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  药店国别: 美国药房
产地国家: 美国
所属类别: 皮肤科药物->糙皮病
处方药:处方药
包装规格: 750毫克/片,90片/瓶
计价单位:
  点击放大  
生产厂家中文参考译名:
雅培制药
生产厂家英文名:
Abbott Laboratories
该药品相关信息网址1:
http://rxabbott.com/u4_prescribing_info.cfm
原产地英文商品名:
NIASPAN ER DISPENSED 750mg/tab,90tabs/bottle
原产地英文药品名:
NIACIN
中文参考商品译名:
NIASPAN缓释片 750毫克/片,90片/瓶
中文参考药品译名:
烟酸
原产地国家批准上市年份:
1997/07/28
英文适应病症1:
pellagra
英文适应病症2:
scurvy
英文适应病症3:
beriberi
英文适应病症4:
rachitis
英文适应病症5:
Vitamin A deficiency
临床试验期:
完成
中文适应病症参考翻译1:
糙皮病
中文适应病症参考翻译2:
坏血病
中文适应病症参考翻译3:
脚气病
中文适应病症参考翻译4:
佝偻病
中文适应病症参考翻译5:
维生素A缺乏症
药品信息:

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 详细处方信息以本药内容附件PDF文件(20098421102516.pdf)的“原文Priscribing Information”为准
---------------------------------------------------------------

 

 部分中文烟酸(Niacin)处方资料(仅供参考)

烟酸(Niacin)介绍:
  
  烟酸也称作维生素B3或维生素PP分子式:C6H5NO2耐热能升华它是人体必需的13种维生素之一是一种水溶性维生素属于维生素B族

  烟酸主要是以辅酶的形式存在于食物中经消化后于胃及小肠吸收吸收后以烟酸的形式经门静脉进入肝脏 过量的烟酸大部分经甲基化从尿中排出

  烟酸在人体内转化为烟酰胺烟酰胺是辅酶Ⅰ和辅酶Ⅱ的组成部分参与体内脂质代谢组织呼吸的氧化过程和糖类无氧分解的过程

  烟酸为维生素B复合物之一作为抗(癞)糙皮病因子而起作用在美国亦称Niacin(烟酸)缺乏症状是(癞)糙皮病其症状特征有三:皮肤炎下痢痴呆对狗会发生黑舌病.

Niacin, also known as vitamin B3 or nicotinic acid, is a water-soluble vitamin that prevents the deficiency disease pellagra. It is an organic compound with the molecular formula C6H5NO2. It is a derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide, nicotinamide ("niacinamide"), where the carboxyl group has been replaced by a carboxamide group (CONH2), as well as more complex amides and a variety of esters. The terms niacin, nicotinamide, and vitamin B3 are often used interchangeably to refer to any one of this family of molecules, since they have a common biochemical activity.

Niacin is converted to nicotinamide and then to NAD and NADP in vivo. Although the two are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects as niacin, which occur as side-effects of niacin's conversion. Thus nicotinamide does not reduce cholesterol or cause flushing,[1] although nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.[2] Niacin is a precursor to NADH, NAD, NAD+, NADP and NADPH, which play essential metabolic roles in living cells.[3] Niacin is involved in both DNA repair, and the production of steroid hormones in the adrenal gland.

Niacin is one of five vitamins associated with a pandemic deficiency disease: these are niacin (pellagra), vitamin C (scurvy), thiamin (beriberi), vitamin D (rickets), and vitamin A deficiency, a syndrome which has no common name but is one of the most common symptomatic deficiencies worldwide.
History
Niacin was first described by Hugo Weidel in 1873 in his studies of nicotine.[4] The original preparation remains useful: the oxidation of nicotine using nitric acid.[5] Niacin was extracted from livers by Conrad Elvehjem who later identified the active ingredient, then referred to as the "pellagra-preventing factor" and the "anti-blacktongue factor."[6] When the biological significance of nicotinic acid was realized, it was thought appropriate to choose a name to dissociate it from nicotine, in order to avoid the perception that vitamins or niacin-rich food contains nicotine, or that cigarettes contain vitamins. The resulting name 'niacin' was derived from nicotinic acid + vitamin.
Carpenter found in 1951 that niacin in corn is biologically unavailable and can only be released in very alkali lime water of pH 11.[7] This process is known as nixtamalization.[8]
Niacin is referred to as Vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as "vitamin PP."
Dietary needs
Depending on the definition used, niacin is one of between 40 to 80 essential human nutrients.
Currently niacin deficiency is rarely seen in developed countries and is usually apparent in conditions of poverty and malnutrition and chronic alcoholism (Pitsavas et al., 2004). Alcoholic patients typically experience increased intestinal permeability leading to negative health outcomes. Studies have indicated that in patients with alcoholic pellagra, niacin deficiency may be an important factor influencing both the onset and severity of this condition (Junqueira-Franco et al., 2006).Severe deficiency of niacin in the diet causes the disease pellagra. Pellagra is characterized by diarrhea, dermatitis and dementia as well as “necklace” lesions on the lower neck, hyperpigmentation, thickening of the skin, inflammation of the mouth and tongue, digestive disturbances, amnesia, delirium, and eventually death if left untreated (Prakash et al., 2008). Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression (Prakash et al., 2008). Mild niacin deficiency has been shown to slow metabolism, causing decreased tolerance to the cold. Dietary niacin deficiency tends to occur in areas where people eat maize ("corn") as a staple food. Maize is the only grain low in niacin and nixtamalization is needed to increase the bioavaiability of niacin during meal/flour production. Nixtamalization refers to the process of alkaline cooking maize with lime. This is the primary processing step during the manufacture of maize products including chips, tortillas, and taco shells. The basic pre-Columbian technique involves cooking whole maize in water for 12–16 hours in large tanks. The steeped maize is referred to as nixtamal and the cooked liquid is nejayote. This process functions to soften the pericarp of the maize and allows the endosperm to absorb water, enabling its milling. The nixtamal is washed and then stone-ground to produce masa which is used to produce a variety of products with improved bioavailability of niacin (Sefa-Dedeh et al., 2004).
The recommended daily allowance of niacin is 2–12 mg/day for children, 14 mg/day for women, 16 mg/day for men, and 18 mg/day for pregnant or breast-feeding women.[9][unreliable source?]. The upper limit for adult men and women is 35 mg/day which is based on flushing as the critical adverse effect.
Hartnup’s disease is an inherited nutritional disorder involving an in-born error of metabolism resulting in niacin deficiency (Prakash et al., 2008). This condition was first identified in the 1950’s by the Hartnup family in London. It is due to a deficit in the intestines and kidneys, making it difficult for the body to break down and absorb dietary tryptophan. The result is a similar condition to pellagra including symptoms of red, scaly rash and sensitivity to sunlight. Oral niacin is given as a treatment in this condition in doses ranging from 40-200 mg with a good prognosis if identified and treated early (Prakash et al., 2008). Niacin synthesis is also deficient in carcinoid syndrome because of metabolic diversion of its precursor, tryptophan, to form serotonin.
Niacin status is generally tested through urinary biomarkers, which are believed to be more reliable than plasma levels.

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更新日期: 2010-12-1
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