天津市婴幼儿维生素D水平及维生素D补充剂应用现状调查北大核心CSCD

目的对天津市3030例婴幼儿维生素D水平及维生素D补充剂应用状况进行调查,了解本地区婴幼儿维生素D营养状况以及维生素D补充剂应用过程中存在的问题。方法对所有研究对象采用酶联免疫吸附法测定血清25羟维生素D[25（OH）D]水平,将研究对象按年龄分为≤6个月、〉6～12个月、〉12—24个月、〉24—36个月4组,分析比较不同年龄／季节婴幼儿维生素D平均水平的差异。从中选取341例进行家长问卷调查,并测定其血红蛋白（Hb）和血清骨碱性磷酸酶（BALP）水平,比较不同喂养方式、孕周、出生体质量、Hb、BALP与维生素D水平的关系。结果婴幼儿25（OH）D平均水平为（60．24-26．2）nmol／L（12．9—286．0nmol／L）,缺乏率约为36．6％（1109／3030例）。〉24～36个月组维生素D水平为（47．22±21．93）nmol／L,明显低于其他各年龄组,差异有统计学意义（F=50．006,P〈0．01）,秋季维生素D水平为（62．00±27．42）nmol／L,明显高于其他季节,差异有统计学意义（F=2．750,P〈0．05）,早产儿25（OH）D水平为（50．21±18．27）nmol／L,显著低于足月儿,差异有统计学意义（F=12．355,P〈0．01）。维生素D补充剂的应用率为97．1％（331／341例）。结论天津地区婴幼儿维生素D补充剂的应用率虽然很高,但仍存在一定比例维生素D缺乏,这与补充过程中的依从性较差有关,因此加强宣教,提高家长的认知和认同,有效建立孕期及出生后各年龄段维生素D补充剂应用状况及维生素D水平的监测机制,可以考虑纳入现有妇幼保健建设体系中。     

维生素D缺乏和人类疾病

维生素D在人体健康和疾病中具有重要作用。研究表明全球约50％的人口存在维生素D缺乏风险。引起维生素D缺乏的主要原因是日照不足或通过膳食补充减少。维生素D缺乏对健康的损害不仅表现为佝偻病和骨软化症,还与癌症、心血管病、内分泌系统疾病、自身免疫性疾病、神经系统疾病及结核易患性有关。     

血清25-羟维生素D在佝偻病诊断中的应用价值

目的：探讨血清25 羟维生素D［25（OH）D］在维生素D缺乏性佝偻病早期诊断中的意义。方法：检测对照组（73例）、可疑组（45例）和佝偻病组（65例）的血清25（OH）D、钙、磷、碱性磷酸酶浓度,并通过ROC曲线对血清25（OH）D的诊断价值进行评价。结果：对照组、可疑组和佝偻病组的血清25（OH）D水平分别为112±37、83±30和72±31 nmol/L,后两者均显著低于对照组（F=26.174,P0.05）。可疑组和佝偻病组的维生素D缺乏率均显著高于对照组（χ2=33.346, P0.05）。结论：血清25(OH)D水平在可疑及确诊佝偻病的患儿中显著降低,可以反映维生素D的营养状况,适用于佝偻病的早期筛查。     

早产儿维生素D两种补充方案的疗效对比：前瞻性随机对照研究

目的 探讨不同维生素D补充方案对出生胎龄 < 34周早产儿生后第28天维生素D营养状况的影响。方法 将59例2018年10月至2019年10月出生胎龄 < 34周的住院早产儿随机分为肌注组（n=30）和口服组（n=29）。肌注组单次肌内注射维生素D₃注射液（10 000 IU/kg）,口服组口服维生素D₃滴剂（900 IU/d）,持续25 d。采集两组患儿生后48 h内（维生素D₃补充前）及第28天静脉血,检测血清25-羟维生素D[25(OH) D]水平。结果 生后48 h内,59例早产儿维生素D缺乏（≤15 ng/mL）率为78%;两组血清25(OH) D水平及维生素D缺乏率比较差异无统计学意义（P > 0.05）。生后第28天,肌注组血清25(OH) D水平显著高于口服组（P < 0.05）,肌注组维生素D缺乏率显著低于口服组（P < 0.05）,且无维生素D过量或中毒病例。结论 单次肌内注射10 000 IU/kg维生素D₃可显著提升出生胎龄 < 34周早产儿生后第28天血清25(OH) D水平,且能安全并有效地降低维生素D缺乏率。     

早产儿维生素D两种补充方案的疗效对比：前瞻性随机对照研究

目的 探讨不同维生素D补充方案对出生胎龄 < 34周早产儿生后第28天维生素D营养状况的影响。方法 将59例2018年10月至2019年10月出生胎龄 < 34周的住院早产儿随机分为肌注组（n=30）和口服组（n=29）。肌注组单次肌内注射维生素D₃注射液（10 000 IU/kg）,口服组口服维生素D₃滴剂（900 IU/d）,持续25 d。采集两组患儿生后48 h内（维生素D₃补充前）及第28天静脉血,检测血清25-羟维生素D[25(OH) D]水平。结果 生后48 h内,59例早产儿维生素D缺乏（≤15 ng/mL）率为78%;两组血清25(OH) D水平及维生素D缺乏率比较差异无统计学意义（P > 0.05）。生后第28天,肌注组血清25(OH) D水平显著高于口服组（P < 0.05）,肌注组维生素D缺乏率显著低于口服组（P < 0.05）,且无维生素D过量或中毒病例。结论 单次肌内注射10 000 IU/kg维生素D₃可显著提升出生胎龄 < 34周早产儿生后第28天血清25(OH) D水平,且能安全并有效地降低维生素D缺乏率。     

血清维生素D水平与儿童反复呼吸道感染的关系

目的检测反复呼吸道感染(RRI)患儿血清25-羟维生素D3[25-(OH)D3]及IgA水平,并行维生素D(VitD)治疗,探讨VitD营养状况与儿童RRI及免疫功能的关系,为临床治疗提供依据。方法选取2010年10月-2011年4月在本院儿科门诊就诊的RRI患儿60例为病例组。年龄1～6(3.91±2.83)岁;男32例,女28例。将病例组随机分为常规治疗组30例和补VitD组30例,均予抗感染及对症治疗,补VitD组另进行补VitD治疗。随机选取同期到门诊体检的健康儿童30例为健康对照组。受检儿童均晨起空腹抽取静脉血3 mL 2份,离心,分离血清。ELISA法检测其血清25-(OH)D3水平,免疫透射比浊法检测其血清IgA水平,进行组间比较。病例组3个月时复查血清25-(OH)D3及IgA水平。病例组儿童随访6个月,观察并记录呼吸道感染的复发次数。结果1.病例组血清25-(OH)D3及IgA水平显著低于健康对照组,2组比较差异均有统计学意义(Pa<0.01)。2.采用不同的方法治疗后补VitD组25-(OH)D3及IgA水平升高,常规治疗组和补VitD组RRI次数比较差异有统计学意义(P<0.01)。结论 RRI患儿血清25-(OH)D3及IgA水平低于健康儿童,低水平25-(OH)D3与RRI有关,提示对RRI患儿应重视VitD的补充。     

早产儿出生时维生素D水平及影响因素分析

目的分析早产儿出生时维生素D水平及其可能影响因素。方法采集600例早产儿出生24 h内静脉血,检测血清25-羟基维生素D[25(OH)D]水平,并分析早产儿性别、出生体重、出生季节、胎龄,以及母亲的年龄、职业、早孕期体重指数(BMI)、分娩方式及妊娠期并发症等对血清25(OH)D水平的影响。结果早产儿维生素D缺乏、不足、充足的比例分别为42.0%、38.7%和19.3%。夏、秋季出生的早产儿血清25(OH)D水平显著高于冬季(P0.05),维生素D缺乏的发生率显著低于春、冬季(P0.003)。与母亲年龄≥30岁者比较,年龄30岁母亲所生早产儿血清25(OH)D水平显著降低(P0.05),维生素D缺乏的发生率显著增高(P0.017)。与母亲肥胖者比较,超重或体重正常母亲所生早产儿血清25(OH)D水平显著增高(P0.05),维生素D缺乏的发生率显著降低(P0.006)。母亲妊娠合并子癎前期者,其早产儿血清25(OH)D水平显著低于无子癎前期者(P0.05),维生素D缺乏的发生率显著高于无子癎前期者(P0.017)。多因素分析结果显示,冬春季出生、母亲年龄30岁及早孕期BMI≥28 kg/m2为早产儿维生素D缺乏的危险因素(P0.05)。结论早产儿维生素D缺乏发生率较高,有维生素D缺乏高危因素的早产儿生后需尽早补充维生素D。     

新生儿维生素D水平与孕母维生素D水平的关系

目的 探讨新生儿维生素D 水平与孕母维生素D 水平的相关性。方法 2015 年6 月1 日至7月10 日采集102 名足月单胎新生儿脐静脉血及其孕母静脉血,采用同位素稀释超高效液相色谱串联质谱法测定血清25(OH)D 水平。结果 孕母维生素D 不足者39 例(38.2%),缺乏者25 例(24.5%)。新生儿维生素D 不足者27 例(26.5%),缺乏者66 例(64.7%)。不同血清25(OH)D 水平孕母组新生儿25(OH)D 水平差异有统计学意义(P<0.001)。孕母25(OH)D 水平与新生儿维生素D 水平呈正相关(r=0.914,P<0.001)。孕母25(OH)DROC 曲线预测新生儿维生素D 缺乏(≤ 15 ng/mL)的曲线下面积为0.962,95%CI: 0.930~0.994,P<0.001。孕母血清25(OH)D ≤ 27.55 ng/mL 为界值预测新生儿维生素D 缺乏的灵敏度为97.2%,特异度为80.3%。结论 新生儿维生素D 水平与孕母维生素D 水平正相关;孕母维生素D 水平可预测新生儿维生素D 缺乏。     

中国儿童维生素D、钙营养的流行病学资料

“钙缺乏”一直是我国儿科领域热议的课题,有关钙缺乏、维生素D缺乏性佝偻病等的诊断、治疗等方面也一直争论不休。近期随着欧美国家对人群维生素D缺乏研究的兴起,国内相关报道也明显增加。然而,由于检测血清25-羟维生素D［25-（OH）D］受限及缺少简便、可靠的判断人体钙营养的生物学指标,目前我国总体缺乏有效的流行病学资料以全面了解儿童青少年维生素D、钙营养状况。     

佝偻病维生素D受体基因多态性与25-羟维生素D3相关性

目的：研究1~3岁佝偻病患儿中维生素D受体基因多态性FokⅠ位点与佝偻病相关性,初步探讨维生素D受体基因多态性FokⅠ位点在佝偻病发病中的作用。方法：病例组（佝偻病患儿）62例与对照组（正常健康儿童）60例,用ELISA方法检测血清25-羟维生素D3水平,比较两组之间血清25-羟维生素D3水平。用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）检测病例组和对照组维生素D受体基因多态性FokⅠ位点,比较两组之间基因型和等位基因分布频率。结果病例组血清25-羟维生素D3水平较对照组明显降低,差异有统计学意义（9.1±4.1 ng/mL vs 16.1±6.9 ng/mL;P＜0.05）。维生素D受体基因多态性FokⅠ位点病例组FF基因型明显高于对照组（53% vs 25%）,基因型分布频率差异有统计学意义（χ2=10.221,P＜0.05）,病例组F等位基因频率明显高于对照组（73% vs 57%）,等位基因分布频率差异有统计学意义（χ2=7.511,P＜0.05）。结论维生素D受体基因多态性FokⅠ位点与佝偻病有相关性,提示其在佝偻病遗传易感性方面起重要作用。［中国当代儿科杂志,2010,12（7）：544-546］     

Ultraviolet B radiation improves serum levels of vitamin D in patients with cystic fibrosis

Background: Ultraviolet B (UVB) radiation can be used in the prevention and treatment of vitamin D deficiency. Aim: To investigate, in a controlled study of patients with cystic fibrosis (CF), whether regular UVB radiation would improve serum levels of calcidiol during the dark season (October-April). Methods: Thirty patients with mild to moderate disease were included (aged 9-40 y). All patients had cholecalciferol supplementation. One group (15 patients) was given UVB one to three times a week for 6 mo and one group (15 sex- and age-matched patients) served as controls. The radiation source consisted of three TL 12/40W UVB fluorescent lamps. Initial treatment duration was 1 min, subsequently increased by 0.5-1 min/treatment to a maximum of 10 min. Results: The mean initial serum calcidiol levels were 21 ng/ml in the controls and 22 ng/ml in the intervention group. Serum calcidiol levels increased to 44 ng/ml after 8 wk and to 50 ng/ml after 24 wk of UVB radiation; the corresponding serum levels in the controls were 19 and 25 ng/ml, respectively. The mean serum calcitriol levels increased in the treated group and were unaltered in the control group.

Conclusions: UVB radiation was effective in increasing vitamin D levels in patients with CF. The study results imply that UVB radiation is valuable in chronic conditions associated with vitamin D deficiency.     

石家庄市夏季汉族4月龄至14岁健康儿童血清25-羟维生素D和甲状旁腺素的关系

目的探讨汉族儿童青少年夏季血清25-羟维生素D(25OHD)和甲状旁腺素(PTH)水平的关系,以及儿童青少年是否存在PTH进入平台期的血清25OHD拐点值。方法河北医科大学第二医院儿科生长发育门诊于2011年6~8月及2012年6~8月向社会招募4月龄至14岁健康儿童青少年。分为1岁、~3岁、~6岁、~10岁和~14岁组。分别采用酶联免疫法和化学发光免疫分析法测定血清25OHD和全段PTH水平。对血清25OHD与PTH水平的关系分别行直线、二次多项式、指数和对数拟合等,计算血清PTH水平进入平台期的血清25OHD阈值。结果共招募632名健康儿童青少年,男童372名,女童260名。1血清25OHD和PTH水平的中位数(P25,P75)分别为56.7(42.2,76.4)nmol·L-1和2.5(2.0,3.3)pmol·L-1。2血清25OHD与PTH在除~10岁组外的其余年龄组中均呈负相关。3二次多项式回归方程能较好反映血清25OHD和PTH之间的曲线关系。回归方程为PTH(pmol·L-1)=4.2698-0.0352·25OHD+0.0002·25OHD2,R2=0.0684。PTH进入平台期时血清25OHD的拐点值为88 nmol·L-1,对应的PTH值为2.72 pmol·L-1。结论 4月龄至14岁汉族儿童青少年的血清25OHD和PTH水平呈负相关,且理想的血清25OHD水平可能为88 nmol·L-1。     

Effect of combined maternal and infant vitamin D supplementation on vitamin D status of exclusively breastfed infants

Severe vitamin D deficiency in mothers and their breastfed infants is a significant health problem in the Middle East. Supplementation of the breastfed infant alone with the recommended dose of vitamin D may be insufficient in high‐risk population. We investigated the effect of combined maternal and infant vitamin D supplementation on vitamin D status of the breastfed infant. We examined also the effect of supplementation on vitamin D antirachitic activity of breast milk in a subset of mothers. Healthy breastfeeding mothers (n = 90) were randomly assigned to 2000 IU daily (group 1) or 60 000 IU monthly (group 2) of vitamin D₂, and all their infants (n = 92) received 400 IU daily of vitamin D₂ for 3 months. Most infants had vitamin D deficiency – 25‐hydroxyvitamin D [25(OH)D] ≤ 37.5 nmol L^?1– at study entry. Serum 25(OH)D concentrations at 3 months increased significantly from baseline in infants of mothers in group 1 (13.9 ± 8.6 vs. 49.6 ± 18.5 nmol L^?1, P < 0.0001) and group 2 (13.7 ± 12.1 vs. 44.6 ± 15.0 nmol L^?1, P < 0.0001). Maternal and infant serum 25(OH)D concentrations correlated positively at baseline (r = 0.36, P = 0.01) and 3 months (r = 0.46, P = 0.002). Milk antirachitic activity increased from undetectable (<20 IU L^?1) to a median of 50.9 IU L^?1. In conclusion, combined maternal and infant vitamin D supplementation was associated with a threefold increase in infants’ serum 25(OH)D concentrations and a 64% reduction in the prevalence of vitamin D deficiency without causing hypervitaminosis D.     

Low vitamin D status in children with sickle cell disease

OBJECTIVES: To examine vitamin D status in children with sickle cell disease (SCD)-SS and its relation to season and dietary intake. STUDY DESIGN: Growth, dietary intake, 25-hydroxyvitamin D (25-OHD), and parathyroid hormone levels were measured. Children with low and normal vitamin D status were compared. Low vitamin D status was defined as a serum concentration of 25-OHD <27.5 nmol/L. Serum 25-OHD and parathyroid hormone levels were compared among children with SCD-SS and healthy children. RESULTS: Children with SCD-SS (n=65), 5 to 18 years of age, were evaluated. Mean (+/-SD) serum 25-OHD concentration was 25.5 +/- 12.8 nmol/L; 65% of subjects had low vitamin D status. Low vitamin D prevalence was highest during spring (100%). Children with SCD-SS were at higher risk for low vitamin D status than healthy children. Vitamin D intake was lower in subjects with SCD-SS and low vitamin D than those with normal serum vitamin D status (P <.05). CONCLUSIONS: Low serum vitamin D status was highly prevalent in black children with SCD-SS. Vitamin D status was associated with season and dietary intake.     

Early response to vitamin D2 in children with calcium deficiency rickets

OBJECTIVE: To assess the effect of vitamin D(2) administration on serum vitamin D metabolite concentrations in calcium deficiency rickets. STUDY DESIGN: We administered vitamin D(2), 50,000 IU orally to 16 Nigerian children 15 to 48 months of age with radiographically active rickets. We measured calcium and vitamin D metabolites at baseline and at 1, 3, 7, and 14 days. RESULTS: At baseline, ranges of serum 25-hydroxyvitamin D (25(OH)D) concentrations were 18 to 40 nmol/L (7-16 ng/mL), and 1,25-dihydroxyvitamin D (1,25-(OH)(2)D) concentrations were 290 to 790 pmol/L (120-330 pg/mL). After vitamin D administration, serum 25(OH)D and 1,25(OH)(2)D concentrations rapidly rose and peaked at 2.8 and 1.9 times the baseline values (P < .001), respectively, at 3 days. Positive correlations between 1,25(OH)(2)D and 25(OH)D were strongest at day 3 (r = 0.84, P < .001) and weakest at day 14 (r = 0.41, P = .11). The relationship of 1,25(OH)(2)D with 25(OH)D at baseline and the increase in 1,25(OH)(2)D in response to vitamin D were similar to those described in children with vitamin D deficiency. However, unlike the pattern in vitamin D deficiency, 1,25(OH)(2)D remained positively correlated with 25(OH)D after administration of vitamin D. CONCLUSION: Dietary calcium deficiency increases the demand for 25(OH)D above that required in vitamin D deficiency to optimize 1,25(OH)(2)D concentrations. Assessment of vitamin D sufficiency in persons or communities may need to be adjusted for habitual dietary calcium intake.     

A Spectrum of Clinical Presentations in Seven Japanese Patients with Vitamin D Deficiency

Recently, the reemergence of vitamin D deficiency in developed countries has been pointed out. Vitamin D deficiency is diagnosed based on the serum 25-hydroxyvitamin D (25OHD) level. However, its normal range is still controversial, making the diagnosis of vitamin D deficiency difficult. Here, we present seven Japanese patients diagnosed with vitamin D deficiency. Three patients complained of leg bowing, and the other four of tetany. The patients with leg bowing were toddlers. Radiographic surveys demonstrated evidence of rickets. Laboratory findings showed decreased levels of serum inorganic phosphorus and increased levels of alkaline phosphatase (ALP) and intact-parathyroid hormone (iPTH). The serum levels of 25OHD were relatively low, ranging from 13 to 15.2 ng/ml. Of the patients with tetany, three were young infants. Laboratory findings showed decreased levels of serum calcium and increased levels of ALP and iPTH. The serum levels of 25OHD were markedly decreased (below 8 ng/ml). Thus, these results indicate that relatively low levels of 25OHD can cause rickets, a symptom of vitamin D deficiency, and that clinicians should therefore carefully evaluate the levels of 25OHD.     

Parathyroid function in different stages of vitamin D deficiency rickets

Direct measurements of parathyroid activity are available in only small numbers of children with vitamin D deficiency rickets (VDR). Therefore serum immunoreactive parathyroid hormone (iPTH) and the urinary cyclic adenosine-3,5-monophosphate excretion (UcAMP) were measured together with other important indices of calcium metabolism in 24 patients (aged 2–42 months) with VDR before vitamin D treatment. iPTH and UcAMP were significantly elevated in comparison to age-matched controls. In patients there was a highly significant positive correlation between iPTH and UcAMP and a negative relationship between both indices of parathyroid activity to serum phosphate and urine calcium, respectively, indicating that the simple measurement of serum phosphate and/or urine cAMP and Ca provides a reliable tool for the assessment of secondary hyperparathyroidism in VDR. In two patients classified as being in the early stage of VDR the parathyroid activity was not elevated despite hypocalcemia indicating relative hypoparathyroidism.Twelve patients with VDR were followed during vitamin D therapy: Within the first 2 weeks of treatment UcAMP slightly increased and thereafter decreased in most patients, but was still elevated in three patients even after 7 weeks, whereas iPTH became normal within 3 weeks of treatment. This favors the concept that vitamin D deficiency diminishes the activation of renal adenylate cyclase by PTH which is overcome by the highly increased PTH secretion in the advanced stages of rickets.The basal and calcium-stimulated serum calcitonin (CT) levels, determined in some of the patients, were normal, ruling out a significant disturbance of CT secretion in VDR.Dedicated to Prof. Dr. H. Bickel on the occasion of his 65th birthday