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SD Movies Point. Black Desert Online Character Download. To browse Academia. Log in with Facebook Log in with Google. Remember me on this computer. Enter the email address you signed up with and we'll email you a reset link. Need an account? Click here to sign up. Download Free PDF. Consensus statement on management of dyslipidemia in Indian subjects Indian Heart Journal, Sanjay Kalra.
A short summary of this paper. Consensus statement on management of dyslipidemia in Indian subjects. Iyengar d, Rajeev Gupta e, Subhash C.
Manchanda f, P. Mohanan g, V. Dayasagar Rao h, C. Manjunath i, J. Sawhney j, Nakul Sinha k, A. Pancholia l, Sundeep Mishra m, Ravi R. Hospital, Poonkunnanm, Thrissur , India h Sr. All rights reserved.
There are an estimated The age-standardized estimates for disability- may differ in Indians with potential implications on the adjusted life-years DALY's lost due to CAD are three times optimum dosages required to achieve the lowest risk- higher in India than in developed countries. A wide va- million deaths annually. At the same time, the CV benefits of riety of cuisines are consumed across different states of lipid lowering have also been well researched.
A review of ten our country. Most of them involve extensive use of large cohort studies reported that a decrease of Sweets those enrolled between 5 and 12 years. The harmful terventions, reduces the occurrence of ischemic events across effects of these unhealthy eating practices are further all age groups.
Although there are distinct epidemiological reinforced by the lack of physical activity among Indians, difference between South-Asians and the western pop- which is becoming increasingly common as a result of ulations, overall CV risk factors are same in both.
In fact, as urbanization and growing affluence. Even when detected, in South-Asians. As the burden of communicable diseases is pidemia in US and Europe, no specific guidelines exist for lipid still substantial in our country, the primary focus of the management among Indians. Consequently, Indian physi- healthcare policies continues to remain on the communi- cians need to resort to the western guidelines only for man- cable diseases.
As outlines below, The present document has therefore been prepared as an Indians are known to have significant socioeconomic, cul- attempt to address the above concerns and to suggest man- tural, lifestyle and genetic differences that directly or indi- agement approaches that are more pertinent to Indians. The intended primarily to assist in clinical-decision making. LDL-C levels are not very high but there is greater pre- However,the final decision regarding care of a particular pa- ponderance of more atherogenic small, dense LDL particles tient has to be made by the treating physician, keeping in as compared to Caucasian subjects.
In addition, the TG consideration all relevant clinical and non-clinical factors levels are usually elevated and HDL-C levels are low. This related to that particular patient. Most published studies from India are 2. Epidemiological aspects from special regional groups, which, by design, are not representative of the entire Indian population. A large cross 2. Burden of CVD in India sectional study, with samples from different socioeconomic strata across different cultural groups with different dietary CVDs are the largest causes of mortality in the world and habits is required to determine normal lipid values amongst majority of deaths occur in low and middle income countries Indians.
Similarly, in absence of prospective studies, it was such as India. Nevertheless, but have since jumped to rank 1 and 3 in The available the other leading causes of YLLs. WHO reports annual age-adjusted available for the western populations. A small study in rural Gujarat8 and a larger study in consensus group, while highlighting the limitations of such an rural Andhra Pradesh9 reported age-adjusted annual mortal- approach. These rates are almost twice that of USA and 3e5 times The government should promote a positive attitude towards greater than many European countries.
As prevention is perhaps the only cure, ological studies in India that have defined prevalence of CHD educating the general public about the importance of lipids and stroke and identified burden of disease. The laws of these studies reported that prevalence rates have more regarding permissible levels of quality and quantity of salts than trebled in the Indian population. Similarly, a uniform lipid testing cations and 0.
In the intervening years the CHD preva- Advisory statement. At the same time, the known CHD or pathological ECG-Q waves a lower prevalence policy initiatives should also focus on improvement in socio- has been reported in various Indian studies. The PURE Study economic status and literacy, adequate healthcare financing reported prevalence of known CHD, stroke or either in high and public health insurance to ensure uniform availability of income, upper middle income, lower middle income and low healthcare to all segments of the society, irrespective of their income mainly India countries.
CV risk factors be able to derive the maximum benefit, the goal should be to influence as large section of the society as possible. Geoffrey There are no prospective CV epidemiological studies that have Rose, who developed concept of continuum of risk associated identified risk factors of importance in India. These risk factors sequent sections. Some of increased significantly.
Risk factor prevalence and trends study using uniform methodology, review of hypertension Review of epidemiological studies suggests that all the major epidemiological studies shows that the prevalence of hyper- CV risk factors are increasing in India. Tobacco production tension is significantly greater in metropolitan cities such as and consumption have increased significantly. Smoking is Mumbai and low in less populated cities.
Diabetes history 9. The prevalence Cardiac causes 6. In a cross sectional reported size Men Women study on such consecutive patients, dyslipidemia was Delhi Urban Slum Study The tri- Urban Slum glyceride levels, however, have not increased and in fact have Indian Women's Health e When compared with the western pop- in other ethnic groups.
Reasons for greater prevalence of atherogenic contrast, mean serum cholesterol levels among Asian Indians dyslipidemia in Indians have been shown to be similar to that of the general popula- The higher prevalence of atherogenic dyslipidemia in Indians tion in the US and lower than the levels in the UK. Environmental factors. The role of dyslipidemia is particularly common in South Asians and has environmental factors in the development of CVRFs has been been shown to have a strong association with type 2 diabetes highlighted by the migrant studies comparing Indian subjects mellitus, metabolic syndrome and CVD.
For example, Bhatnagar et al compared forms of lipid abnormalities among Indians. A cross-sectional study of South Asians are increasingly consuming diets high in children aged 9e18 years and their mothers, using quali- saturated fats, cholesterol, and refined carbohydrates and tative focus group and quantitative semi-structured low in polyunsaturated fatty acids and fiber. These food items contain high 2. Genetic factors. Genetic susceptibility of Asian Indians amount of trans-fatty acids due to deep-frying using low to development of dyslipidemia and obesity has been shown cost and widely available partially hydrogenated vege- in some studies.
Association of Apo B gene polymorphisms table oils. Urbanization exposes people to a APOC3 SstI gene polymorphism S1S1, S1S2 and S2S2 geno- number of challenges such as imbalanced diets, physical types was shown to be associated with plasma triglyceride inactivity, long working hours and other urban stresses, levels. Another study reported that variants of Myostatin gene In an earlier study, it was shown that migrant post- predispose to obesity, abdominal obesity and low lean body menopausal women settled in urban slums had high mass in north Indians.
Larger studies are required. Evaluation of a patient with dyslipidemia energy expenditure. Other social factors for physical inac- tivity include priority for academics at the cost of playing 3. Measurement of lipid values time in children, increasing use of television and com- puters, lack of playfields and open spaces, and security Measurement of lipids is the first step towards management concerns in the outdoors, especially for women.
In a study of dyslipidemia. The NECP-ATP III guidelines recommend involving different ethnic groups, lower level of physical that a lipid profile should be obtained at least once every 5 activity in Asian Indians, Pakistanis and Bangladeshis was years in adults age 20 years or above. CV risk stratification tors and evidence of pre-existing CVD. This recommenda- tion of higher age-threshold for initial lipid estimation is 3.
This presents a practical challenge as many-a-times circumstances do not allow fasting sampling. In such settings, 3. Non- gorithm. It includes all the developed in to predict the overall CVD risk. As a Some prospective studies have reported that non-fasting result, FRS tends to overestimate CV risk in populations in serum triglyceride levels may be a useful predictor of CV which the CVD incidence is much lower, as in the Europeans.
Finally, FRS adequately standardized. Conse- rating all Apo B containing lipid particles in blood, can provide quently, in a young individual, the estimated year CV risk a similar, albeit slightly less accurate, information in a more according to FRS is invariably low, despite the presence of cost-effective and simpler manner.
This has important implications for Indians in whom CVD tends to occur at a younger age than the Summary western populations. As a result, FRS is likely to underesti- The present consensus committee recommends that lipid mate CV risk in Indians, as has been amply highlighted in measurement should be performed in all adults beginning at some of the studies.
As all the currently existing guidelines are based on LDL-C levels, it is advisable to obtain complete 3. Alternate CV risk scores. A number of other scoring fasting lipid profile. However, when fasting sample cannot be systems, as mentioned above, have been developed to over- obtained, measurement of TC, HDL-C and non-HDL-C from a come the limitations of FRS but none of them has been vali- non-fasting sample should be sufficient and if required, a dated in Indians.
These risk assessment charts have been derived with the findings on the initial assessment. These charts predict year risk of a fatal or non-fatal cardiovascular event.
For rural Indians, the suggested correction geographical regions. Though these charts have not been factor is 1. South Asian populations. More recently, two new risk scoring systems have become Summary. Estimation of the future CV risk is an essential available. Unfortunately, none of the currently pooled data from multiple cohorts, including the Framingham available risk scoring algorithms have been specifically vali- original and off-springs cohorts.
Role of sub-clinical atherosclerosis imaging Although this risk score is applicable to the populations in The conventional risk assessment algorithms have yet the UK, it includes data on non-resident Indians also and may another important limitation thatwhile they work well at the therefore be able to provide relatively more accurate risk es- population level, their accuracy at the individual level is timates for resident Indians than other risk algorithms.
Thus, it is not uncommon to find individuals with no A yet another approach, as has been suggested by several apparent CV risk factors to develop CVD while many of those investigators, is to recalibrate the FRS by multiplying the with multiple CV risk factors remain free from CVD for years.
A potential solution to advices. Experience with subclinical atherosclerosis assessment factors. If a person has evidence of sub-clinical atheroscle- in Indians. Several cross-sectional studies have been per- rosis, he or she has high probability of developing clinically formed in resident Indians to assess the utility of CIMT and manifest CVD later on, irrespective of the presence or absence CCS in them.
CIMT has been shown to correlate with the of the CV risk factors and will therefore deserve aggressive presence and extent of existing CAD as well as the presence of risk factor modification.
Several tools for detection of sub- conventional CV risk factors. In addition, the normal reference values of CIMT in brachial artery flow-mediated dilatation, coronary calcium Indian subjects are also not available at present. The data with score CCS , ankle-brachial index, pulse wave velocity, etc.
CCS is even more limited with hardly few studies published so Among them, carotid imaging and CCS appear to be the most far. Carotid ultrasound imaging allows detection and charac- Summary. The assessment of subclinical atherosclerosis terization of carotid plaques and measurement of CIMT. However, their rotid artery.
The basic premise underlying carotid vascular routine use cannot be recommended at present because of imaging is that atherosclerosis is a generalized process, which the lack of outcome data with these techniques and also affects all vascular beds sooner or later.
Hence, the evidence of because the normal reference values for these various atherosclerosis in carotid arteries is likely to indicate high risk atherosclerosis markers are not yet available for Indians. This hypothesis has been adequately Nevertheless, the physicians or cardiologists with adequate validated in autopsy studies as well as a number of large experience with these techniques may continue to use them clinical trials. In coronary arteries, calcium is deposited only in the athero- 3.
Biochemical markers for risk assessment sclerotic plaques and therefore the presence of coronary cal- Atherosclerosis is now well-recognized to be an inflamma- cium serves as an indirect evidence of ongoing atherosclerotic tory disease. Consequently, a number of markers of process in the coronary arteries. The total CCS is directly inflammation have been shown to be associated with the related to the total atherosclerotic burden in the coronaries extent of atherosclerosis and the risk of adverse CV events.
However, the calcium in the coronaries is not site- been the most extensively studied marker. This occurs as a result of positive remodeling in be a target for initiation of statin therapy, irrespective of the which the coronary arterial wall undergoes expansion sec- lipid levels. Therefore, any significant inflam- future risk of CV events.
The main incremental role of these tools is in patients deemed At present, there is only limited data available to assess the to be at intermediate risk. While several those who are shown to have the evidence of ongoing cross-sectional studies have demonstrated relationship be- atherosclerosis whereas a less aggressive approach can be tween hsCRP and various conventional and non-conventional adopted in those having no evidence of atherosclerosis.
An CV risk factors,e no prospective study is available as yet added advantage of these imaging techniques is that they may to show the prognostic utility of hsCRP measurement in also help in improving patient compliance to the treatment.
When available, the imaging for subclinical atherosclerosis Summary. The use of these markers to further provide direct evidence of atherosclerosis and to further refine refine CV risk in intermediate risk patients is optional. Lp a the CV risk. Management of dyslipidemia 3. Other markers for CV risk assessment Urinary albumin excretion has been suggested to be a useful 4. Lipid goals and overall approach to treatment tool for CV risk prediction as microalbuminuria is considered to be a manifestation of vascular damage.
However, the value of micro- albuminuria as a CV risk marker is restricted largely to the 4. Primary prevention patients with diabetes or hypertension. However, as recommendations are summarized in Box 1. Long-standing diabetes, particularly with other CV statescharacterized by elevated triglyceride levels such as risk factors or with evidence of target organ damage and metabolic syndrome and diabetes-the conditions commonly presence of chronic kidney disease also signify high CV risk seen among Indians.
Conversely, if there is no for lowering non-HDL-C is same as that for lowering LDL-C, evidence of pre-existing atherosclerotic vascular disease and using non-HDL-C as the primary target for therapy does not the patient has no or only one major CV risk factor, the risk of require any deviation from the standard clinical practice.
At adverse CV events is generally low. An exception to this is the same time, as LDL-C is lowered with the help of statin when there is an extreme of the single risk factor such as therapy, non-HDL-C becomes an increasingly superior pre- strong family history of premature CAD, chronic heavy dictor of residual CV risk than the on-treatment LDL-C smoking, markedly deranged lipid values, etc.
In all the levels. Since majority of which the goals for lipid lowering and means of achieving it the asymptomatic patients encountered in the regular clinical are decided. As refinement of the risk estimate is required in them to permit there are no prospective studies available to determine the better matching of the intensity of the therapeutic approach optimal LDL-C levels and the treatment thresholds in Indians, with the true CV risk.
In such patients, it is advisable to look these recommendations are based on the available western for the presence of one or more of the non-conventional risk guidelines only.
The rationale behind this recom- desired range. Nutritionist's involvement often helps. A large number of studies in a Cardiovascular risk categories as applicable to Indians. The treatment should begin with a statin dose ex- disease CAD, carotid artery disease, peripheral arterial pected to lower LDL-C by the desired margin and the dose disease, abdominal aortic aneurysms, atherosclerotic should be up-titrated if the initial dose fails to achieve the renal artery stenosis, etc desired LDL-C reduction.
Smoking cessation is drome, impaired fasting glucose, impaired glucose also very helpful and should be encouraged. At the same time, tolerance, psychosocial stress, microalbuminuria, etc. Pharmacotherapy is also rec- ommended from the beginning itself in individuals perceived 4. Life-style modifications to be at high risk of CV events Table 4.
Diet most cost-effective methods to control dyslipidemia and Dietary modification is a powerful non-pharmacological for overall primary and secondary prevention of heart strategy for improving blood lipids.
The goals of nutrition disease. In general, nutrition advice for people with dyslipidemia is the same as The treatment should begin with a statin dose expected to lower LDL-C by the desired margin. The dose can be up titrated if the initial dose fails to achieve the desired LDL-C reduction.
Nutrition in all forms of dyslipidemia management should be individualized. All patients should be on a statin All patients should be on a statin All patients should be on a statin 4. Energy intake should be limited to the amount of energy needed to maintain or obtain a healthy weight, i. Energy requirement for any individual is calculated by multiplying the activity factor by ideal body weight of that individual Table 6.
For example, an Asian In- dian man with medium built frame, cm tall, should ideally weigh 62 kg and would require Kcal to maintain healthy weight if he is sedentary. The primary source of complex carbohydrates in the diet should be cereals whole wheat, brown rice etc.
Complex carbohydrates should be preferred over refined carbohydrates and its products, e. While deciding for carbohydrates, the glycemic index GI Patients with established atherosclerotic vascular disease Low risk 0e1 CV risk factor and year risk of hard CV of foods should also be considered.
GI is a measure of the effects of carbohydrates on blood Does not include patients presenting with an acute CV event. In contrast, high GI foods [refined flour, root all the other subjects. Along with GI, glycemic load GL of the food should also be Purpose Primary considered, which depends on the amount of carbohydrate consumed. Source: Williams, provided by a food and dividing the total by For one Men serving of a food, a GL lower than 10 is considered low; between 11 and 19 is considered medium, and 20 or more is considered high.
Whole grains, ce- reals, pulses, vegetables and fruits contain high dietary fiber. A minimum of four to five servings per day of fruits and vegetables are recommended i.
Fruits lbs Simple sugars like crystalline sugar, sugarcane juice, sweetened carbonated beverages, fruit juices and sugar syrups should be avoided. A high dietary intake of fat has been reported in Asian Indians. Regular consumption of foods with high ALA content proportion of total fatty acids as n-6 PUFA and a lower pro- wheat, pearl millet, pulses, green leafy vegetables, portion of long-chain n-3 PUFA in plasma and cellular mem- fenugreek, flaxseed, mustard seeds.
Partial substitution of visible fat and invisible fats from has been suggested that an imbalance in dietary n-6 and n-3 animal foods with whole nuts such as pistachios and PUFA may be important for the development of insulin almonds. Moderation in the use of animal foods containing high fat, saturated fats and cholesterol. The 3. While low-fat diets are generally recommended, it is 6. Food-based guidelines to ensure optimal fat quality in Asian Indian diets 4.
Proteins 1. The recommendation for oils are as follows 1. Protein intake should be based on body weight. This should a. Combina- Indian vegetarian diet. In conjunction with energy intake, the protein intake mended. Non-vegetarian: Egg white, fish, and lean chicken. Salt b. Consumption of butter and ghee clarified butter should 1. Salt intake should be less than 5 g of sodium chloride or be kept to minimum.
To limit the intake of trans fats, strictly avoid the use of 2. Addition of extra salt at the dining table should be avoided. Coconut oil, palm kernel oil, palm oil and palmolein or popcorn, salty biscuits, preserved meat products, other their solid fractions should be substituted for partially- pre-prepared and preserved foods, soups, cheese, fast hydrogenated vegetable oils in foods that require solid foods should be limited.
Avoid processed foods that have fats bakery fats, shortening etc. These oils are high in high salt content. Reading of food labels to determine sodium content of the commercial foods should be encouraged. Sodium, in 2. To ensure correct balance of fatty acids from dietary such foods may be added in the form of sodium benzoate, components other than visible fat, the following dietary monosodium glutamate, baking powder, and baking guidelines are recommended, soda.
Alternatives to sweetened beverages can be water, skim- lipids. Indian sweets, halwa a gelatinous sweet dish made from variability in the HDL-C raising effect of PE, probably due to grain flour, ghee, sugar and nuts , kheer a sweet dish made differences in baseline characteristics and genetic factors. In from boiling rice with milk, sugar, cardamoms, saffron and addition, PE has been shown to reduce TG as well as improve nuts , puddings, ice creams, sweetened biscuits, cakes, the LDL-C particle size.
Therefore, PE may prove to be particularly 4. Encourage reading of food labels to determine sugar con- helpful in reducing CVD in Indians. Some of the names in the ingredients list for the presence of added sugars include: brown sugar, corn syrup, 4. Several cross sectional dextrose, honey, malt syrup, sugar, molasses and sucrose.
Artificial sweeteners could be used in moderation. How- are higher in physically active people as compared to less ever, these do not contain any beneficial nutrients and active counterparts. Although males and females compared with baseline with significant doubts have been raised regarding safety of saccharin, FDA individual variability. Stevia Stevi0cal, PE are not entirely clear. Data are inconsistent regarding Gwiser and some sugar alcohols Sorbitol, xylitol, whether greater benefit occurs with low vs normal to high mannitol, maltitol etc.
Lipid lowering foods. There is also a need to iden- levels. Kraus et al found lowering properties. Oats, fraction. Nutse tent relationship between the intensity of exercise and in- 3. Psyllium husk crease in HDL-C.
Cinnamon, that genetics might play a key role in response of HDL-C to 5. Flaxseeds, exercise. Soy, notype, and lipoprotein lipase LPL genotype. Amla 9. Garlic 4. Effects of PE on TG. PE has a consistent favorable Finger Millet effect on serum TG levels especially in patients with disorders Observational studies have shown an in- verse association between PE and TG levels.
Non-dietary measures subset analysis of men in the Heritage Family Study 4. Physical exercise PE. LDL-C is the most smoking cessation. Smokers should quit smoking because it fect on LDL-C as reported in several systemic reviews. Though, separate data on bidi smoking and reduction of LDL-C by PE also showed significant reduction in chewable tobacco are not available, they should also be body fat and weight.
Alcohol consumption. Resistance training non drinkers and heavy drinkers in several prospective cohort over longer periods may also reduce LDL-C. However, binge drinking and heavy drinking increase portions of small-dense LDL. CV mortality. Summary and recommendations regarding phys- blood pressure and TG, inmale patients with diabetes.
Similarly a cross sectional study by Roy et al among The following recommendations are made as per WHO's alcohol users in India shows that alcohol intake increased the Global Recommendations on Physical activity for health risk for CAD.
In moderate-intensity such as brisk walking PE throughout addition, as heavy drinking can increase TG and blood pres- the week, or do at least 75 min of vigorous-intensity aerobic sure and cause metabolic syndrome, apart from causing other exercise throughout the week, or an equivalent combina- non-lipid harmful effects, it should completely be avoided.
Yoga is an ancient Indian and holistic tech- PE is similar to adults aged 18e64 years but when adults of nique which has been shown to control stress. It has also been this age group cannot do the recommended amounts of shown to have several cardio protective effects in several exercise due to health conditions, they should try to be as small studies like control of hypertension, body weight, physically active as their abilities and conditions may blood sugar, and improvement in lipids.
In addition, exercise. Smoking cessation. Smoking intensity has been asso- A recent study suggests that yoga may improve lipid profile in ciated with reduction in HDL-C with small but statistically patients with end stage renal disease.
Psychosocial stress is an important but and improvements in lipids after smoking cessation, though neglected risk factor for CAD. Several Simvastatin Semi-synthetic Short acting small studies suggest that yoga can affect lipids favorably. Pharmacological therapy Rosuvastatin 4. Of the long acting statins, rosuvastatin has a longer action than atorvastatin, which acts longer than pitavastatin. Statin pharmacokinetics and clinical benefits. Table 9 Pitavastatin summarizes the pharmacology of commonly available sta- tins.
Pitavastatin has minimal effects on CYP P, while pravastatin has none. Statins metabolized Lovastatin by alternate pathways are to be chosen if there is evidence of hepatic or muscle toxicity by a statin with CYP P 3A4 pathway.
Short acting 4. The standard dosages as use with caution well as maximal dosages of various statins are shown in Table Short acting 8. This of course does statin therapy, other causes of muscle symptoms should be not apply to patients presenting with an acute CV event, in looked for. If persistent muscle symptoms are determined to whom intensive statin therapy is recommended from the arise from a condition unrelated to statin therapy, or if the outset ref.
Section 6. In addition, it is advisable to avoid consumption etc. Liver function abnormality. Liver enzyme 4.
Adverse effects. Statins are safe drugs. In large clinical changes generally occur in the first 3 months of therapy trials, side effects of statins have been quite rare. Serious muscle injury being much rarer at 0. Muscle toxicity. Statins may cause different checked prior to the initiation of therapy and when clinically types of muscle toxicity which can be classified as follows- indicated.
These patients should be monitored until the abnormalities resolve. Once abnormal- ating statin therapy. However, in patients at high risk of muscle ities resolve, statin can be restarted cautiously, using a toxicity, such as elderly patients, patients on concomitant drug smaller dose and possibly a different statin than the previ- therapy likely to increase the risk of myotoxicity or those with ously used one.
If liver injury recurs and an alternate etiology hypothyroidism, reduced renal or hepatic function, rheuma- is not found, statin therapy may have to be permanently tologic disorders such as polymyalgia rheumatica, steroid discontinued. If muscle symptoms resolve, and if no contra- 4. Other important adverse effects. Statin therapy is indication exists, the original or a lower dose of the same associated with very modest excess risk of new onset diabetes statin should be restarted establish a causal relationship be- 1 excess case per individuals treated 1 year with tween the muscle symptoms and the statin therapy.
If a moderate-intensity statin therapy and 3 excess cases per causal relationship exists, the original statin should be dis- individuals treated for 1 year with high-intensity statin ther- continued and a low dose of a different statin should be apy. However, the benefit with statin therapy clearly out- started once muscle symptoms have resolved.
If this is toler- weighs this small risk of new-onset diabetes. Clinical evidence. Tables 10 and 11 summarize the evidence showing beneficial effects of statins in large clinical trials in primary and secondary prevention settings, respectively.
Yes Yes Yes Yes Yes 4. Available fibrates are: fenofibric acid derivatives, gemfi- brozil and bezafibrate. After oral administration, Gemfi- brozil reaches peak plasma concentration at around 1e2 h.
The absorption of the drug is best when given before meals. Gemfibrozil is High-risk men aged 45e64 y without prior MI, followed up for 4. The elimination half-life is approximately 1. Fenofibrate is the most commonly Population used fibrate in clinical practice. After absorption in to the circulation, it is hydrolyzed to fenofibric acid, which is the active metabolite.
The elimination half-life is approximately 20 h. A major problem with fenofibrate is its poor water solubi- lity resulting in low and unpredictable oral bioavailability. Micronized and nano-particle formulations have been devel- C required oped to overcome these challenges but oral bioavailability related issues still remain. More recently, choline salt of higher fenofibric acid has been developed which does not have most of these problems.
Table 11 e Cardiovascular benefits of statins in secondary prevention clinical trials. Choline salt of fenofibric acid is the only fibrate approved complications. A number of trials have evaluated 4.
Dosage fibrates, either alone or in combination with statin therapy. However, fenofibrate therapy 4. The recommended dose of gemfi- resulted in significantly lower risk of non-fatal MI and coro- brozil is mg twice a day, given 30 min before the meals. The recommended dosage of beza- stroke and CHD death or individual components, despite fibrate is mg twice or thrice a day or mg modified reduction of triglycerides and increase in HDL-C.
Dose adjustment according to However, a subgroup analysis involving patients with TG renal function is indicated. There 4. In addition, extreme caution results were confirmed in a meta-analysis that included 5 needs to be exercised when prescribing fibrates to those with large trials with fibrates. Bile acid sequestrants BAS 4. Fibrate use can cause myotoxicity Cholestyramine, colestipol and colesevelam are the three including myopathy and rhabdomyolysis especially when co- commonly available BASs.
Cholestyramine and colestipol administered with a statin, particularly in patients with dia- were initially available as water insoluble powder, but coles- betes mellitus, renal failure, hypothyroidism and in elderly tipol was subsequently developed as a tablet form to improve patients. If gemfibrozil needs to be combined with a statin, flu- vastatin may be preferred, since there is no significant effect 4. Mechanism of action. Bile acids are secreted in the bile of gemfibrozil on its concentration.
They emul- Fenofibratestatin combination was evaluated in around sify the fat in food, facilitating absorption. A major portion of patients of the total population of patients who the secreted bile acid is reabsorbed from the intestines and received both the drugs, in the Fenofibrate Intervention and returned to the liver via the portal circulation, thus, forming Event Lowering in Diabetes FIELD trial.
There were no re- the enterohepatic cycle. Mono- drug was discontinued by 2. It is therefore recommended that serum creatinine should be checked before initiating fibrate therapy, 4. BASs are not absorbed or metabolized, and routine creatinine monitoring is required in patients with and there is no interference with systemic drug metabolizing preexisting chronic kidney disease.
Colesevelam is approved for use as disorders, those who have had major gastrointestinal adjunct to diet and exercise. Dosage tion. Because of the tablet size, colesevelam and colestipol 4. The recommended starting should be used with caution in patients with dysphagia or dose is 4 g once or twice a day followed by maintenance daily swallowing disorders, since they may cause dysphagia or dose is 8e16 g, divided into 2 doses.
Dose increments should esophageal obstruction. For example, colesevelam of 4 weeks. The maximum recommended daily dose is 24 g. Chronic use of BAS may divided doses. The starting doses should be 5 g granules once a be associated with increased bleeding tendency due to hypo- day, or two 1 g tablets once or twice a day and should be prothrombinemia and vitamin K deficiency.
BAS may decrease absorption of fat-soluble vitamins. Patients on vitamin therapy should take vitamins at least 4 h 4. Colesevelam can be used at lower before the BAS. If a patient is taking other medications in doses since it has greatest bile acid binding capacity among addition to cholestyramine or colestipol, the other medica- BAS. The recommended dose is six mg tablets once a day tions should be taken 1 h before or 4 h after the BAS. Cole- or divided in two doses with meals. It can be dosed at the same sevelam is a more specific BAS, but may reduce GI absorption time as a statin or the two drugs can be dosed apart.
After of some drugs. Also, the couple chose to go about as outsiders under a similar rooftop and win over each other. Daana Paani next Punjabi movie scheduled to be released on 4 May, The cast also includes Nirmal Rishi. It is a drama directed by Tarnvir Singh Jagpal. Punjabi cinema just started to grow their wings to fly high. And our Actors directors producers doing tremendously. From last 5 years standard of Punjabi cinema jumped high.
To keep it continue and to make high standard movie, they need funds, at least minimum as they spend of making of same movie.
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