠外营养虽然给早产儿提供必要的营养素使其得以存活，但是也可以导致一系列的代谢并发症，给早产儿的脏器功能和生长发育带来严重影响。早产儿代谢性骨病（Metabolic bone disease of prematurity）便是其中之一，该疾病不仅影响婴儿期的生长，而且可以影响成年后的骨骼健康。虽然该疾病并非罕见，但在我国一直未得到重视，国内几乎没有相关报道。随着早产儿胃肠外营养技术在各地的推广，我们认为很有必要对该疾病进行报道，以引起广大新生儿科医师的关注。     

早产儿代谢性骨病防治进展

早产儿代谢性骨病是早产儿常见的并发症,对其生存质量会造成重要影响,甚至增加成年期骨质疏松的风险。早期干预能有效地减少代谢性骨病的发生,改善早产儿预后。该文对早产儿代谢性骨病的防治进展作一综述。     

早产儿代谢性骨病诊治的研究进展

早产儿代谢性骨病(MBD)是由于多种因素引起钙磷代谢紊乱导致骨矿物质含量减少,从而引起临床、生化及骨影像学相关改变,多发生于极低和超低出生体重儿。临床症状通常发生在生后6~12周,主要表现为呼吸困难、长时间依赖呼吸机治疗、佝偻病样表现,严重者甚至骨折。目前MBD主要依赖生化标记物、放射学及超声学等进行诊断。由于早产儿MBD的临床表现发生较晚,故对于高危人群进行早期筛查及预防有重要意义。     

合并骨折的早产儿代谢性骨病临床分析及随访

目的分析合并骨折的早产儿代谢性骨病患儿临床资料及随访情况,为其防治提供指导依据。方法对2009年11月至2013年12月我院新生儿重症监护室确诊合并骨折的早产儿代谢性骨病患儿临床资料进行回顾性分析,包括一般资料、临床表现、辅助检查、治疗、转归及随访情况。结果共确诊5例患儿,均为男性,出生胎龄〈32周,出生体重≤1000 g,3例为小于胎龄儿,3例母亲重度子痫前期或重度子痫。5例均有反复喂养不耐受,胃肠外营养时间≥30天,3例呼吸机辅助通气时间≥20天。发现骨折时间分别为：生后6-7周3例,生后11周1例,生后17周1例;4例表现局部肢体肿胀。X线显示骨折形成,血钙无异常,碱性磷酸酶高于正常,4例血磷低于正常。2例绷带固定,1例双下肢皮牵引、双下肢悬吊位、小儿髋关节吊带固定治疗,1例患侧上肢功能位制动,1例未予特殊处理。随访患儿骨折均愈合良好,肢体对称、活动无明显异常。结论合并骨折的早产儿代谢性骨病多见于男性超低出生体重儿,好发于校正胎龄36~40周,与钙磷储备少、生后早期钙磷摄入不足及应用类固醇激素等药物有关,近期预后良好。     

未成熟儿代谢性骨病

骨质矿物质含量低下(或佝偻病)为低出生体重早产儿的特征。佝偻病生化改变通常可自动恢复。但是,出生体重<1000g的小儿有50%左右可发生骨折、呼吸困难及生长发育障碍。未成熟儿代谢性骨病包括生理性骨质疏松,通过光子吸收比色计所显示的骨矿物质含量低下,生物化学性佝偻病,骨碱性磷酸酶增高伴有X线检查的轻微改变,以及未成熟儿明显佝偻病表现。     

早产儿代谢性骨病—新生儿科和小儿内分泌科诊治现状的全国性调查

目的:研究旨在调查英国早产儿代谢性骨疾病(MBDP)的诊治现状。方法:在英国所有新生儿网络内开展全国性调查,小儿内分泌科医生作为对照也包括在内。加权平均值用于比较筛查和诊断方法的相对重要性(1表示不重要,5表示完全有必要)。结果:53个新生儿病房中69位参与者做出回应。新生儿科医生认为血磷和碱性磷酸酶水平在筛查(加权平...     

Metabolic bone disease of prematurity and secondary hyperparathyroidism

Aim: To illustrate, via case histories, the importance of laboratory investigations for the early diagnosis and management of metabolic bone disease (MBD). Methods: We report three cases of extreme premature infants with MBD. Results: These three infants had several risk factors for MBD of prematurity: very low birthweight, delayed enteral feeds, cholestatic liver disease, intolerance of fortification, the use of glucocorticoids and diuretics. Serum alkaline phosphatase and parathyroid hormone (PTH) were elevated despite relatively normal calcium and phosphate levels. These parameters were corrected with additional supplementation of calcium, phosphate and vitamin D. Conclusions: Infants born extremely prematurely have significant calcium and phosphate depletion by the time they reach full term compared with the normal fetal accretion rate. This is exacerbated if there is poor tolerability to feeds where extra calcium and phosphate could not be added either by additives or via human milk fortifier. Serum calcium and phosphate levels may be normal despite inadequate intake or stores due to the counter‐regulatory effect of PTH. In infants at risk of MBD, testing serum alkaline phosphatase, vitamin D and PTH with calcium and phosphate may assist in the monitoring and management of MBD.     

Metabolic bone disease

Metabolic bone disease results from a complex variety of causes but can generally be divided into conditions that mainly cause osteoporosis and those that result principally in osteomalacia. Some conditions show a mixture of these two states. Investigation of metabolic bone disease should follow a logical progression and a diagnosis can usually be made if this sequence is adhered to. Many of the syndromes resulting in metabolic bone disease are genetic in origin, especially in children, though the commonest form of osteomalacic rickets results from environmental vitamin D deficiency. DNA analysis is often available to confirm the diagnosis. Treatment should be aimed primarily at removing the cause of the metabolic bone disease if possible, but it may be possible only to counteract the effects of the disease rather than achieving a ‘cure’. A multidisciplinary approach to treatment may be required, particularly in the more disabling conditions.     

Screening for Metabolic Bone Disease of prematurity

Metabolic bone disease (MBD) of prematurity remains a significant comorbid condition in preterm, low birth weight infants. As the majority of in utero calcium (Ca) and phosphorus (Phos) accretion occurs during the third trimester, many of these children have inadequate mineral stores and are at risk for deficiencies of Ca and Phos. While fortification of formula has allowed for increased mineral delivery to premature infants, intestinal immaturity prevents optimal absorption. This is compounded by immobilization, delayed establishment of enteral feeds, long term parenteral nutrition and medications that may alter mineral levels. Over time, biochemical changes occur and accompany MBD, with poor bone mineralization during this period increasing the risk for complications such as osteopenia, rickets and fractures. Screening is largely based on risk factors, but despite the 2013 AAP Consensus Statement, there remains significant variation in screening practices across institutions. A combination of laboratory and radiologic testing is often used to diagnose and manage MBD of prematurity, but there exists a lack of consensus on which screening tests and thresholds to use. This is in part related to a lack of normative data and clinical trials for preterm infants, and a result, a lack of evidence-based guidelines on the diagnosis and timing of potential treatment. Biochemical markers, such as serum Phos, alkaline phosphatase (ALP) and parathyroid hormone (PTH), have shown some benefit in the diagnosis of MBD in some studies, but have not always been reproducible. Radiographs may identify different degrees of skeletal changes, but these changes may not be detected until later in MBD development. Other modalities, such as DXA and ultrasound, have also been used, but these may be limited by lack of standards in preterm infants or lack of availability in some centers. Further research, more specifically clinical trials, are needed to determine which combination of tests can detect MBD at its earliest, in order to promote early treatment and prevent short- and long-term complications of MBD.     

Bone disease of prematurity

Bone disease of prematurity is a complication of preterm birth. This article reviews the aetiology, treatment and prevention of bone disease of prematurity. Provision of adequate nutrition including energy, protein, and minerals is required for both treatment and prevention. Screening for bone disease is controversial. While further research is required quantitative ultrasound appears to be a promising tool for screening and monitoring response to therapy. Further research is needed before recommending physical activity to prevent bone disease of prematurity.     

早产儿代谢性骨病临床管理专家共识（2021年）（英文翻译）

早产儿代谢性骨病（metabolic bone disease of prematurity,MBDP）是由于机体钙磷代谢紊乱导致骨矿物质含量减少的全身性骨骼疾病。我国目前对MBDP尚缺乏深入研究和系统认识,在临床管理方面存在很多不规范之处。现基于国内外相关研究,采用证据推荐分级的评估、制定与评价方法（Grading of Recommendations Assessment,Development and Evaluation）,制定MBDP临床管理专家共识,从MBDP的高危因素、筛查/诊断、预防、治疗及出院后随访等5个方面提出推荐意见,旨在为相关从业人员提供 MBDP临床管理的建议,以减少MBDP的发生及改善其近远期预后。