【精品】维生素ad胶丸42

【精品】维生素ad胶丸42 维生素AD胶丸 、适应症:1、治疗佝偻病和夜盲症。2、治疗小儿手足抽搐症。3、预防2 和治疗维生素A和D缺乏症 。 4、每种成分的名称和数量: 规格 物料名称 植物油(kg) 滴丸胶(kg) 6、生产方法:(见如下生产工艺流程) 7、质量控制的管理体制理路径和条件:(见如下生产工艺流程) 工艺流程图 维生素A、维生素D、植物油明胶、甘油、纯化水2 品名、外观、数量QAQA品名、外观、数量 配油溶胶 QCQA含量水分、粘度 滴丸 QA胶丸外观、含油量、含胶量 定型 温湿度 洗丸 面清洁度 干燥 温湿度 整理图例QA胶丸外观 物料QC胶丸丸重差异、含量、胶皮水分 洁净度工序内包装材料内包装物料走向与工序衔接QA数量、外观 质量检验QC与控制QA 外包装材料外包装 中间品存放QA文字内容品名、批号、数量 质量数量300 000级洁净区成品、入库 8、剂型:胶丸剂 9、副作用:尚无数据 10、禁忌症:慢性肾衰竭、高钙血症、高磷血症伴肾性佝偻病患者禁用。 11、不良反应:按推荐剂量服用，无明显不良反应。 12、服用过量时所需用的解毒剂:催吐，泻药，弱碱性食品、饮料。 13、致畸性: 维生素A ?动物实验:视黄醇对实验动物有致畸性，各类动物的易感性按下列顺序 依次增加:大小鼠、仓鼠、猴和兔。对大鼠、猴和兔的最低致畸剂量分别为35000、6000和2500μgRE/(kg?d)。这种致畸作用于合成的类胡萝卜素对人体的致畸性很相似，如无脑儿，脊柱裂，唇裂，腭裂，眼睛过小，眼睛、牙齿、涎腺和主动脉弓的畸形，心室间隔缺损，肛门闭锁，脐膨出，肾缺如，多囊肾，肾盂积水 ，短肢畸形，指(趾)畸形，生殖器、垂体、甲状腺、胸腺、头颅、脊椎、肋骨和肌肉的某些缺陷以及内脏错位。暴露剂量》3000μgRE/(kg?d)时，F344大鼠出现永久性学习能力丧失。 维生素A对动物致畸性的研究资料如下: 1997a，b)、Wiegand等人(1998)和Miller等人(1998)Hendrickx等( 报道了一项致畸性研究，在孕早期(孕16-27d)分别给予猕猴口服剂量为0、2250、6000、12000和24000μgRE/(kg?d)的视黄基棕榈酸后发现摄入量与流产和畸形的发生率呈剂量相关性递增关系。剂量在6000和24000μgRE/(kg?d)时畸形的发生率分别为1/21和5/11(中间剂量未作报道)。更高的剂量对发生于颅神经嵴的结构产生影响。这些畸形类似于在猴和人体中观察到的由异维甲酸(13-顺-视黄酸)引起的畸形，但其症状又略有不同，后者颅面部畸形的发生频率更高、甲状腺和心脏的缺陷较轻并且不引起脑部畸形，同时还观察到对母体的毒性。 ?人群研究:对人体的致畸性方面，异维甲酸是一种已知的人体致畸剂。因此发育毒性对维生素A的危险度评价很关键。与维生素A有关的出生缺陷已有许多报道。但只有一个病例的维生素A暴露剂量小于7500μg/d。1990年以来，已有7项流行病学研究(5项病例对照研究和两项前瞻性研究)。其中的4项未能发现维生素A的暴露剂于出生缺陷的关系，而另外3项研究在不同的剂量水平发现有致畸作用。 维生素 D 尚未证实维生素D在体内或体外有致畸性。 14、每种成分的分析方法:化学 本品系取维生素A与维生素D或维生素D,加鱼肝油或精炼食用植物油(在 23 0?左右脱去固体脂肪)溶解并调整浓度后制成。每丸含维生素A应为标示量的 90.0,,120.0,;含维生素D应为标示量的85.0,以上。标签上应注明本品含维生素D或维生素D。 23 【性状】 本品内容物为黄色至深黄色油状液。 【鉴别】 (1) 取本品内容物，加三氯甲烷稀释成每1ml 中含维生素A10,20单位的溶液;取1ml,加25,三氯化锑的三氯甲烷溶液2ml ，即显蓝色至蓝紫色，放置后，色渐消褪。 (2) 照高效液相色谱法(附录? D)测定。用十八烷基硅烷键合硅胶为填充剂;以甲醇,乙腈(3:97)为流动相;检测波长为254nm。取等量维生素D、D混合液23各约相当于5,10个单位的对照品溶液注入液相色谱仪，调节流动相比例，分离度应大于1.0。取维生素D测定法(附录? K)中的供试品溶液B或收集定量分析柱系统中的维生素D流出液，用无氧氮气吹干，加流动相少许溶解后，注入液相色谱仪，色谱图，供试品溶液中应有与对照品溶液相应的维生素D 或2D主峰相同保留时间的色谱峰。 3 【检查】 应符合胶囊剂项下有关的各项(附录? E)。 检验项目 单位 限度 崩解时限 分钟 ?60 装量差异限度 % ?10 细菌数 (个/g) ?1000 霉菌，酵母菌数 (个/g) ?100 大肠埃希菌 (个/g) 不得检出 【含量测定】 维生素A 取装量差异项下的内容物，照维生素A测定法(附录? J)测定，根据每丸内容物的平均装量计算，即得。 维生素D 取装量差异项下的内容物，照维生素,测定法(附录? K)测定，即得。采用维生素D 或D对照品应与标签所注的相符。 23 16、毒理学数据资料: 维生素A ? 急性毒性:维生素A急性毒性的症状包括腹痛、厌食、呕吐、视觉模糊、易激怒、头痛以及新生儿和婴儿囱门突起。发生急性毒性的剂量成人和儿童分别远大于100000μgRE和10000μgRE。小于6个月的婴儿在一次剂量为 7500-15000μgRE即可产生急性毒性，而大一些的婴儿(6个月和9个月)能耐受30000μgRE这一剂量。 ?慢性和亚慢性毒性:慢性毒性的症状包括皮肤干燥、增厚，嘴唇干裂，结膜炎，红色斑疹，脱发，骨密度下降，骨关节疼痛，慢性头痛，颅内高压和肝脏毒性。中毒症状的出现和严重程度随剂量、时间的长短和症状本身的不同而不同。对眼镜、骨骼和肝脏的破坏作用可能是永久性的，而其他许多症状是可逆的。成人的慢性毒性作用发生于数周、数月或数年的补充剂量>7500-15000μgRE/d.但也有病例的毒性作用发生于较低剂量1500-3000μgRE/d.慢性毒性作用的阈值的制定受已患疾病、酗酒、治疗药物以及膳食摄入量不明等因素的影响。维生素A严重不耐受有遗传因素的作用，但具体的代谢缺陷尚未阐明。 流行病学资料表明，当膳食视黄醇的摄入量>1500μg/d时,绝经后妇女髋骨骨折的发病危险性(比膳食视黄醇的摄入量为500μg/d时)增加了一倍.其他支持这一观点的流行病学研究表明北欧国家,尤其是斯堪的纳维亚地区髋骨骨折的发病危险性较高,而这一地区膳食视黄醇的摄入量也较高.瑞典男性髋骨骨折的发生率高于英国和瑞士女性. 在β-胡萝卜素视黄醇功效研究(CARET)实验中,每天联合补充7500μg视黄醇和 30000μgβ-胡萝卜素可导致男性吸烟者以及男性石棉行业工人肺癌发生率的增大.这一研究以及ABTC研究表明这一作用是有β-胡萝卜素产生的。一项对接触蓝石棉的工人的化学保护研究发现，512个每日服用7500μgRE的对象中有45人因为发生相关的头痛而改变治疗。与异维甲酸组和对照组相比，每天给与7500μg视黄醇的研究对象皮肤癌的发生率中度增大。在化学预防研究中，每日给予肺癌和头颈部癌症患者90000μgRE的视黄基棕榈酸一年后，下一年每天给与45000μgRE，结果对45%的人有副作用，包括皮肤干燥、瘙痒、出血和毛发脱落。 维生素D 过量摄入维生素D可导致高钙血症和高钙尿症。维生素D促使钙的吸收和骨骼的重吸收，引起钙在软组织中的沉积、弥散性骨矿丢失以及不可逆的肾脏和心血管毒性。由于肉芽肿组织中的维生素D可无限制地转化为其活性形式，所 以结节病患者对维生素D异常敏感。虽然结节病并不常见，但如果患者补充维生素D的话会产生潜在危险性。 有研究提示，中等剂量的维生素D可增加易感者肾结石的形成。 缺少对维生素D2和维生素D3的人体毒性进行比较的资料。 许多补充试验报道维生素D的摄入量在0.010~0.045mg/d时没有不良作用。更高剂量时的作用差别较大。比如，给予63名老年人(女性大于60岁，男性大于65岁)补充剂量为0.05mg/d的维生素D(未说明剂量)6个月后，2人发生高钙血病(Johnson等人，1980)。但在另一项为期5个月的研究中，给予61名成年人(平均年龄41岁)补充剂量为0.10mg/d的维生素D3，其血清钙没有显著增加(Vieth等人，2001)。这种差异可能反映了老年人在干预前已发生甲状旁腺功能亢进症或维生素D缺乏症。 17、临床数据资料: 维生素A 数百年前，人们已经将夜盲症、干眼病于感染性疾病的发病率和死亡率联系在一起;20世纪30年代，维生素A作为一种抗感染维生素得到了广泛的研究和应用。维生素A缺乏时，不同组织中核受体的配体构成方式发生了改变，表现出多层次的免疫功能损伤。在黏膜免疫水平，维生素A缺乏不仅使 眼、呼吸道、胃肠道以及泌尿生殖道黏膜上皮的完整性受到破坏，而且也会使局部分泌型IgA的水平下降。近年来，临床和群体试验表明:幼儿补充维生素A能显著降低各种原因导致的疾病发生率和死亡率。 1.儿童病毒感染 维生素A已被试用于儿童不同种类的病毒感染，例如麻疹、呼吸道合胞病毒感染(Respiratory Syncytial Virus)、水痘和艾滋病。12项研究综述表明:维生素A能预防上述病儿死亡，应当广泛使用。国内有人报道，血清维生素A水平低与儿童好发肺炎、腹泻等疾病有关，补充维生素A可预防和辅助治疗消化道、呼吸道感染性疾病。 2.糖尿病 糖尿病患者易出现维生素A缺乏。有人报道:补充维生素A可改善糖尿病患者的血糖控制。糖尿病患者应按遗嘱决定是否补充维生素A制剂。 3.皮肤疾病 维生素A已被试用于各种皮肤疾病，包括痤疮、牛皮癣、酒糟鼻、脂溢性皮炎、湿疹，但其疗效不是很大。一般来说，要到接近中毒剂量，才能获得良好疗效。 4.月经过多 有人报道:月经过多的女性每日摄入25000IU维生素A可减少月经量。但这不能作为长期持续治疗，因为停经的妇女一旦怀孕，高剂量维生素A就可能导致胎儿畸形。 5.艾滋病 有人报道:摄入较高剂量的维生素A6~8年可能对艾滋病病人有益，但摄入超过20268IU/d的患者，其降低艾滋病危险性和死亡率的效果反而下降。 6(缺铁性贫血 最近的研究发现，维生素A缺乏而铁充足的膳食也会导致缺铁性贫血。人群干预实验也证实，单独补充维生素A或同时补充铁均可改善贫血，但两者同时补充效果最好。 7.眼结膜和角膜病 维生素A可维持角膜结膜上皮细胞的正常分化和完整性，已广泛应用于临床。最近国内有人采用维生素A滴眼液治疗角膜病变，取得了良好的疗效。 维生素D 1. 佝偻病 1989年吴光驰和1990年李同等报道:由于婴幼儿身体快速生长、维生素D的需要量相对增加。在我国南方每日提供维生素D350IU可预防婴幼儿佝偻病，而北方需要提供550IU。1995年Guillemant等发现:7月份儿童的25-(OH)D3 29.96μg/L?7.46μg/L明显高于3月份的6.61μg/L?2.04μg/L(0.0001),结果提示:季节会造成维生素D亏空，应注意额外补充。 2.骨质疏松症 1993年Komar等报道:86%的养老院老人血25-(OH)D低于50mmol/L,85%3 老人骨矿含量示骨质疏松。1997年Dawson-Hughes等发现:维生素D缺乏可增 加髋骨骨折发生率。多项研究表明:适当增加维生素D摄入量(400~800IU/d)，可降低骨质丢失及骨折发生率。1992年Chapuy等给1634例妇女每日服维生素D800IU和钙1200mg，对照组1636例服安慰剂，共18个月。结果表明:补充组的骨密度上升2.6%，而对照组下降4.6%(P<0.001);补充组髋部骨折数比对照组减少43%(P=0.043);补充组非脊椎骨折总数比对照组减少32%(P=0.015)。 3.骨软化病 1981年Brooke等报道:给孕妇补充维生素D400IU/d,可以降低母体骨软化病、新生儿低钙血病和手足搐搦的发生率。1994年Alexande等调查结果表明:素食者，特别是蔬食者的维生素D摄入明显低于杂食者。1992年Finch等已发现:15例骨软化病人和13例接近骨软化病人中，大部分是印度素食者。1988年Fonseca等认为:素食者，即使无症状，也应该额外补充维生素D。 4(癌症 多项研究表明:维生素D可能有助于对乳腺癌、结肠癌、胰腺癌、前列腺癌的预防。 5.多囊性卵巢综合征 一项初步的研究表明:补充含有维生素D的钙剂可能有益于预防多囊性卵巢综合征。 6、牛皮癣 维生素D可能用来治疗牛皮癣。丹麦的一项研究推荐使用维生素D3的衍生物calcipotrol用来治疗牛皮癣。 7.糖尿病 近几年的基础研究发现，胰腺中有维生素D受体和维生素D依赖性钙结合蛋白，维生素D缺乏可引起胰岛素分泌减少，且维生素D受体基因多态性与I型糖尿病有关。维生素D有免疫抑制因子样作用，可抑制淋巴细胞增殖和细胞因子的产生。英国科学家发现，I型糖尿病的发生于维生素D缺乏及佝偻病的发生相关。维生素D在某种程度上可抑制针对胰腺β细胞的自身免疫反应。亦有研究发现，大剂量维生素D可能于高胰岛素血症及胰岛素抵抗有关。 8.冠心病 最近的一项研究结果显示，65岁以上妇女服用维生素D，其冠心病死亡危 险性比未服用者低1/3。早期的研究提示，血清维生素D水平降低，在冠心病动 脉粥样斑块的钙化中起一定作用。骨质疏松症妇女死于心血管的危险大于无骨质 疏松症者。事实上，在骨质疏松症妇女，钙在其血管壁的沉积率大于正常骨质妇 女。导致骨钙丢失和动脉粥样斑块的钙化可能属于同一生理过程。当然，研究者 也同时指出，提倡补充维生素D防治冠心病之前尚有大量工作要做。 Vitamin A & D Soft Capsules 2. Indications: 1. For the treatment of rickets and nyctalopia 2. For the treatment of child tetany 3. For prevention of vitamin A and D deficiency diseases 4. Components and their contents Specification Components Vegetable oil (kg) Gel for dropping pills (kg) 6. Methods of production (as shown in the following production process) 7. Pathway and condition of quality management system (as shown in the following production process) Flow chart of process 8. Formulation: soft capsules 9. Side effect: (No data available) 10. Contraindications: chronic renal failure, hypercalcemia, hyperphosphatemia associated with renal rickets 11. Adverse reactions: No obvious adverse reaction will occur if it is taken according to the suggested dose. 12. Antidote for overdose application: emetic, cathartic, alkalescent foods and beverages. 13. Teratogenicity Vitamin A ? Zoopery: Retinol has a teratogenic effect on laboratory animals. The susceptibility of animals in an ascending order is as follows: rat and mouse, hamster, monkey and rabbit. The minimum teratogenic dose for rat, monkey and rabbit is 35000, 6000 and 2500μgRE/ (kg?d) respectively. This teratogenic effects on laboratory animals are very similar to those on human body caused by carotenoid, including anencephalus, spina bifida, cheiloschisis, cleft palate, microphthalmia, malformation of eyes, teeth, salivary glands and aortic arch, ventricular septal defect, anal atresia, omphalocele, renal agenesis, polycystic kidney, hydronephrosis, phocomelia, abnormality of finger (toe), some defects of genital organ, pituitary, hyroid glands, thymus glands, skull, spondyle, rib and muscle, and transposition of t viscera. Permanent learning incapacitation would occur to Rat F344 exposed to over 3000μgRE/ (kg?d). The teratogenic effect of VA on animals is summarized as follows: Based on a teratogenic research reported by Hendrickx et al (1997a, b), Wiegand et al (1998) and Miller et al (1998), for Rhesus monkey at the early stage of pregnancy (16-27 d) administered with 0, 2250, 6000, 12000 and 24000μgRE/(kg?d) of retinoic palmic acid respectively through oral taking, the occurrence rate of abortion and abnormal embryos is progressively raised with the dose administered rises. The occurrence rates of abnormal embryos are 1/21 and 5/11 respectively at the dose of 6000 and 24000μgRE/(kg?d) respectively (that at the medium dose is not reported). A higher dose would exert an influence on the structures developed in cranial neural crest. These deformities are similar to those observed in monkey and human embryos caused by isotretinoic acid (13-cis-retinoic acid), but the symptom is slightly different. In the latter, the occurrence rate of facies dysmorphosis is higher, defects in thyroid gland and heart are not so serious and head dysmorphosis won’t be caused; meantime, toxicity to mothers is detected. ? Human population-based studies: Isotretinoic acid is a known human teratogenic agent, therefore its toxicity to the development is critical for assessing the risk of VA. Many birth defects related to VA have been reported, but only in one case, the exposure dose of VA is less than 7500μg/d. Seven epidemiological researches (5 case control researches and 2 prospective researches) have been done since 1990, among which 4 researches did not reveal the relationship between VA exposure dose and birth defect and other 3 researches revealed the teratogenic effect at different doses. Vitamin D The teratogenic effect of VD hasn’t been verified both in vivo and in vitro. 14. Analytical method of ingredients: chemical To make this product, VA and VD or VD are dissolved in cod-liver oil or refined 23 vegetable oil (solid fats have been removed at around 0?), and then the concentration is modulated. The content of VA in one pill is 90.0%~120.0% of the labeled quantity, and that of VD is more than 85.0% of the labeled quantity. The label should indicate whether this product contains VD or VD.23 [Characters] This product is a yellow to deep yellow oily liquid. [Identification] (1) Take out the content of this product, dilute it with chloroform to get a solution whose VA concentration is 10~20U/ml, and then add 2ml of 25% antimony chloride (diluted with chloroform) to 1ml of the above solution; the color of the solution becomes blue to blue violet, and then fades after standing.. (2) High performance liquid chromatography (see appendix VD). Octadecylsilane bonded silica gel is used as filler, methanol- acetonitrile (3:97) as mobile phase, and detection wavelength is set to 254nm. Inject the intermixture of VD and VD 32 (their quantities are the same and each amounts to 5~10 units in the control solution) into high performance liquid chromatograph, modulate the proportion of mobile phase, and make sure that the resolution is more than 1.0. Take test solution B shown in VD assay method (appendix ? K) or collect VD effluent in quantitative column system, dry it with nitrogen (free of oxygen), add a little mobile phase to dissolve it, inject it to the liquid chromatograph, and then record the chromatogram. At the same retention time, in the sample solution there should be chromatographic peaks of VD or VD corresponding to the peak of VD or 232 VDin the control solution. 3 [Examination] The requirement under Inspection item should be met (appendix ? E). Inspection item Unit Limit Disintegration time minute ?60 Content uniformity % ?10 Bacterial count (Number/g) ?1000 Mold and yeast count (Number/g) ?100 Escherichia coli (Number/g) Should not be detected [Content determination] Vitamin A Take out the content under the item of Content uniformity, determine it according to VA assay method (appendix ? J), and the average of contents in each pill is regarded as its content. Vitamin D Take out the content under the item of Content uniformity, and determine it according to VD assay method (appendix ? K). VD or VDused in the control should coincide 23 with that labeled on the tag. 16. Toxicological information Vitamin A ? Acute toxicity: symptoms of acute VA toxicity include bellyache, anorexia, vomiting, blurring of vision, fussiness, headache, and fontanel protuberance of neonate and baby. The dose that may cause the acute toxicity is much more than 100000μgRE and 10000μgRE for adult and child respectively. Single dose of 7500-15000μgRE may lead to acute toxicity to babies under six months. A little elder baby (six or nine months old) may tolerate the dose of 30000μgRE. ? Chronic and subchronic toxicity: The symptoms of chronic toxicity include dry skin, skin thickening, chapped lips, conjunctivitis, red maculae, hair loss, decline of bone density, arthrodynia, chronic headache, intracranial hypertension and liver toxicity. Occurrence and severity of the poisoning symptom depend on dosage, length of time and symptom itself. The destructive effects on eye, skeleton and liver are permanent, whereas many other symptoms are reversible. Toxic action occurs in adults after gRE/d for several weeks, taking a replenishing dose of more than 7500-15000μ months or years. But the toxic action is detected also in some cases at a dose less than 1500-3000μgRE/d. The threshold value is influenced by existing illness, excessive drinking, therapeutic medications and dietary intakes. Serious intolerance to VA is also influenced by genetic factors, but details of this metabolic defect haven’t been clarified. Epidemiologic data shows that when dietary retinol intake is more than 1500μg/d, hipbone fracture attack rate in postmenopausal women will be doubled as compared with the intake dose of 500μg/d. Other epidemiologic researches supporting this view show that hipbone fracture attack rate is higher in Nordic countries, especially in Scandinavian Peninsula where more dietary intakes of retinol are observed. Hipbone fracture attack rate of Swedish men is higher than that of British and Swedish women. In β-carotene and retinol efficacy test (CARET), occurrence of lung cancer in male smokers and male asbestos workers would increase when they ingest jointly 7500μg of retinol and 30000μg of β-carotene. This test and ABTC research indicate that this effect is caused by β-carotene. A research about the chemical protection for workers exposed to blue asbestos revealed that 45 of 512 subjects who take a dose of 7500μgRE every day changed their treatment because of associated headache caused. Compared with isotretinoic acid treatment and the control, occurrence of skin cancer in subjects who take a dose of 7500μg retinol every day was increased moderately. In the chemical protection research, side effects are found in 45% of patients with lung cancer and cancers of head and neck who had been injected with a daily dose of 90000μgRE for one year, and then 45000μgRE for the next year after observation. These side effects include dry skin, pruritus, hemorrhage, and trichomadesis. Vitamin D Excessive intake of vitamin D could result in hypercalcemia and hypercalciuria. Vitamin D promotes calcium absorption and skeletal re-absorption, and causes calcium deposition in soft tissues, diffuse bone mineral loss as well as irreversible renal and cardiovascular toxicity. Vitamin D in granulomatous tissues could be unlimitedly transformed into its active form, so patients with sarcoidosis are exceptionally sensitive to Vitamin D. Sarcoidosis is uncommon, but if patients take additional vitamin D, there will be a potential danger. It has been suggested that moderate dose of vitamin D could enhance the formation of renal calculi in susceptible individuals. There is no information for the comparison of toxicity to the human body between vitamin D2 and vitamin D3. A lot of supplemental tests showed that there were no adverse effects with a 0.010 ~ 0.045mg /d vitamin D intake. The effects of higher doses were greatly different. For example, among 63 aged persons (the female was more than 60 years old, the male more than 65 years old) provided with a replenishing dose of 0.05mg /d vitamin D (unspecified dose) for 6 months, two persons developed hypercalcinemia (Johnson et al, 1980). However, in another study lasted for five months, 61 adults (the average age was 41 years old) were given a replenishing dose of 0.10mg /d vitamin D3, and their serum calcium level did not increase significantly (Vieth et al, 2001). This difference may reflect that the aged has developed hyperparathyroidism or vitamin D deficiency before the intervention. 17. Clinical data Vitamin A A few hundred years ago, Night blindness and xerophthalmia were associated with the incidence and mortality of infectious disease. In 1930s, vitamin A as an anti-infective vitamin has been widely researched and applied. With a lack of vitamin A, the way to constitute ligand of nuclear receptor is changed in different tissues, and the damage of immune function at multiple levels is shown. As for mucosal immunity, vitamin A deficiency not only damages the integrity of mucosal epithelia of eyes, respiratory tract, gastrointestinal tract and genitourinary tract, but also lowers the local secretion of IgA. In recent years, clinical and human population tests have shown that for infants supplemented with vitamin A, incidence and mortality of diseases of various causes could be significantly reduced. 1. Child viral infection Vitamin A has been tested in different kinds of child viral infectious diseases, such as measles, respiratory syncytial virus, chicken pox and AIDS. Twelve researches have shown that Vitamin A could prevent children with above diseases from death, and therefore it should be widely used. It is reported that low level of serum vitamin A was related to predisposition of child pneumonia, diarrhea and other diseases, and supplement of VA can prevent infectious diseases in digestive tract, respiratory tract and could be used as an auxiliary therapy for these infectious diseases. 2. Diabetes Diabetics are prone to vitamin A shortage. It was reported that Vitamin A supplement could improve the blood glucose control of diabetics. Diabetics should decide whether they would take additional vitamin A preparations based on the medical advice 3. Skin diseases Vitamin A has been tested in various kinds of skin diseases, including acne, psoriasis, brandy nose, seborrheic dermatitis, eczema, but the curative effect was not so noticeable. In general, the does close to the poisoning dose may obtain a good curative effect. 4. Menorrhagia It was reported that for the female with menorrhagia, the amount of menstrual flow may be reduced through daily intake of 25000IU vitamin A. It could not be used as a long-term therapy, because once amenorrheic women were pregnant, high-dose vitamin A may lead to fetal anomaly. 5. AIDS It’s reported that the intake of higher-dose of vitamin A for 6 ~ 8 years may be beneficial for patients with AIDS, but if the intake is over 20268IU/d, the effect to reduce risks and mortality of AIDS will be decreased instead. eficiency anemia 6. Iron d Recent studies have found that diet short of vitamin A and iron could also lead to iron deficiency anemia. Population intervention trials also confirm that the supplementation of single vitamin A or iron may improve anemia, but the jointed supplementation of vitamin A and iron may gain the best effect. 7. Palpebral conjunctiva and keratonosus Vitamin A may maintain the normal differentiation and integrity of corneal and conjunctival epithelial cells, and it has been widely applied clinically. Recently, In China someone treated the keratopathy with vitamin A eye drops and achieved satisfactory therapeutic effect. Vitamin D 1. Rickets It has been reported that the demand of vitamin D would be increased relatively for infants because of their rapid physical growth (Wu Guangchi, 1989; Li Tong, 1990). The daily intake of 350IU vitamin D may prevent infant rickets in south China, and 550IU in the north China would be needed daily. In 1995, Guillemant et al found that the level of 25 - (OH) D3 in children in July (29.96μg / L ? 7.46μg / L) was significantly higher than that in March (6.61μg / L ? 2.04μg / L (0.0001) ), suggesting that the season would cause Vitamin D deficit and the due attention should be paid to the extra supplementation of it. 2. Osteoporosis It was reported that the level of 25 - (OH) D3 in 86% of the aged in Rest Home was below 50mmol/L, and the bone mineral content in 85% of the aged suggested osteoporosis (Komar et al, 1993). It is found that a lack of vitamin D could increase the incidence of hipbone fracture (Dawson-Hughes et al, 1997). A number of studies have shown that appropriate vitamin D intake (400 ~ 800IU/d) could reduce the loss of bone material and the incidence of bone fracture. 1634 women were supplemented with 800IU vitamin D and 1200mg calcium every day for 18 months; meanwhile 1636 women in the control group were given placebos (Chapuy et al, 1992). The results showed that bone density in the group supplemented with VD and calcium was increased by 2.6%, meanwhile it was reduced by 4.6% in the control group (P <0.001). Compared with the control group, the number of cases with hipbone fracture in the group supplemented with VD and calcium was reduced by 43% (P = 0.043), and the total number of cases with non-vertebral fractures was reduced by 32% (P = 0.015). 3. Osteomalacia It was reported that offering 400IU/d vitamin D to pregnant women could reduce the incidence of maternal osteomalacia, neonatal hypocalcemia and tetany of extremities (Brooke et al, 1981). The investigation results indicated that vitamin D intake for vegetarians was significantly lower than that for omnivorous persons (Alexander et al, 1994). It has been found that in 15 cases of osteomalacia and 13 cases of quasi-osteomalacia, most patients were India vegetarians ( Finch et al, 1992). It was believed that vegetarians, though asymptomatic, should also take additional vitamin D (Fonseca et al, 1988). 4. Cancer A number of studies have showed that vitamin D may contribute to the prevention of breast cancer, colon cancer, pancreatic cancer, and prostate cancer. 5. Polycystic ovary syndrome A preliminary study has implied that calcium agent with vitamin D supplement may be beneficial to the prevention of polycystic ovary syndrome. 6. Psoriasis Vitamin D may be used to treat psoriasis. Calcipotrol as Vitamin D3 derivative is recommended for the treatment of psoriasis in a study in Denmark. 7. Diabetes In recent years, the basic research on vitamin D suggests that there may be vitamin D receptors and calbindin-D 28 k in pancreas, that a lack of vitamin D could cause reduction of insulin secretion, and that vitamin D receptor gene polymorphism may be related to Type I Diabetes. Vitamin D acts as an immunosuppressive factor to inhibit lymphocyte proliferation and production of cytokines. British scientists have discovered that the incidence of Type I Diabetes may be related to vitamin D deficiency and the generation of rickets. To some extent, Vitamin D could inhibit the pancreatic β-cell autoimmune response. It was also found that high-dose of vitamin D may be associated with hyperinsulinemia and insulin resistance. 8. Coronary heart disease A recent study showed that for women over 65 years old who were with coronary heart disease and took Vitamin D, the death risk may be reduced by one third as compared with those who did not take Vitamin D. Early researches suggested that the reduction of serum vitamin D level played a certain role in calcification of atherosclerotic plaque in patients with coronary heart disease. The risk to die of cardiovascular diseases for women with osteoporosis was greater than those without osteoporosis. In fact, the rate of calcium deposition in the wall of blood vessels for women with osteoporosis is greater than those with the normal bone material. The physiological process that leads to bone calcium loss and calcification of atherosclerotic plaque may be the same. Of course, the researchers pointed out simultaneously that there would be still much work to be done before advocating supplementing vitamin D for preventing coronary heart disease.