Combination of niacin extended-release and simvastatin results in a less atherogenic lipid profile than atorvastatin monotherapy.

OBJECTIVE: To compare the effects of combination niacin extended-release + simvastatin (NER/S) versus atorvastatin alone on apolipoproteins and lipid fractions in a post hoc analysis from SUPREME, a study which compared the lipid effects of niacin extended-release + simvastatin and atorvastatin in patients with hyperlipidemia or mixed dyslipidemia. PATIENTS AND METHODS: Patients (n = 137) with dyslipidemia (not previously receiving statin therapy or having discontinued any lipid-altering treatment 4-5 weeks prior to the study) received NER/S (1000/40 mg/day for four weeks, then 2000/40 mg/day for eight weeks) or atorvastatin 40 mg/day for 12 weeks. Median percent changes in apolipoprotein (apo) A-1, apo B, and the apo B:A-I ratio, and nuclear magnetic resonance lipoprotein subclasses from baseline to week 12 were compared using the Wilcoxon rank-sum test and Fisher's exact test. RESULTS: NER/S treatment produced significantly greater percent changes in apo A-I and apo B:A-I, and, at the final visit, apo B < 80 mg/dL was attained by 59% versus 33% of patients, compared with atorvastatin treatment (P = 0.003). NER/S treatment resulted in greater percent reductions in calculated particle numbers for low-density lipoprotein (LDL, 52% versus 43%; P = 0.022), small LDL (55% versus 45%; P = 0.011), very low-density lipoprotein (VLDL) and total chylomicrons (63% versus 39%; P < 0.001), and greater increases in particle size for LDL (2.7% versus 1.0%; P = 0.007) and VLDL (9.3% versus 0.1%; P < 0.001), compared with atorvastatin. CONCLUSION: NER/S treatment significantly improved apo A-I levels and the apo B:A-I ratio, significantly lowered the number of atherogenic LDL particles and VLDL and chylomicron particles, and increased the mean size of LDL and VLDL particles, compared with atorvastatin.

Micronutrients and genomic stability: a new paradigm for recommended dietary allowances (RDAs).

Diet as a key factor in determining genomic stability is more important than previously imagined because we now know that it impacts on all relevant pathways, namely exposure to dietary carcinogens, activation/detoxification of carcinogens, DNA repair, DNA synthesis and apoptosis. Current recommended dietary allowances for vitamins and minerals are based largely on the prevention of diseases of deficiency such as scurvy in the case of vitamin C. Because diseases of development, degenerative disease and aging itself are partly caused by damage to DNA it seems logical that we should focus better our attention on defining optimal requirements of key minerals and vitamins for preventing damage to both nuclear and mitochondrial DNA. To date, our knowledge on optimal micronutrient levels for genomic stability is scanty and disorganised. However, there is already sufficient evidence to suggest that marginal deficiencies in folate, vitamin B12, niacin and zinc impact significantly on spontaneous chromosome damage rate. The recent data for folate and vitamin B12 in humans with respect to micronucleus formation in blood and epithelial cells provide compelling evidence of the important role of these micronutrients in maintenance of genome integrity and the need to revise current RDAs for these micronutrients based on minimisation of DNA damage. Appropriately designed in vitro studies and in vivo placebo controlled trials with dose responses using a complementary array of DNA damage biomarkers are required to define recommended dietary allowances for genomic stability. Furthermore these studies would have to be targeted to individuals with common genetic polymorphisms that alter the bioavailability of specific micronutrients and the affinity of specific key enzymes involved in DNA metabolism for their micronutrient co-factor. That there is a need for an international collaborative effort to establish RDAs for genomic stability is self-evident.

Intoxicación alimentaria por consumo de chacinados con alto contenido de ácido nicótico / Food intoxication through consumption of spiced pork with high nicotinic acid content

Con frecuencia, las enfermedades transmitidas por alimentos en general y la alteración de los mismos, es el resultado de la negligencia, ignorancia o ambos hechos. El objetivo general de este trabajo es conocer el agente implicado en los casos de una intoxicación alimentaria, siendo el propósito contribuir a la vigilancia epidemiológica de las enfermedades transmitidas por alimentos. Se investigó una intoxicación alimentaria ocurrida en una cena del día 10 de junio de 1995, en la ciudad de Coronel Vidal, provincia de Buenos Aires, teniendo en consideración la metodología de investigación del brote. Se tomaron muestras de los alimentos sospechados (ingeridos en dicha cena) para su análisis, indentificándose también la hora de su ingesta. Las personas afectadas, 50 casos aproximadamente, presentaron prurito e hinchazón generalizada, rush cutáneo y algunos pocos, síntomas gastrointestinales. Se comprobó que la fuente de infección fue el chorizo fresco a la parrilla y el agente causal, el ácido nicotínico presente en exceso en dicho alimento. A partir de las recomendaciones hechas, debidas a éste y a otros episodios de intoxicación, el Laboratorio Central de Salud Pública de la Provincia de Buenos Aires ha incorporado a su planilla de inscripción de productos manufacturados de origen cárneo, el análisis de niveles de ácido nicotínico en forma rutinaria, haciéndose efectivo de esta manera, el control sanitario que indica el código alimentario argentino

Intoxicación alimentaria por consumo de chacinados con alto contenido de ácido nicótico / Food intoxication through consumption of spiced pork with high nicotinic acid content

Con frecuencia, las enfermedades transmitidas por alimentos en general y la alteración de los mismos, es el resultado de la negligencia, ignorancia o ambos hechos. El objetivo general de este trabajo es conocer el agente implicado en los casos de una intoxicación alimentaria, siendo el propósito contribuir a la vigilancia epidemiológica de las enfermedades transmitidas por alimentos. Se investigó una intoxicación alimentaria ocurrida en una cena del día 10 de junio de 1995, en la ciudad de Coronel Vidal, provincia de Buenos Aires, teniendo en consideración la metodología de investigación del brote. Se tomaron muestras de los alimentos sospechados (ingeridos en dicha cena) para su análisis, indentificándose también la hora de su ingesta. Las personas afectadas, 50 casos aproximadamente, presentaron prurito e hinchazón generalizada, rush cutáneo y algunos pocos, síntomas gastrointestinales. Se comprobó que la fuente de infección fue el chorizo fresco a la parrilla y el agente causal, el ácido nicotínico presente en exceso en dicho alimento. A partir de las recomendaciones hechas, debidas a éste y a otros episodios de intoxicación, el Laboratorio Central de Salud Pública de la Provincia de Buenos Aires ha incorporado a su planilla de inscripción de productos manufacturados de origen cárneo, el análisis de niveles de ácido nicotínico en forma rutinaria, haciéndose efectivo de esta manera, el control sanitario que indica el código alimentario argentino (AU)

Liquid chromatographic analysis of niacin in fortified food products.

An ion exchange liquid chromatographic (LC) method using an anion exchange resin column was developed for the determination of niacin in fortified foods. Samples were extracted by autoclaving with H2SO4 (1 + 1). Florisil open column chromatography was used to remove interferences from the sample extracts. Niacin levels were quantitated by an LC system using a 250 x 4.1 mm Hamilton PRP-X100 column, a mobile phase of 2% glacial acetic acid in water, and UV detection at 254 nm. The limit of detection was 0.11 micrograms niacin/mL, and the standard curve was linear from 0.24 to 0.80 micrograms niacin/mL. The system reproducibility was evaluated by completing 10 repetitive analyses on an infant formula and a macaroni product, which gave an average CV of 2.7%. Mean recovery (+/- standard deviation) was 99.8 +/- 7.7 (n = 15). The results compared favorably with those by the AOAC microbiological method.

[Nicotinic acid in dust-gas emissions from the biochemical industrial plants producing yeast for animal feed]. / Nikotinovaia kislota v pylegazovykh vybrosakh biokhimicheskikh zavodov po proizvodstvu kormovykh drozhzhei.

The presence of nicotine acid in the dustgaseous pollution from biochemical plants producing fodder yeast has been shown. Its allergic and sensitizing role compared to the same properties of protein-containing dust has been pointed out. It has been suggested that MAC of nicotine acid should be established for the sanitary-protective zone of microbiological industry enterprises.