储液囊早期埋植引流治疗婴儿晚发性维生素K缺乏性脑室出血合并脑积水

目的探讨晚发性维生素K依赖因子缺乏(delayed vitamin Kdeficiency,DVDH)所致的婴儿脑室出血合并脑积水的治疗方法.方法通过Ommaya储液囊早期脑室埋植反复引流治疗婴儿晚发性维生素K依赖因子缺乏脑室出血合并脑积水8例.结果所有病例在发病后3d内手术,并予持续脑室引流,脑脊液引流量每天30～60ml,共5d,以后每3～4d穿刺Ommaya囊引流脑脊液.3例在术后20d、5例术后6～8周脑脊液检测达正常水平.CT复查,8例患儿脑积水全部较术前好转.10～20月随访,7例患儿生长发育良好,无神经系统异常表现,1例有轻度脑积水交通性脑积水,头围较正常同龄儿上限大1cm,未检得神经系统损害体征.结论;本疗法的手术指征是晚发性维生素K依赖因子缺乏脑室出血早期合并脑积水的婴儿.对降低本病致死、致残率有较大价值.     

储液囊早期埋植引流治疗婴儿晚发性维生素K缺乏性脑室出血合并脑积水

目的:探讨晚发性维生素K依赖因子缺乏(delayed vitamin Kdeficiency,DVDH)所致的婴儿脑室出血合并脑积水的治疗方法。方法:通过Ommaya储液囊早期脑室埋植反复引流治疗婴儿晚发性维生素K依赖因子缺乏脑室出血合并脑积水8例。结果:所有病例在发病后3d内手术,并予持续脑室引流,脑脊液引流量每天30～60ml,共5d,以后每3～4d穿刺Ommaya囊引流脑脊液。3例在术后20d、5例术后6～8周脑脊液检测达正常水平。CT复查,8例患儿脑积水全部较术前好转。10～20月随访,7例患儿生长发育良好,无神经系统异常表现,1例有轻度脑积水交通性脑积水,头围较正常同龄儿上限大1cm,未检得神经系统损害体征。结论;本疗法的手术指征是晚发性维生素K依赖因子缺乏脑室出血早期合并脑积水的婴儿。对降低本病致死、致残率有较大价值。     

维生素K缺乏症引起小儿颅内出血的原因分析及预防

目的回顾分析100例颅内出血患儿出血原因,预防小儿颅内出血,提高对小儿维生素K缺乏症的认识、诊断和治疗,防止后遗症发生。方法分析本院2006-2010年收治的100例维生素K缺乏症引起颅内出血患儿的临床资料。结果治愈35例,死亡20例,因经济原因放弃治疗10例,留有中枢神经系统后遗症35例。结论要充分认识和重视小儿维生素K缺乏症,及早诊断和治疗,不但在新生儿出生时肌注维生素K1,而且还应在孕妇、婴儿及乳母中大力推广口服维生素K1,以补充母乳中维生素K的不足,减少维生素K缺乏症的发病,防止后遗症的发生。     

婴儿晚发性维生素K缺乏症的治疗与健康教育

婴儿晚发性维生素K缺乏症是婴儿期最常见的出血性疾病,以颅内出血多见,该病起病突然,病死率及致残率高,并发颅内出血者存活后多有不同程度的神经系统后遗症,但早期发现、及时治疗可明显减少并发症。本院儿科于2005年1月-2010年1月共收治38例晚发性维生素K缺乏症婴儿,通过对患儿家属加强健康宣教,及时治疗与精心护理,均取得良好疗效,现报告如下。     

晚发型维生素K缺乏症39例临床分析

目的：分析维生素K引起出血性疾病的原因及预防，提高诊治水平，减少发病率及致残率。方法：回顾性分析近8年来的39例婴儿晚发性维生素K缺乏症的临床资料。结果：早期诊断，及时合理治疗，治愈率92．3％，病死率5．1％，后遗症7．7％。结论：维生素K缺乏引起颅内出血死亡率高、致残率高，关键是预防和早期治疗。     

17例婴儿期晚发性维生素K缺乏症临床分析

目的对17例婴儿期晚发性维生素K缺乏症的发病因素、临床特征、预后进行分析.方法分析2000年1月～2005年1月我院17例婴儿期晚发性维生素K缺乏症临床资料.结果17例婴儿期晚发性维生素K缺乏症男女比例1.83∶1(11∶6),母乳喂养15例(88.2%),17例患儿9例为颅内出血(53%),消化道出血10例(58.8%),颅内出血随诊5例,智力异常3例,神经系统后遗症3例.结论婴儿期晚发性维生素K缺乏症以颅内出血为主,预后严重,致残率高,故应早期诊断、早期治疗、早期预防本病.     

母乳喂养中的维生素K缺乏及预防

最近维生素K缺乏及预防再度引起国际学术界的重视,并开展了相应的研究,因为由于维生素K缺乏造成出血在纯母乳喂养儿中占极大比例,此种出血致死率高,后遗症棘手,不仅影响存活儿的生理健康,而且累及日后智力发育和行为发展,引发一系列社会问题,所以,这也是推广母乳喂养、创建爱婴医院必需加以解决的问题.生后2周至1岁的婴儿由于维生素K(Vk)缺乏而致出血称为晚发性Vk缺乏症,1980年日本报告了晚发性婴儿Vk缺乏出血病发生率为1/4000,其中87％的患儿为单纯母乳喂养儿.国内近些年来也有大量病历报道此病.发展中国家此病发生率估计为0.6～3/1000,其中单纯母乳喂养儿占87～98％.     

婴儿迟发性维生素k缺乏致颅内出血的外科治疗

[目的]探讨婴儿迟发性维生素K缺乏致颅内出血的诊断及手术。[方法]针对血肿的部位分采用开颅小骨瓣血肿清除,钻孔血肿外引流,侧脑室穿刺外引流术。[结果]1例放弃治疗,2例术后有轻微抽搐,余患儿治愈出院。无1例死亡。[结论]对迟发性维生素K缺乏致颅内出血的患儿,特别是对出血量较大,病情危重患儿早期诊断,采用积极的手术治疗,术后采取远期综合干预措施,可降低病死率及致残率。     

迟发型维生素K缺乏致颅内出血54例临床分析

目的:探讨迟发型维生素K缺乏致颅内出血的发病原因。方法:对54例迟发型维生素K缺乏致颅内出血患儿的临床资料进行回顾性分析。结果:该病患儿年龄2周～3个月,均为母乳喂养史后未及时给予维生素K,突然发病呈进行性加重,面色苍白、甚至抽搐乃至昏迷,严重者可出现脑疝表现,头部CT显示颅内出血。轻者给予维生素K1后出血停止,并辅以止痉、降颅压等对症治疗预后良好。重者因并发多脏器功能衰竭死亡,幸存者遗留后遗症。结论 :维生素K缺乏症是由于维生素K缺乏而引起的凝血障碍性疾病,迟发型维生素K缺乏症所致的颅内出血症状重,死亡率高,幸存者遗留神经系统后遗症(脑发育不良,癫痫、语言落后等)。     

晚发型维生素K缺乏出血患儿颅内血肿的微创外科治疗

晚发型维生素K缺乏性出血（vitaminKdeficiencybleeding，VKDB）致婴儿颅内血肿发生率为92．09／6，致死率约为22．0％，致残率为67．5％。随着神经外科手术技术的不断进步和方法的改进，神经外科微创手术可有效清除晚发型VKDB患儿颅内血肿，降低患儿病死率、减轻神经系统后遗症、改善患儿生活质量。对晚发型VKDB患儿颅内血肿神经外科微创手术适应证的选择及手术时机的掌握，迄今尚无统一标准。现将本院对晚发型VKDB患儿颅内血肿神经外科微创手术治疗结果，分析报道如下。     

小儿维生素K缺乏致颅内出血的临床特点及诊治方法探讨

[目的]了解小儿维生素K缺乏致颅内出血的临床特点,探讨其诊治方法,提高临床治愈率。[方法]选择2007年1月～2010年12月收治的43例维生素K缺乏致颅内出血患儿的病案资料,对其临床表现、影像学特点、实验室检查、诊断方法、治疗方案进行回顾性分析总结,依据临床症状,采用手术治疗的患儿18例,采用药物保守治疗的患儿25例。[结果]不同治疗方案的患儿总体愈合情况,手术治疗组中,遗留后遗症或死亡1例(5.6%),好转11例(55.6%),痊愈7例(38.9%);保守治疗组中,死亡1例(8.0%),好转18例(68.0%),痊愈6例(24.0%)。幕上出血﹥15ml时不同治疗方案的患儿愈合情况,手术治疗组中,遗留后遗症或死亡1例(7.7%),好转7例(53.8%),痊愈7例(38.5%);保守治疗组中,死亡2例(28.6%),好转4例(57.1%),痊愈1例(14.3%)。[结论]小儿维生素K缺乏致颅内出血的患儿发病较急,临床应依据症状采取及时有效的抢救方案,减少后遗症的发生率。     

Vitamin K deficiency bleeding in an infant despite adequate prophylaxis

Vitamin K deficiency in infants can cause life-threatening haemorrhages. To prevent this, neonates in the Netherlands receive an oral dose of 1 mg vitamin K directly after birth. In addition, because breast milk contains little vitamin K, breast-fed infants receive a daily dose of 25 micrograms the first three months. Of three female infants aged 4 weeks, 5 months and 3 months, respectively, two developed an intracranial haemorrhage, which caused death in one. In two cases there were signs of a bleeding tendency, but no tests were done because the patients appeared healthy otherwise. The underlying resorptive disorders, cholestasis and fat malabsorption, caused few symptoms and were discovered only after a vitamin K deficiency bleeding had occurred. In an infant with a bleeding tendency, one should consider the possibility of vitamin K deficiency, even if adequate prophylaxis has been given.     

Prothrombin and acarboxyprothrombin activity in neonates after oral and intramuscular administration of vitamin K

The effect of prophylaxis with oral or intramuscular vitamin K1 (Konakion) on the hypoprothrombinaemia and on the rate of detectable acarboxyprothrombin of full-term newborns was investigated. Factor II clotting activity, factor II activity by Echis carinatus venom, factor II protein concentration and acarboxyprothrombin were determined in four groups of breast-fed infants. In the untreated group and in the group where the babies received vitamin K1 orally at birth the factor, II clotting activity was decreased and the rate of acarboxyprothrombin positive cases was increased significantly (from 30% and 28% to 55% and 52% respectively) at the 3d and 5-7th days of age. By the other two groups where 1 mg vitamin K1 was given intramusculary or 2-3 mg vitamin K1 was given orally with the first milk-feed, the factor II clotting activity increased at 3d and 5-7th days of life. In these groups the rate of acarboxyprothrombin positive babies was reduced at 3d day of life from 36% and 35% (cord blood values) to 16% and 13% respectively, and there was found acarboxyprothrombin in none of the babies at 5-7th days of life. These findings support that vitamin K1 given orally at birth is ineffective to prevent vitamin K deficiency, but when it was given with the first feed orally to well, mature babies it seems to be enable to protect the early haemorrhagic disease of the newborns.     

晚发性维生素K缺乏伴颅内出血30例分析

目的探讨晚发性维生素K缺乏伴颅内出血的影响因素及防治情况。方法回顾性分析我院2005年11月—2009年2月收治的30例晚发性维生素K缺乏伴颅内出血患儿的临床资料。结果晚发性维生素K缺乏伴颅内出血的发病与性别、年龄无关（P〉0.05）,与母乳喂养、腹泻、使用抗生素和肝功能异常有关（P〈0.01）。本组28例治愈出院,2例放弃治疗死亡。结论针对晚发性维生素K缺乏伴颅内出血发病的影响因素进行预防,减少发病率;一旦发病,在使用维生素K止血的同时进行输血及对症处理,预后较好。     

维生素K和钙对去卵巢大鼠骨质疏松的影响

切除雌鼠双侧卵巢以造成骨快速丢失作为模拟女性绝经后骨质疏松症的动物模型,从骨计量学、骨生物力学等方面综合观察单纯补充维生素Ｋ（９０ｍ ｇ／ｋｇ）、钙（５ｇ／ｋｇ）及两者联合作用６个月对骨丢失的影响。结果发现：与正常对照组（Ａ）大鼠相比,模型对照组（Ｂ）大鼠骨量显著减少,骨脆性增加。与模型对照组相比,单纯补充维生素Ｋ组（Ｄ） 股骨中点骨密度值显著提高,股骨干骺端及腰椎骨密度、股骨近侧端矿物质含量都有增高趋势,表明补充维生素Ｋ 可在一定程度上减少骨丢失;同时补充维生素Ｋ及钙组（Ｅ）股骨的最大挠度与最大应变值,与模型对照组相比也有增高趋势,表明补充维生素Ｋ可提高骨的柔韧性,改善股骨的力学性能。综合骨计量学与骨力学观察结果,发现各种实验措施对密质骨的效果皆优于松质骨,并且维生素Ｋ与钙的联合作用效果优于单纯补充维生素Ｋ 或钙。本实验结果提示：绝经后妇女,作为骨质疏松危险人群,增加膳食维生素Ｋ 与钙的摄入是有帮助的     

牛磺酸及微量营养素对人体夜视功能的影响

目的　研究补充适量牛磺酸、VA、B族维生素、Zn、Se等微量营养素对低照度作业人员夜视功能的改善作用。方法　低照度作业成年男子 34人 ,年龄 1 8～ 2 9岁 ,分为实验组和对照组 ,实验组人员每天加服一定剂量牛磺酸及多种微量营养素。实验期限为 4wk,分别在服药前、服药 2 wk、服药 4wk和停药 3d检测受试人员快速暗适应时间、微光近视力 ,并测定暗适应恢复曲线。结果　服用牛磺酸和多种复合微量营养素制剂 2 wk后 ,微光近视力和快速暗适应功能即大幅度提高 ,服用 4wk后效果更佳 ,同时暗适应恢复曲线明显下移 ,绝对阈值降低。另外 ,停药 3d后 ,微光近视力并未降低 ,表明良好的营养贮备对维持夜视功能具有重要意义。结论　适当补充牛磺酸和 VA、B族维生素、VC、微量元素 Zn、Se能有效提高低照度作业人群夜间视力     

Effects of Combined Vitamin K2 and Vitamin D3 Supplementation on Na[18F]F PET/MRI in Patients with Carotid Artery Disease: The INTRICATE Rationale and Trial Design

INTRICATE is a prospective double-blind placebo-controlled feasibility study, assessing the influence of combined vitamin K2 and vitamin D3 supplementation on micro-calcification in carotid artery disease as imaged by hybrid Sodium [¹⁸F]Fluoride (Na[¹⁸F]F) positron emission tomography (PET)/ magnetic resonance imaging (MRI). Arterial calcification is an actively regulated process and results from the imbalance between calcification promoting and inhibiting factors. Considering the recent advancements in medical imaging, ultrasound (US), PET/MRI, and computed tomography (CT) can be used for the selection and stratification of patients with atherosclerosis. Fifty-two subjects with asymptomatic carotid artery disease on at least one side of the neck will be included in the study. At baseline, an Na[¹⁸F]F PET/MRI and CT examination will be performed. Afterwards, subjects will be randomized (1:1) to a vitamin K (400 µg MK-7/day) and vitamin D3 (80 µg/day) or to placebo. At the 3-month follow-up, subjects will undergo a second Na[¹⁸F]F PET/MRI and CT scan. The primary endpoint is the change in Na[¹⁸F]F PET/MRI (baseline vs. after 3 months) in the treatment group as compared to the placebo arm. Secondary endpoints are changes in plaque composition and in blood-biomarkers. The INTRICATE trial bears the potential to open novel avenues for future large scale randomized controlled trials to intervene in the plaque development and micro-calcification progression.     

晚发性维生素K缺乏致颅内出血62例临床分析

目的:对晚发性维生素K缺乏致颅内出血患儿的临床诊治进行分析,并探讨防治措施。方法:对2002年1月～2006年12月期间我科收治的62例晚发性维生素K缺乏致颅内出血患儿的临床资料进行汇总、分析。结果:62例患儿中,治愈36例,好转16例,放弃6例,死亡4例。对存活者中26例进行随访6个月～5年,17例存在不同程度后遗症。结论:晚发性维生素K缺乏致颅内出血是小儿死亡和致残的主要因素,早期诊断,早期治疗,减少误诊,加强预防,对提高治愈率,降低发病率,减少后遗症,有重要的临床意义。     

Total body phylloquinone and its turnover in human subjects at two levels of vitamin K intake

The aims of this study were to determine the total body phylloquinone and its metabolic turnover in human subjects using a tracer dose of [5-H3]phylloquinone containing 4 MBq/mmol. Seven subjects aged 22 to 49 years were given 0.3 microg isotopic phylloquinone intravenously on a control diet (75 microg phylloquinone/d) and blood, urine and faeces were sampled periodically for 6 d. Five of these subjects were studied a second time after 3-8 weeks on a low-vitamin K diet (8 microg/d). The changes in the radioactivity of plasma phylloquinone with time were analysed by the method of residuals and fitted to a curve composed of two exponential components. The size of the exchangeable body pool was calculated by isotope dilution. Plasma phylloquinone levels fell during vitamin K restriction but the vitamin K-dependent coagulation factors did not change. After injection the first exponential decay curve t1/2 was 1.0 (sd 0.47) h in the subjects on the control diet and 0.49 (sd 0.27) h after vitamin K restriction. On the control diet, the second exponential t1/2 was 27.6 (sd 124) h that did not change on the low-vitamin K diet ( (sd 13.5) h). These results indicate that the turnover time for phylloquinone in human subjects is about 1.5 d. Urinary excretion of 3H-metabolites ranged from 30 % of the administered dose on the control diet to 38 % on the restricted diet and had the same turnover rate as the second component of the plasma decay curves. The exchangeable body pool of phylloquinone declined from about 1.0 microg/kg before restriction to lower values after vitamin K restriction. The faecal excretion of phylloquinone and its metabolites fell from 32 % of the administered dose on the control diet to 13 % on the restricted diet.