INCREASED BY UNCONTROLLED DIABETES MELLITUS, OBESITY & SEDENTARY HABITS & IS RISK FACTOR FOR CORONARY DISEASE. IN PRIMARY HYPERTRIGLYCERIDEMIA, SCREEN OTHER FAMILY MEMBERS
Medical Care
" When hTG is diagnosed, secondary causes should be sought out and controlled.
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o Direct treatment of elevated TGs should be undertaken after aggravating conditions, such as uncontrolled diabetes mellitus, are controlled as well as possible.
o In some cases, hTG will resolve completely when the other condition(s) are managed successfully. These conditions include obesity, a sedentary lifestyle, and smoking. Thus, the initial management of hTG should include weight reduction, increased physical activity, and elimination of ingesting large concentrations of refined carbohydrates.
o The latest Adult Treatment Panel guidelines (ATP III) have reclassified serum triglycerides as follows:
Table 1. Classification of Triglycerides
Classification TG Level (mg/dL)
Normal TG level <150
Borderline-high TG level 150-199
High TG level 200-499
Very high TG level >500
" If the secondary conditions that raise TG levels cannot be managed successfully and if TGs are 200-499 mg/dL, the non-HDL-c becomes the initial target of drug therapy using LDL-lowering medication. The non-HDL-c is the sum of the LDL-c and the VLDL cholesterol (total cholesterol - HDLc). The goals for non-HDL-c levels, similar to the goals for LDL-c levels, are dependent on risk and are 30 mg/dL higher than the corresponding LDL-c goals. The classification of LDL-c and non-HDL-c is as follows:
Table 2. Classification of Low-Density Lipoprotein Cholesterol and Non-High-Density Lipoprotein Cholesterol
Classification LDL Goal
(mg/dL) Non-HDL Goal
(mg/dL)
CHD* and CHD risk equivalent, diabetes mellitus, and the following: 10-year risk for CHD >20% <100 <130
Two or more risk factors and the following: 10-year risk <20% <130 <160
0-1 risk factor <160 <190
*Congestive heart disease
" If secondary conditions are not present, no specific care is required other than treatment to improve hTG.
" The importance of obesity, a sedentary lifestyle, and a deconditioned state should not be underestimated in the treatment of hTG. Instituting a program of progressive aerobic and toning exercise along with dietary management of obesity can cause TG levels to decrease several hundred points (in mg/dL).
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" During pregnancy, severe hTG is an unusual complication and may cause pancreatitis.
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o Many case reports have been published describing interventions to manage this condition.
o Most commonly, a very low-fat diet was sufficient to control TGs and prevent pancreatitis.
o Intermittent and, in persistent cases, continuous total parenteral nutrition has been used-usually in the third trimester.
o Reports also have been published describing plasma exchange or apheresis, as well as early third trimester termination of pregnancy by cesarean section.
Diet
" Total fat intake should be restricted if this intervention assists in weight loss. If TG levels are greater than 1000 mg/dL, allowing no more than 10% of total calories from fat usually will lower TGs promptly and dramatically.
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o Fat restriction is a 2-edged sword. When reducing fat intake causes needed weight loss, TGs usually will improve. When TGs are severely elevated (>1000 mg/dL), suggesting impaired or absent LPL activity, a low-fat diet will decrease chylomicron and VLDL production and improve the metabolism of these TG-rich lipoproteins.
o On the other hand, in the setting of stable weight and moderately elevated TGs, a low-fat diet will increase TGs and may, in addition, decrease HDL-c levels. Patients who are extremely compliant and motivated may choose to follow such a diet in the hope of improving their cholesterol levels. If they have a mixed hyperlipidemia, their LDL-c certainly will decrease. However, such a diet will, if anything, cause further deterioration in the HDL-c and TGs. If the patient has an isolated TG elevation and does not lose weight on the diet, the TGs may increase. In such cases, addition of a healthy fat (monounsaturated or polyunsaturated fat) will lower TGs, increase HDL-c, and sometimes decrease LDL-c.
" In cases where dietary intake of sugar and white flour products is substantial, restricting simple carbohydrates and increasing dietary fiber are important adjuncts that can lower TGs substantially.
" Alcohol should be eliminated or restricted to no more than 1 standard alcoholic beverage per day.
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" Omega-3 (N-3) fatty acids
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o The class of polyunsaturated fats known as omega-3 fatty acids, which are derived mainly from fatty fish and some plant products (flax seed), has a unique impact on TGs.
o In large amounts (10 or more g/d), N-3 fatty acids lower TGs 40% or more.
o To achieve this dose, purified capsules usually are necessary, but some patients may prefer to eat large amounts of fatty fish. The fish highest in N-3 fatty acids are sardines, herring, and mackerel; daily servings of 1 pound or more may be necessary.
o If weight gain ensues, TG-lowering will be compromised.
Activity
" Exercise, particularly sustained aerobic activity, can have a dramatic impact on TG levels and may increase HDL-c slightly.
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" The American Heart Association recommends 30-60 minutes of aerobic exercise most days of the week and toning for 20-30 minutes twice a week. This prescription has substantial benefits beyond lipid effects as follows:
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o Reduced weight
o Decreased insulin resistance
o Decreased blood pressure
o Improved cardiovascular conditioning
" Overall reduction in acute cardiovascular events is also a likely benefit of regular exercise.
" Toning of large muscles groups (abdomen, back, legs, arms) also improves metabolism of TG-rich lipoproteins and lowers TGs.
DRUG TREATMENT :
1. FIBRIC ACID DERIVATIVES :
- GEMFIBROZIL
- FENOFIBRATE
2. NIACIN ( NICOTINIC ACID ) :
- NIACIN ( VITAMIN B3 ) SUSTAINED RELEASE :
- IMMIDIATE RELEASE NIACIN
ALTERNATIVE DRUGS :
β’ HMG-CoA reductase inhibitors [lovastatin (Mevacor, Altocor), pravastatin (Pravachol), simvastatin (Zocor),
fl uvastatin (Lescol), atorvastatin (Lipitor), rosuvastatin (Crestor)] lower triglycerides 10-30%
β’ Fish oil
β’ Glitazones - pioglitazone and rosiglitazone
β’ Clofibrate (Atromid-S)
PATIENT MONITORING :
. Fasting lipid profile
. Liver function test, CPK, CBC diff
. Target goals :
* For pancreatitis - TG < 500 mg/dL (< 5.65 mmol/L)
* For CHD: patients with CHD, diabetes, and 2 or more risk factors TG<150 mg/dL (<1.7 mmol/L)
POSSIBLE COMPLICATIONS :
. Acute pancreatitis
. Atherosclerosis
EXPECTED COURSE/PROGNOSIS :
. Good in secondary disorder if the underlying causes are eliminated
. In primary, may need life-long treatment