Pravastatin Sodium 4. Tablets - Summary of Product Characteristics (SPC)Pravastatin Sodium 4. Tablets. Each tablet contains 4. Excipient: Lactose monohydrate 2. Salt is made up of sodium and chlorine (chemical name: "sodium chloride"). But there are other forms of sodium in food, including baking soda (sodium bicarbonate) and. Salt or sodium is a vital part of a diet, but many people get too much. Too much sodium can cause high blood pressure and other problems. Learn about low sodium diets. Schiff® MegaRed® contains oil from 100% pure Antarctic krill, tiny crustaceans that thrive in the frigid waters of the Antarctic. MegaRed® provides an optimal. The following sections describe a healthy eating pattern and how following such a pattern can help people meet the Guidelines and its Key Recommendations. The easiest way to achieve this imbalance is by consuming a diet of processed foods, which are notoriously low in potassium while high in sodium. Sodium R-Lipoate 300 mg Neuroprotective pain relief (R-lipoic acid) Improves several neuropathic symptoms: pain, burning, numbness, tingling Daily Nutritional Goals for Age-Sex Groups Based on Dietary Reference Intakes and Dietary Guidelines Recommendations. Pravastatin Sodium 40 mg Tablets - Summary of Product Characteristics (SPC) by Accord Healthcare Limited. Calcium in the Vegan Diet. Summary: Calcium, needed for strong bones, is found in dark green leafy vegetables. Baking Soda it contains so much sodium,it will damage your kidneys and give you high blood pressure! Pravastatin Tablets 4. Yellow colored, rounded rectangular shaped, biconvex, uncoated tablets debossed 'PDT' on one side and '4. Hypercholesterolaemia. Treatment of primary hypercholesterolaemia or mixed dyslipidaemia, as an adjunct to diet, when response to diet and other non- pharmacological treatments (eg. Pravastatin sodium is administered orally once daily preferably in the evening with or without food. Hypercholesterolaemia: The recommended dose range is 1. The therapeutic response is seen within a week and the full effect of a given dose occurs within four weeks, therefore periodic lipid determinations should be performed and the dosage adjusted accordingly. The maximum daily dose is 4. Cardiovascular prevention: In all preventive morbidity and mortality trials, the only studied starting and maintenance dose was 4. Dosage after transplantation: Following organ transplantation a starting dose of 2. Depending on the response of the lipid parameters, the dose may be adjusted up to 4. Children and adolescents (8- 1. The recommended dose range is 1. Elderly patients: There is no dose adjustment necessary in these patients unless there are predisposing risk factors (see section 4. Renal or hepatic impairment: A starting dose of 1. The dosage should be adjusted according to the response of lipid parameters and under medical supervision. Concomitant therapy: The lipid lowering effects of pravastatin sodium on total cholesterol and LDL - cholesterol are enhanced when combined with a bile acid – binding resin (e. Pravastatin sodium should be given either one hour before or at least four hours after the resin (see section 4. For patients taking ciclosporin with or without other immunosuppressive medicinal products, treatment should begin with 2. Hypersensitivity to the active substance or to any of the excipients. Therapy is not suitable when hypercholesterolaemia is due to elevated HDL- cholesterol. As for other HMG- Co. A reductase inhibitors, combination of pravastatin with fibrates is not recommended. In children before puberty, the benefit /risk of treatment should be carefully evaluated by physicians before treatment initiation. Hepatic disorders: As with other lipid- lowering agents, moderate increases in liver transaminase levels has been observed. In the majority of cases, liver transaminase levels have returned to their baseline value without the need for treatment discontinuation. Special attention should be given to patients who develop increased transaminase levels and therapy should be discontinued if increases in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) exceed three times the upper limit of normal and persist. Caution should be exercised when pravastatin is administered to patients with a history of liver disease or heavy alcohol ingestion. Muscle disorders: As with other HMG- Co. A reductase inhibitors (statins), pravastatin has been associated with the onset of myalgia, myopathy and very rarely, rhabdomyolysis. Myopathy must be considered in any patient under statin therapy presenting with unexplained muscle symptoms such as pain or tenderness, muscle weakness, or muscle cramps. In such cases creatine kinase (CK) levels should be measured (see below). Statin therapy should be temporarily interrupted when CK levels are > 5 x ULN or when there are severe clinical symptoms. Very rarely (in about 1 case over 1. Rhabdomyolysis is an acute potentially fatal condition of skeletal muscle, which may develop at any time during treatment and is characterised by massive muscle destruction associated with major increase in CK (usually > 3. ULN) leading to myoglobinuria. The risk of myopathy with statins appears to be exposure- dependent and therefore may vary with individual drugs (due to lipophilicity and pharmacokinetic differences), including their dosage and potential for drug interactions. Although there is no muscular contraindication to the prescription of a statin, certain predisposing factors may increase the risk of muscular toxicity and therefore justify a careful evaluation of the benefit/risk and special clinical monitoring. CK measurement is indicated before starting statin therapy in these patients (see below). The risk and severity of muscular disorders during statin therapy is increased by the co- administration of interacting medicines. The use of fibrates alone is occasionally associated with myopathy. The combined use of a statin and fibrates should generally be avoided. The co- administration of statins and nicotinic acid should be used with caution. An increase in the incidence of myopathy has also been described in patients receiving other statins in combination with inhibitors of cytochrome P4. This may result from pharmacokinetic interactions that have not been documented for pravastatin (see section 4. When associated with statin therapy, muscle symptoms usually resolve following discontinuation of statin therapy. Creatine kinase measurement and interpretation: Routine monitoring of creatine kinase (CK) or other muscle enzyme levels is not recommended in asymptomatic patients on statin therapy. However, measurement of CK is recommended before starting statin therapy in patients with special predisposing factors, and in patients developing muscular symptoms during statin therapy, as described below. If CK levels are significantly elevated at baseline (> 5x ULN), CK levels should be re- measured about 5 to 7 days later to confirm the results. When measured, CK levels should be interpreted in the context of other potential factors that can cause transient muscle damage, such as strenuous exercise or muscle trauma. Before treatment initiation: Caution should be used in patients with predisposing factors such as renal impairment, hypothyroidism, previous history of muscular toxicity with a statin or fibrate, personal or familial history of hereditary muscular disorders, or alcohol abuse. In these cases, CK levels should be measured prior to initiation of therapy. CK measurement should also be considered before starting treatment in persons over 7. If CK levels are significantly elevated (> 5 x ULN) at baseline, treatment should not be started and the results should be re- measured after 5- 7 days. The baseline CK levels may also be useful as a reference in the event of a later increase during statin therapy. During treatment: patients should be advised to report promptly unexplained muscle pain, tenderness, weakness or cramps. In these cases, CK levels should be measured. If a markedly elevated (> 5 x ULN) CK level is detected, statin therapy must be interrupted. Treatment discontinuation should also be considered if the muscular symptoms are severe and cause daily discomfort, even if the CK increase remains . If symptoms resolve and CK levels return to normal, then reintroduction of statin therapy may be considered at the lowest dose and with close monitoring. If a hereditary muscular disease is suspected in such patients, restarting statin therapy is not recommended. Interstitial lung disease. Exceptional cases of interstitial lung disease have been reported with some statins, especially with long term therapy (see section 4. Presenting features can include dyspnoea, non- productive cough and deterioration in general health (fatigue, weight loss and fever). If it is suspected a patient has developed interstitial lung disease, statin therapy should be discontinued. This risk, however, is outweighed by the reduction in vascular risk with statins and therefore should not be a reason for stopping statin treatment. Patients at risk (fasting glucose 5. L, BMI> 3. 0kg/m. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose- galactose malabsorption should not take this medicinal product. Fibrates: The use of fibrates alone is occasionally associated with myopathy. An increased risk of muscle related adverse events, including rhabdomyolysis, have been reported when fibrates are co- administered with other statins. These adverse events with pravastatin cannot be excluded, therefore the combined use of pravastatin and fibrates (e. If this combination is considered necessary, careful clinical and CK monitoring of patients on such regimen is required. Colestyramine / Colestipol: Concomitant administration resulted in approximately 4. There was no clinically significant decrease in bioavailability or therapeutic effect when pravastatin was administered one hour before or four hours after colestyramine or one hour before colestipol (see section 4. Ciclosporin: Concomitant administration of pravastatin and ciclosporin leads to an approximately 4- fold increase in pravastatin systemic exposure. In some patients, however, the increase in pravastatin exposure may be larger. Clinical and biochemical monitoring of patients receiving this combination is recommended (see section 4. Warfarin and other oral anticoagulants: Bioavailability parameters at steady state for pravastatin were not altered following administration with warfarin. Chronic dosing of the two products did not produce any changes in the anticoagulant action of warfarin. Products metabolised by cytochrome P4. Pravastatin is not metabolised to a clinically significant extent by the cytochrome P4. This is why products that are metabolised by, or inhibitors of, the cytochrome P4. The absence of a significant pharmacokinetic interaction with pravastatin has been specifically demonstrated for several products, particularly those that are substrates/inhibitors of CYP3. A4 e. g. In a similar study with clarithromycin a statistically significant increase in AUC (1. Cmax (1. 27%) was observed. Although these changes were minor, caution should be exercised when associating pravastatin with erythromycin or clarithromycin. BENZOIC ACID AND SODIUM BENZOATE. INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY. CONCISE INTERNATIONAL CHEMICAL ASSESSMENT DOCUMENT NO. BENZOIC ACID AND SODIUM BENZOATE. This report contains the collective views of an international group of. United Nations Environment Programme, the International. Labour Organization, or the World Health Organization. Mangelsdorf, and Dr C. Melber, Fraunhofer Institute. Toxicology and Aerosol Research, Hanover, Germany. Published under the joint sponsorship of the United Nations. Environment Programme, the International Labour Organization, and the. World Health Organization, and produced within the framework of the. Inter- Organization Programme for the Sound Management of Chemicals. The overall objectives. IPCS are to establish the scientific basis for assessment of. The purpose of the IOMC is to promote. Participating Organizations, jointly or separately, to achieve the. Errors and omissions excepted, the names of. IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE4. Natural sources of benzoic acid. Anthropogenic sources. Estimated global release. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, TRANSFORMATION, AND ACCUMULATION5. Transport and distribution between media. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE6. Environmental levels. COMPARATIVE KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS7. Precursors of benzoic acid. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS8. Irritation and sensitization. Short- term exposure. Inhalation exposure. Long- term exposure. Subchronic exposure. Chronic exposure and carcinogenicity. Carcinogenicity of benzyl acetate, benzyl alcohol, and benzaldehyde. Genotoxicity and related end- points. Reproductive and developmental toxicity. Developmental toxicity. Reproductive toxicity of benzyl acetate, benzyl alcohol, and benzaldehyde. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND FIELD1. Aquatic environment. Terrestrial environment. EFFECTS EVALUATION1. Evaluation of health effects. Hazard identification and dose- response assessment. Criteria for setting tolerable intakes or guidance values for benzoic acid and sodium benzoate. Sample risk characterization. Evaluation of environmental effects. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES. REFERENCES. APPENDIX 1 - - SOURCE DOCUMENTS. APPENDIX 2 - - CICAD PEER REVIEW. APPENDIX 3 - - CICAD FINAL REVIEW BOARD. APPENDIX 4 - - INTERNATIONAL CHEMICAL SAFETY CARD. R. CICADs. join the Environmental Health Criteria documents (EHCs) as. They are based on. EHCs. Before acceptance for publication as CICADs by IPCS, these. CICADs are not a summary of. The critical studies are, however, presented in. For additional. information, the reader should consult the identified source documents. CICAD has been based. Responsible. authorities are strongly encouraged to characterize risk on the basis. To assist the. reader, examples of exposure estimation and risk characterization are. CICADs, whenever possible. These examples cannot be. The reader is referred to EHC 1. Geneva, World. Health Organization (Environmental Health Criteria 1. Unless otherwise stated, CICADs are based on a search of. Authors of the first draft are usually, but not. The first draft undergoes primary review by IPCS to ensure that. CICADs. Authors are required to take reviewers' comments into. The resulting second. Final Review Board together with the. They are selected. Boards are. chosen according to the range of expertise required for a meeting and. Representatives of. Final Review Board. Observers may participate in. Board discussions only at the invitation of the Chairperson, and they. The two compounds are being considered together because it is. As benzoic acid itself is only slightly soluble in water. A comprehensive literature search of. September 1. 99. 9 to identify any. Information on the preparation and peer review of the. Appendix 1. Information on the peer. CICAD is presented in Appendix 2. This CICAD was. approved as an international assessment at a meeting of the Final. Review Board, held in Sydney, Australia, on 2. November 1. 99. 9. The International Chemical Safety Card (ICSC 0. International Programme on Chemical Safety. IPCS, 1. 99. 3), has also been reproduced in this document (Appendix 4). Sodium benzoate (CAS No. Benzoic acid is used as an intermediate. Other end products. Sodium benzoate is. Benzoic acid and sodium benzoate are used as food. H range. Their use as. The. estimated global production capacity for benzoic acid is about. Worldwide sodium benzoate production in 1. Benzoic acid occurs. It is therefore a natural. Anthropogenic. releases of benzoic acid and sodium benzoate into the environment are. Concentrations of naturally occurring benzoic acid in. To a lesser extent. Owing to. rapid metabolism and excretion, an accumulation of the benzoates or. In. cats, which seem to be more sensitive than rodents, toxic effects and. For benzoic acid, the available studies. Other effects included. The information. concerning long- term oral exposure of experimental animals to benzoic. From a limited. four- generation study, only a preliminary no- observed- (adverse- )effect. NO(A)EL) of about 5. However, the documentation of. NO(A)EL values can be derived. Data on its precursors support the. Sodium benzoate was also inactive in Ames tests, whereas. In one. in vivo study (dominant lethal assay with rats), a positive result. At present, a genotoxic activity of sodium benzoate. With sodium benzoate. In a dietary. study in rats, a NO(A)EL of about 1. Data on its precursors support the notion that benzoic. However, both substances are known to cause non- immunological. This effect is scarce in healthy. A provisional tolerable intake. As there are no adequate studies. From the. results of numerous removal experiments, the main elimination pathway. Data from. laboratory tests showed ready biodegradability for both substances. Several isolated microorganisms (bacteria. From the experimental data on bioconcentration. EC5. 0/LC5. 0 values for the other aquatic. Immobilization. of Daphnia magna has been demonstrated to be p. H dependent, with a. EC5. 0 (1. 02 mg/litre) at acidic p. H. For the freshwater fish. Leuciscus idus), a 4. LC5. 0 of 4. 60 mg/litre has been. Developmental effects have been found in frog (Xenopus). EC5. 0 for. malformation). For sodium benzoate, exposure of juvenile stages of. Daphnia magna, Gammarus fasciatus, Asellus intermedius, Dugesia tigrina, Helisoma trivolvis, and Lumbriculus variegatus) resulted in 9. LC5. 0 values of greater than. A 9. 6- h LC5. 0 of 4. Pimephales promelas). Owing to the limited available data on. Except for the antimicrobial action of benzoic acid. For sodium benzoate, bacterial. H- dependent manner by. Owing to the lack. C7. H6. O2; C6. H5. COOH. benzenecarboxylic acid, phenyl carboxylic acid . Regulation on Labelling of Foodstuffs). Its solubility. in water is low (2. It is soluble in ethanol. It has an. octanol/water partition coefficient (log Kow) of 1. Its. vapour pressure at 2. Its calculated. Henry's law constant at 2. Additional physical and chemical properties are. International Chemical Safety Card reproduced in. Appendix 4). 5. 32- 3. C7. H5. O2. Na; benzoic acid. Regulation on Labelling of Foodstuffs). It is very. soluble in water (5. Its p. H is about 7. It is soluble in ethanol, methanol, and ethylene. Dry sodium benzoate is electrically charged by friction and. Maki &. Suzuki, 1. Liquid. chromatographic methods were developed to overcome this (e. Bennett. & Petrus, 1. Puttemans et al., 1. Tyler, 1. 98. 4). For the. sensitive determination of benzoic acid in fruit- derived products, a. UV absorbance detection is described (Mandrou et. The detection limit is 0. For soft drinks, a simultaneous. Castro et al., 1. Sodium. benzoate was measured in soya sauce, fruit juice, and soft drinks. HPLC with a UV spectrophotometric detector. Before injection. Villanueva et al., 1. Detection was by 6. Ni electron capture. HPLC methods. have been developed for the simultaneous determination of benzoic acid. Hippuric acid and. HPLC, and. measured hippuric acid levels corrected for urinary creatinine. Villanueva et al., 1. High concentrations are. Benzoic acid has also been. Benzoic acid therefore occurs. Sieber et al., 1. The major producers of. Netherlands (2. 20 0. Japan. (1. 40 0. 00 tonnes per year), followed by the USA (1. Another reference gives the total European capacity as less. SRI, 1. 99. 8). It can also be produced. Shibamoto & Umano, 1. Shibamoto, 1. 98. Worldwide sodium benzoate production in 1. Srour, 1. 99. 8). The. largest producers are the Netherlands, Estonia, the USA, and China. These percentages are still approximately correct today. Srour, 1. 99. 8). Caprolactam seems to be produced only by European. Srour, 1. 99. 8). It is also used to improve. Its use as a. rubber polymerization retarder is diminishing (Srour, 1. Owing to their inhibitory effect on yeast, they cannot be used. Friedman & Greenwald, 1. Examples of. upper concentrations allowed in food are up to 0. USA). and between 0. Chipley, 1. 98. 3). The. European Commission limits for benzoic acid and sodium benzoate are. EC, 1. 99. 5). Benzoic acid is also used in. H values under 4, up to 0. Wallh. Sixteen out of 7. Rastogi et al., 1. Benzoic acid is reported to leach from. Koda et al., 1. 98. Sodium benzoate is also widely used as. Srour, 1. 99. 8). A new use is the formulation of sodium. BFGoodrich Kalama Inc., 1. Sodium benzoate is used as a. BUA, 1. 99. 5). No data were available from other countries. There were no data available on the emission of benzoic. Minor amounts are expected to be. From its physicochemical properties (vapour. Henry's law constant; see section 2), a significant. Experimental data on wet and dry deposition from air. Owing to its use pattern, which. However, benzoic acid adsorbed on silica gel (Si. O2) and. irradiated with UV light (lambda > 2. Freitag et al., 1. This may be due to a. Zn. O) and titanium dioxide (Ti. O2). When benzoic. Kinney & Ivanuski, 1. Matthews, 1. 99. 0). Hydroxyl radical rate constants (k.
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