澳洲保健品Swisse女士复合维生素(120片瓶)说明书
swisse liver detox用法
swisse liver detox用法
Swisse Liver Detox是一种能够帮助肝脏排毒的保健品。
它含
有多种天然成分，包括乳薊提取物、水飞蓟、甘草和小卫矛等。
使用方法如下：
1. 每日成人服用1-2片，与饭后用水一同服用。
2. 不建议孕妇、哺乳期妇女和儿童使用。
3. 请在使用之前仔细阅读并遵循产品包装上的说明。
4. 如有任何持续性症状或对该产品成分过敏的情况，请咨询医生。
重要提示：
1. 本产品不能代替均衡的饮食。
2. 饮食习惯和生活方式对于肝脏健康至关重要。
3. 如果您有任何肝脏疾病或正在服用其他药物，请在使用之前咨询医生。
4. 如果您正在接受医疗过程，请在使用之前咨询医生。
总结而言，使用Swisse Liver Detox时应按照产品包装上的说
明进行，并在使用之前咨询医生以确保其安全和适合性。
复合维生素片说明书作用
复合维生素片说明书作用批准文号：国药准字J20210155生产厂家：Bayer S.A.药品说明书【主要成分】本品为复方制剂，每片含： 12种维生素...【功能主治】本品用于妊娠期和哺乳期妇女对维生素、矿物质和微量元素的额外需求;并预防妊娠期因缺铁和叶酸所致的贫血。
【用法用量】本品口服。
一次1片，一日1次，与早餐同时服用;如存在晨起恶心现象，可在中午或晚上服用。
【不良反应】1. 本品耐受性良好，少数病例会出现胃肠道功能紊乱如便秘，但一般不须停药。
某些敏感的妇女可能会出现一定程度的过度兴奋，故此类病人避免在晚间服用。
2. 如出现任何不良事件或反应，请咨询医师。
【禁忌症】1. 高维生素A血症、高维生素D血症、高钙血症、高钙尿症者禁用。
2. 肾功能不全、铁蓄积、铁利用紊乱者禁用。
【剂型】片剂注意事项：1. 本品不推荐儿童使用。
2. 请严格按推荐剂量服用。
3. 可是粪便颜色变黑，但无临床意义。
4. 对本品过敏者禁用，过敏体质者慎用。
5. 本品性状发生改变时禁止使用。
6. 请将本品放在儿童不能接触的地方。
7. 如正在使用其他药品，使用本品前请咨询医师或药师。
成份：本品为复方制剂，每片含：12种维生素7种矿物质和微量元素1、维生素A 4,000国际单位1.2毫克;钙 0.125克。
2、维生素B 11.6毫克;镁 0.1克。
3、维生素B 21.8毫克;磷 0.125克。
4、维生素B 62.6毫克;铜 1毫克。
5、维生素B 24.0微克;铁 60毫克。
6、维生素C 0.1克;锰 1毫克。
7、维生素D3 500国际单位12.5微克;锌 7.5毫克。
8、维生素E 15毫克。
9、生物素 0.2毫克。
10、叶酸 0.8毫克。
11、烟酰胺 19毫克。
12、泛酸钙 10毫克。
作用类别：本品为维生素及矿物质类非处方药药品。
药物相互作用：1. 不宜与四环素类药物同用。
必要时两药须间隔两小时以上分别服用。
2. 不宜与其他含维生素A和维生素D的药物同用。
swisse liver detox用法
swisse liver detox用法摘要：1.Swisse Liver Detox 产品简介2.Swisse Liver Detox 的主要成分3.Swisse Liver Detox 的使用方法4.Swisse Liver Detox 的功效及适用人群5.Swisse Liver Detox 的注意事项6.总结正文：Swisse Liver Detox 是一款肝脏排毒产品，旨在帮助身体清除毒素，提高肝脏功能。
本篇文章将详细介绍Swisse Liver Detox 的用法、成分、功效及注意事项等内容。
1.Swisse Liver Detox 产品简介Swisse Liver Detox 是一款澳大利亚品牌Swisse 推出的肝脏排毒产品。
本产品采用天然成分，无添加糖分、人造香料及色素，适用于希望改善肝脏功能、提高身体排毒能力的人群。
2.Swisse Liver Detox 的主要成分Swisse Liver Detox 的主要成分包括：朝鲜蓟、奶蓟草、姜黄、胡椒薄荷、荨麻、山楂和葡萄籽提取物。
这些成分均具有抗氧化、抗炎、保护肝脏等功能，共同协作以达到肝脏排毒的效果。
3.Swisse Liver Detox 的使用方法Swisse Liver Detox 的使用方法非常简单。
首先，请确保每天饮用足够的水，以便帮助身体排毒。
然后，每天早晨空腹服用两粒Swisse Liver Detox 胶囊。
建议持续使用8 周，以达到最佳效果。
在使用过程中，如遇到不适，请及时停止使用并咨询专业医生。
4.Swisse Liver Detox 的功效及适用人群Swisse Liver Detox 具有以下功效：- 帮助肝脏清除毒素，减轻肝脏负担- 抗氧化，保护肝脏细胞- 提高肝脏功能- 缓解酒后不适适用人群包括：- 长期饮酒者- 饮食不规律者- 经常熬夜者- 生活压力大者- 有肝脏疾病家族史者5.Swisse Liver Detox 的注意事项在使用Swisse Liver Detox 时，请注意以下事项：- 本产品不适合孕妇、哺乳期妇女及儿童使用- 患有疾病者在使用前请咨询医生- 若出现不适，请停止使用并咨询医生- 请存放于阴凉干燥处，避免阳光直射综上所述，Swisse Liver Detox 是一款有助于肝脏排毒的产品，适用于希望改善肝脏功能的人群。
Viltepso (Viltolarsen) 使用说明说明书
UnitedHealthcare ® Community PlanViltepso ® (Viltolarsen)Policy Number : CS2023D0095KEffective Date : September 1, 2023 Instructions for Use Table of Contents Page Application ..................................................................................... 1 Coverage Rationale ....................................................................... 1 Applicable Codes .......................................................................... 2 Background ................................................................................... 2 Clinical Evidence ........................................................................... 3 U.S. Food and Drug Administration ............................................. 4 References ..................................................................................... 4 Policy History/Revision Information ............................................. 5 Instructions for Use ....................................................................... 5 This Medical Benefit Drug Policy does not apply to the states listed below; refer to the state-specific policy/guideline, if noted: State Policy/Guideline FloridaRefer to the state’s Medicaid clinical policy KansasNone LouisianaRefer to the state’s Medicaid clinical policy New JerseyViltepso ® (Viltolarsen) (for New Jersey Only) North CarolinaNone OhioViltepso ® (Viltolarsen) (for Ohio Only) PennsylvaniaViltepso ® (Viltolarsen) (for Pennsylvania Only) TexasRefer to drug-specific criteria found within the Texas Medicaid Provider Procedures ManualViltepso (viltolarsen) may be covered for the treatment of Duchenne muscular dystrophy (DMD) in patients who meet all of the following criteria :• For initial therapy , all of the following:o Diagnosis of Duchenne muscular dystrophy by, or in consultation with, a neurologist with expertise in the diagnosis of DMD; and o Submission of medical records (e.g., chart notes, laboratory values) confirming the mutation of the DMD gene is amenable to exon 53 skipping; ando One of the following: ▪ Submission of medical records (e.g., chart notes, laboratory values) confirming that the patient has a 6-MinuteWalk Test (6MWT) ≥ 300 meters while walking independently (e.g., without side-by-side assist, cane, walker,wheelchair, etc.) prior to beginning Viltepso therapy; or▪ Both of the following:Commercial Policy • Viltepso ® (Viltolarsen)Submission of medical records (e.g., chart notes) confirming that the patient is ambulatory without needing anassistive device (e.g., without side-by-side assist, cane, walker, wheelchair, etc.); and o One of the following:▪Patient has achieved a score of greater than 17 on the North Star Ambulatory Assessment (NSAA); or▪Patient has achieved a time to rise from the floor (Gower’s test) of less than 7 seconds;ando Viltepso is prescribed by, or in consultation with, a neurologist with expertise in the treatment of DMD; ando Viltepso dosing for DMD is in accordance with the United States Food and Drug Administration approved labeling; and o Viltepso is not used concomitantly with other exon skipping therapies for DMD; ando Initial authorization will be for no more than 6 monthsFor continuation of therapy, all of the following:o Patient has previously received Viltepso; ando Viltepso is prescribed by, or in consultation with, a neurologist with expertise in the treatment of DMD; ando Submission of medical records (e.g., chart notes) confirming that the patient is ambulatory without needing an assistive device (e.g., without side-by-side assist, cane, walker, wheelchair, etc.); ando Viltepso dosing for DMD is in accordance with the U.S. Food and Drug Administration (FDA) approved labeling; and o Viltepso is not used concomitantly with other exon skipping therapies for DMD; ando Reauthorization will be for no more than 12 monthsViltepso will not be covered for other forms of muscular dystrophy.The following list(s) of procedure and/or diagnosis codes is provided for reference purposes only and may not be all inclusive. Listing of a code in this policy does not imply that the service described by the code is a covered or non-covered health service. Benefit coverage for health services is determined by federal, state, or contractual requirements and applicable laws that may require coverage for a specific service. The inclusion of a code does not imply any right to reimbursement or guarantee claim payment. Other Policies and Guidelines may apply.HCPCS Code DescriptionJ1427 Injection, viltolarsen, 10 mgDiagnosis Code DescriptionG71.01 Duchenne or Becker muscular dystrophyDuchenne muscular dystrophy (DMD) is an X-linked disease that affects 1 in 3,600-6,000 live male births. DMD occurs as a result of mutations (mainly deletions) in the dystrophin gene. These mutations lead to an absence or a defect of the protein, dystrophin, resulting in progressive muscle degeneration, leading to loss of ambulation and additional respiratory, orthopedic, and cardiac complications. If left untreated, mean age of death is approximately 19 years of age.2-4Viltolarsen is an antisense oligonucleotide of the phosphorodiamidate morpholino oligomer (PMO) subclass. PMOs are synthetic molecules in which the five-membered ribofuranosyl rings found in natural DNA and RNA are replaced by a six-membered morpholino ring. Each morpholino ring is linked through an uncharged phosphorodiamidate moiety rather than the negatively charged phosphate linkage that is present in natural DNA and RNA. Each phosphorodiamidate morpholino subunit contains one of the heterocyclic bases found in DNA (adenine, cytosine, guanine, or thymine).1Viltolarsen is designed to bind to exon 53 of dystrophin pre-mRNA, resulting in exclusion of this exon during mRNA processing in patients with genetic mutations that are amenable to exon 53 skipping. Approximately 8% of DMD patients have out of frame deletion mutations amenable to exon 53 skipping. Exon skipping is intended to allow for production of an internally truncated dystrophin protein.1Eteplirsen (Exondys 51) was the first PMO approved by the U.S. Food and Drug Administration for treatment of DMD patients with confirmed genetic mutations amenable to exon 51 skipping. Approximately 13% of DMD patients have out of frame deletion mutations amenable to exon 51 skipping. This indication was approved under accelerated approval based on an increase in dystrophin in skeletal muscle observed in some patients treated with eteplirsen. A clinical benefit of eteplirsen has not been established. Continued approval for this indication may be contingent upon verification of a clinical benefit in confirmatory trials.5Golodirsen (Vyondys 53) was the second PMO approved by the US Food and Drug Administration for treatment of DMD patients with confirmed genetic mutations amenable to exon 53 skipping, the same population as viltolarsen. Approximately8-10% of DMD patients have out of frame deletion mutations amenable to exon 53 skipping. This indication was also approved under accelerated approval based on an increase in dystrophin in skeletal muscle.6Casimersen (Amondys 45) is an antisense oligonucleotide that is designed to bind to exon 45 of dystrophin pre-messenger RNA, resulting in exon 45 skipping during messenger RNA processing in patients with amenable deletion mutations of the DMD gene. The FDA granted accelerated approval of casimersen for the treatment of patients with DMD who have a confirmed mutation of DMD that is amenable to exon 45 skipping, which is thought to cause approximately 8 percent of DMD cases.14Viltolarsen is indicated for the treatment of Duchenne muscular dystrophy (DMD) in patients who have a confirmed mutation of the DMD gene that is amenable to exon 53 skipping.1A phase II study evaluated two doses of viltolarsen in 16 ambulatory boys aged 4 to 9 years with a DMD diagnosis and DMD gene amenable to exon 53 skipping over 24 weeks. Ambulatory boys on a stable corticosteroid regimen for at least 3 months who could complete time to stand from supine, time to run/walk 10 m, and time to climb four stairs assessments were included. The study was a multicenter, two period dose-finding clinical trial. The first study period, which corresponded to the first 4 weeks of treatment following enrollment, was double-blinded and placebo-controlled. Participants in both dose cohorts were randomized 3:1 to receive viltolarsen or placebo. The second study period began at week 5 for each participant. During this period, all participants received viltolarsen according to their cohort dose for a 20-week open-label treatment. Primary study outcomes included safety, tolerability, and pharmacokinetics of low-dose (40 mg/kg per week) and high-dose (80 mg/kg per week) viltolarsen in ambulant boys with DMD. Efficacy was assessed based on change from baseline in dystrophin protein level (measured as % of the dystrophin level in healthy subjects, i.e., % of normal) at week 25. Muscle dystrophin production was assessed as protein production by Western blot for the primary study efficacy outcome and as dystrophin mRNA splicing on RT-PCR, dystrophin protein production by MS, and dystrophin localization by IF staining for secondary study efficacy outcomes. Additional secondary efficacy outcomes were gross motor skill assessments of timed function tests, including time to stand from supine, time to run/walk 10 m, time to climb four stairs, North Star Ambulatory Assessment, and 6-minute walk test as well as quantitative muscle testing. These outcomes were compared with a matched natural history control group from the Cooperative International Neuromuscular Research Group (CINRG) Duchenne Natural History Study (DNHS).In patients who received viltolarsen 80 mg/kg once weekly, mean dystrophin levels increased from 0.6% of normal at baseline to 5.9% of normal by week 25, with a mean change in dystrophin of 5.3% of normal levels (p = 0.01) as assessed by validated Western blot; the median change from baseline was 3.8%. All patients demonstrated an increase in dystrophin levels over their baseline values. As assessed by mass spectrometry, mean dystrophin levels increased from 0.6% of normal at baseline to 4.2% of normal by week 25, with a mean change in dystrophin of 3.7% of normal levels; the median change from baseline was 1.9%.Comparison of viltolarsen-treated participants with 65 age-matched and treatment matched natural history controls from CINRG DNHS suggested evidence of clinical benefit of viltolarsen treatment. Viltolarsen-treated participants showed improvement or stabilization of function over the 25-week period, whereas the CINRG DNHS external comparator group exhibited a decline in all timed function tests, except for time to climb four stairs. Velocity in the time to run/walk 10 m test significantly improved in viltolarsen-treated participants at weeks 13 and 25 compared with a decline in controls from CINRG DNHS (change at 25 weeks compared with baseline: viltolarsen, 0.23 m/s; control, −0.04m/s). The 6-minute walk test showed significant improvement at week 25 in viltolarsen treated participants, whereas results from CINRG DNHS controls declined over the same period (change at 25 weeks compared with baseline: viltolarsen, 28.9 m; control, −65.3 m). Significant improvements in time to stand from supine were observed (change at 25 weeks compared with baseline: viltolarsen, −0.19 s; control, 0.66 s). Velocity in the time toimprovement or stabilization, but the differences between viltolarsen treatment and external comparator controls were not significant. Measures of muscle strength by isometric testing showed no differences between viltolarsen-treated participants and the CINRG DNHS external comparator control group.7RACER53 is an ongoing 48-week, phase 3 double-blind, placebo controlled, randomized clinical trial that will evaluate the efficacy of viltolarsen in ambulatory DMD patients with out-of-frame deletion mutations amenable to skipping exon 53. The study will enroll 74 boys from 4 to 8 years of age with genotypically confirmed DMD on a stable dose of corticosteroids who can walk independently without assistive devices with a time to stand of less than 10 seconds. The primary endpoint is the change from baseline to week 48 in the time to stand. Secondary outcomes include the change in time to run/walk 10 meters, change in 6MWT, change in the NSAA, change in time to climb four steps, and change in muscle force contraction measured by dyanometry.8The SKIP-NMD trial of golodirsen is a U.S.-based, blinded, placebo-controlled, dose-escalation two-part Phase I/II RCT of male patients aged six to 15 years with a DMD diagnosis and DMD gene amenable to exon 53 skipping. Patients age 6 to 15 years with stable cardiac and pulmonary function, and on a stable dose of corticosteroids for at least six months were included. Additional inclusion criteria included a baseline six-minute walk test (6MWT) of greater than 250 m, a North Star Ambulatory Assessment (NSAA) score of greater than 17 or a rise time of less than 7 seconds. In part one, 12 patients were randomized to receive once-weekly intravenous infusions at escalating doses of 4, 10, 20, 30 mg/kg of golodirsen or matching placebo for 12 weeks. Part two consists of an open-label period of all patients from part one and 13 newly recruited patients who are receiving once-weekly infusions of 30 mg/kg of golodirsen for up to 168 weeks.Part one of the SKIP-NMD trial assessed safety and tolerability. In part two, the primary endpoints are change from baseline in 6MWT at 144 weeks and change in dystrophin protein levels at 48 weeks. Secondary endpoints include drug pharmacokinetics, change from baseline in FVC percent predicted, and change from baseline in dystrophin intensity at 144 weeks.At the time of pre-planned interim analysis, data from baseline and week 48 muscle biopsies, exon 53 skipping, and dystrophin localization were available for 25 patients on golodirsen. The study is ongoing, and results for the primary efficacy endpoint of 6MWT at week 144 are not yet available. Mean baseline of dystrophin in the trial was reported to be 0.095% of normal. At 48 weeks, the mean level of dystrophin had increased to 1.019% of normal resulting in an absolute increase of 0.918% of normal (p < 0.001). A clinically meaningful change in level of dystrophin has not yet been established in humans. As such, the clinical significance of these results is not clear. Among individual patients, dystrophin levels at week 48 ranged from 0.09% to4.30%.9-11ESSENCE is an ongoing 96-week, Phase 3, double-blind, placebo controlled, randomized clinical trial that will evaluate the efficacy of golodirsen and casimersen in DMD patients with out-of-frame deletion mutations amenable to skipping exon 53 and exon 45, respectively. The study will enroll 222 boys from 7 to 13 years of age with genotypically confirmed DMD and 6MWT ≥ 300 m and ≤ 450 m. The primary endpoint is the change from baseline to week 96 in 6MWT.12Viltolarsen or golodirsen have not been studied in DMD that is not amenable to exon 53 skipping, nor in other forms of muscular dystrophy (e.g., Becker muscular dystrophy).1,6This section is to be used for informational purposes only. FDA approval alone is not a basis for coverage.Viltepso is indicated for the treatment of Duchenne muscular dystrophy (DMD) in patients who have a confirmed mutation of the DMD gene that is amenable to exon 53 skipping. This indication is approved under accelerated approval based on an increase in dystrophin in skeletal muscle observed in some patients treated with Viltepso. Continued approval for this indication may be contingent upon verification of a clinical benefit in confirmatory trials.1.Viltepso [package insert]. Paramus, NJ; NS Pharma, Inc, March 2021.2.Bushby K, Finkel R, Birnkrant DJ, Case LE, Clemens PR, Cripe L, et al. Diagnosis and management of Duchenne musculardystrophy, part 1: diagnosis, and pharmacological and psychosocial management. Lancet Neurol; 2010 Jan; 9(1):77 93.3.Bushby K, Finkel R, Birnkrant DJ, et al. (2010) Diagnosis and management of Duchenne muscular dystrophy, part 2:implementation of multidisciplinary care. Lancet Neurol; 2010 Jan; 9(2):177-189.4.Birnkrant DJ, Bushby K, Bann CM, et al. Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis,and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management. Lancet Neurol.2018;17(3):251-267. doi: 10.1016/S1474-4422(18)30024.5.Exondys 51 [package insert]. Cambridge, MA: Sarepta Therapeutics, Inc, January 2022.6.Vyondys 53 [package insert]. Cambridge, MA: Sarepta Therapeutics, Inc, February 2021.7.Clemens PR, Rao VK, Connolly AM, et al. Safety, tolerability, and efficacy of viltolarsen in boys with Duchenne musculardystrophy amenable to exon 53 skipping: a phase 2 randomized clinical trial. JAMA Neurol. 2020; 26;77(8):1-10. doi:10.1001/jamaneurol.2020.2025.8.Study to Assess the Efficacy and Safety of Viltolarsen in Ambulant Boys With DMD (RACER53)https:///ct2/show/NCT04060199?term=viltolarsen&draw=2&rank=1. Accessed June 5, 2023.9.Frank DE, Mercuri E, Servais, L, et al. Golodirsen induces exon skipping leading to sarcolemmal dystrophin expression inpatients with genetic mutations amenable to exon 53 skipping. Poster presented at: Annual Clinical Genetics Meeting of the American College of Medical Genetics and Genomics; April 2-6, 2019; Seattle, WA.10.Muntoni F, Frank DE, Morgan J, et al. Golodirsen induces exon skipping leading to sarcolemmal dystrophin expression inpatients with genetic mutations amenable to exon 53 skipping [abstract]. Neuromuscul Disord. 2018;28:S5. Abstract D01.11.Muntoni F, Frank DE, Sardone V, et al. SRP-4053 induces exon skipping leading to sarcolemmal dystrophin expression inDuchenne muscular dystrophy patients amenable to exon 53 skipping. Poster presented at: 22nd International Annual Congress of the World Muscle Society; October 3-7, 2017; Saint Malo, France.12.Study of SRP-4045 and SRP-4053 in DMD Patients (ESSENCE)https:///ct2/show/NCT02500381?term=golodirsen&cond=Duchenne+Muscular+Dystrophy&rank=3.Accessed June 5, 2023.13.Institute for Clinical and Economic Review (ICER). Deflazacort, eteplirsen, and golodirsen for Duchenne musculardystrophy: Effectiveness and value: Evidence Report. https:///wp-content/uploads/2020/10/Corrected_ICER_DMD-Final-Report_042222.pdf. April 22, 2022. Accessed June 5, 2023. 14.Amondys 45 [package insert]. Cambridge, MA; Sarepta Therapeutics, Inc.: March 2023.Date Summary of Changes09/01/2023 ApplicationLouisianaReplaced reference link to the state-specific policy version with instruction to refer to the state’sMedicaid clinical policySupporting InformationArchived previous policy version CS2023D0095JThis Medical Benefit Drug Policy provides assistance in interpreting UnitedHealthcare standard benefit plans. When deciding coverage, the federal, state, or contractual requirements for benefit plan coverage must be referenced as the terms of the federal, state, or contractual requirements for benefit plan coverage may differ from the standard benefit plan. In the event of a conflict, the federal, state, or contractual requirements for benefit plan coverage govern. Before using this policy, please check the federal, state, or contractual requirements for benefit plan coverage. UnitedHealthcare reserves the right to modify its Policies and Guidelines as necessary. This Medical Benefit Drug Policy is provided for informational purposes. It does not constitute medical advice.UnitedHealthcare may also use tools developed by third parties, such as the InterQual® criteria, to assist us in administering health benefits. The UnitedHealthcare Medical Benefit Drug Policies are intended to be used in connection with the independent professional medical judgment of a qualified health care provider and do not constitute the practice of medicine or medical advice.。
复合维生素说明书
复合维生素【药品名称】商品名称：复合维生素英文名称：decavitamin拼音全码：Fu he wei sheng su【主要成份】本品主要成份为复合维生素。
【性状】本品为【适应症/功能主治】1、用于维生素A缺乏症，如干眼病、夜盲症、角膜软化症和皮肤粗糙等，据称本品对预防上皮癌，食管癌的发生也有一定作用。
2.维生素B缺乏时影响机体的生物氧化，使代谢发生障碍。
表现为口角炎、唇炎、舌炎、眼结膜炎和阴囊炎等。
本品可用于防治上述疾病。
3.临床用于维生素C缺乏引起的坏血病、贫血、过敏性疾病、心肌炎、慢性肝炎、克山病及急慢性中毒等，并能促进创伤愈合。
4.临床用于防治维生素D缺乏引起的软骨病、佝偻病以及因缺乏维生素引起的低血钙，骨质疏松症，龋齿，手足搐搦症及甲状旁腺功能减退等。
5.临床用于缺乏维生素B所致的各种疾病。
如脚气病、糙皮病及食欲不振等的辅助治疗。
本药含有机体正常代谢所必需的多种维生素及微量元素，补充多种维生素、矿物质及微量元素，用于维生素和微量元素缺乏的预防。
参与体内糖类、氨基酸、脂肪代谢、用于维生素及微量元素缺乏症的治疗与预防。
【用法用量】幼雏每100公斤饲料中添加本品50克；育成鸡每100公斤饲料中添加本品80克；产蛋鸡每100公斤饲料中添加本品100克；种鸡每100公斤饲料中添加本品100克；生长猪体重5-10公斤，每100公斤饲料中添加本品44克，体重10-20公斤，每100 公斤饲料中添加本品35克，体重20-100公斤，每100公斤饲料中添加本品26克。
【适用范围】本品适用于雏鸡、育成鸡、产蛋鸡和乳猪、幼猪、育肥猪、奶牛、兔、狐狸、貉、貂、等畜禽及动物。
六．贮藏密闭、遮光、干燥处保存。
七．保质期十八个月。
汤臣倍健多种维生素片(女士)的说明书
汤臣倍健多种维生素片(女士)的说明书维生素和矿物质是体内必须品，这些微量元素在日常生活中可以通过食物中获取，但是如果出现了意外情况的话，人体会缺少某些维生素等必要的微量元素，对于人体的健康影响是比较大的。
目前出现了一种叫做汤臣倍健多种维生素片(女士)的维生素矿物质药物，该药物对于人体无任何副作用，它能有助于身体的健康。
【药品名称】通用名称：多种维生素片(女士)商品名称：汤臣倍健多种维生素片(女士)拼音全码：TangChenBeiJianDuoZhongWeiShengSuPian(NvShi)【主要成份】β-胡萝卜素321μg,维生素B20.75mg,维生素B121.31μg,维生素 D3.01μ等。
【适应症/功能主治】1.均衡补充女性所需的多种维生素、矿物质；2.独特的均匀释放营养素技术；3.精确配方，不含磷、铜。
【规格型号】1000mg*70s【用法用量】每日1次，每次1片。
建议饭后食用，更有利于身体的吸收。
【贮藏】密封。
【有效期】24 月【批准文号】国食健字G2*******【生产企业】广东汤臣倍健生物科技股份有限公司★【产品说明】汤臣倍健多种维生素系列产品，以源自德国BASF 及荷兰DSM维生素A、E、B6、B12、D、β-胡萝卜素、叶酸等为主要原料，严格遵照《中国居民膳食营养推荐摄入量》RNIs标准，专为中国居民设计，营养全面均衡，配方科学精确。
★【产品特点】1.源自德国BASF及荷兰DSM的优质维生素A、E、B6、B12、D、β-胡萝卜素、叶酸。
2.独特的均匀释放营养素技术，24小时呵护身体健康。
3.采用先进的微囊技术、脂溶膜技术，使营养成分被包裹起来，防止被氧化，同时也保持了营养成分的活性。
4.专为中国人设计的营养配方，营养全面均衡，配方科学安全。
严格遵照《中国居民膳食营养推荐摄入量》RNIs标准，全面均衡补充中国人所需的维生素及矿物质。
5.精确配方，满足每日营养补充需求，避免某些维生素和矿物质摄入过量可能产生的蓄毒问题。
营养品说明
(大豆卵磷脂)Swisse 卵磷脂Lecithin 护肝通血管调血脂1200mg 卵磷脂是血管清道夫，中老人健康之宝。
“卵磷脂+深海鱼油”属黄金组合。
如果深海鱼油是体内血管的“清洁工”，把血管里多余的胆固醇及其他垃圾扫到一起，这时，卵磷脂就担当“运输车”，将垃圾运出体外。
卵磷脂的保健作用：卵磷脂泛指磷脂、甘油三酸酯和脂肪酸混合物，被誉为“细胞的保护神”。
1、调节血脂，预防和改善心脑血管疾病2、增强记忆力，预防老年痴呆的发生3、保持皮肤水分，促进多余脂肪分解4、促进肠蠕动，防止便秘5、防止脂肪在肝脏的堆积，预防脂肪肝的发生【产品功效】卵磷脂有助于保持健康的肝脏。
卵磷脂是一种天然来源的卵磷脂这是一个重要的组成部分，所有的细胞膜。
卵磷脂胶囊为您补充足够身体所需的卵磷脂，帮助降低血液中的胆固醇和中性脂肪的含量。
虽然身体产生自己的卵磷脂，饮食摄入量决定了卵磷脂的进展。
卵磷脂也有利于帮助维持正常的健康皮肤和头发。
卵磷脂是构成细胞膜的最重要的成分之一，以脑神经系统、血液、肝脏等重要组织最为重要，卵磷脂中含有的主要成份，磷脂酰胆碱能强化神经，使思维敏捷、记忆力增强、降低胆固醇，还能够避免胆固醇凝结，预防血管堵塞，预防因动脉硬化造成的高血压、脑中风、血栓症、狭心症。
卵磷脂被称为“血管清道夫”、“肝脏的保护神”，能健脑益智，预防老年痴呆的发生，还是糖尿病患者的最佳营养品。
此外，卵磷脂还可预防、化解胆结石。
卵磷脂作为一种健康食品，有着全面、长远、稳定的效果，同时又没有药物的副作用，在增进健康和预防疾病方面起重要作用.卵磷脂又称蛋黄素，是天然生化强劲排毒剂。
被誉为与蛋白质、维生素并列的“三大营养素”。
其主要功效如下：一、乳化脂肪卵磷脂具有乳化、分解油脂的作用，可增进血液循环，改善血清脂质，清除过氧化物，使血液中胆固醇及中性脂肪含量降低，减少脂肪在血管内壁的滞留时间，促进粥样硬化斑的消散，防止由胆固醇引起因血管内膜损伤，保持血循环的畅通无阻。
swisse维c片的功能主治
Swisse维C片的功能主治简介Swisse维C片是一种含有高剂量维生素C的膳食补充剂，广泛应用于改善身体健康和增强免疫力。
维生素C是一种重要的水溶性维生素，对人体具有多种重要作用。
功能主治Swisse维C片主要具有以下功能和主治特点：1.增强免疫力：Swisse维C片中的高剂量维生素C可以增强免疫系统的功能，提高抵抗力，减少感冒和其他疾病的发生。
维生素C可以促进白细胞的产生和活性，增强机体对病原体的抵御能力。
2.抗氧化作用：维生素C是一种强效的抗氧化剂，可以帮助清除体内的自由基，减轻氧化应激对身体健康的损害。
维生素C还可以促进抗氧化物质谷胱甘肽的再生，保护细胞免受氧化损伤。
3.促进胶原蛋白合成：Swisse维C片中的维生素C可以促进胶原蛋白的合成，有助于维持皮肤、血管、骨骼等结缔组织的正常功能。
胶原蛋白是人体重要的结构蛋白，对保持皮肤弹性、提高肌肤亮度等具有积极作用。
4.增强铁的吸收：维生素C可以提高肠道对铁的吸收效率，促进铁的转运和利用，有助于防治缺铁性贫血。
缺铁性贫血是常见的一种贫血类型，维生素C的补充可以提高身体对铁的利用率，缓解贫血症状。
5.降低血清尿酸水平：维生素C可以通过增加尿酸的排泄，帮助降低血清尿酸水平，减少痛风和尿酸肾结石等尿酸相关疾病的发生。
适用人群Swisse维C片适用于以下人群：•免疫力低下者：身体抵抗力较弱、易感冒的人群。
•常年疲劳、亚健康人群：维C片可帮助改善疲劳感，提升身体健康。
•缺乏新鲜水果蔬菜摄入者：维生素C是水溶性维生素，摄入不足时可以通过维生素C片来补充。
•需要增加胶原蛋白合成者：如皮肤干燥、皱纹增多者，可选择适量补充维生素C。
使用方法•每日常规保健：成人每天建议服用1片，随餐服用。
•养颜护肤：可视个体需求增减用量。
注意事项：•请按照产品说明和医生建议使用，不可过量服用。
•对维生素C过敏者、肾脏功能异常者请事先咨询医生。
•孕妇和哺乳期妇女请在医生指导下使用。
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Swisse女士复合维生素（120片/瓶）
产地：
澳大利亚
产品简介：
Swisse女士多维片全面为女士提供每日所需的维生素、矿物质和草本元素，还添加了抗氧化元素，有效舒缓压力疲劳，改善女性生理机能，激发女性活力。
适宜人群：
爱美的女性、缺乏维生素、长期喝酒的女性、生活压力大的女性
使用方法：
每日一粒，随餐或餐后服用，或遵医嘱服用
禁忌及注意事项：
本品为海外保健膳食补充剂，不能代替药物。
已服用其他含硒药物或维生素的人群须谨慎服用，请勿过量。
本品含有B族维生素，可导致尿液变黄，此为正常现象。
16岁以下儿童不建议服用。