Hyperlipidemia combined

Hyperlipidemia Diet HMG-CoA reductase inhibitors (stati ns) Gemfibrozil Ezetemibe CSA greater than TAC consider switch to TAC discontinue or hold SRL CSA/TAC may increase statin levels start at lowest dose Monitor for muscle cramps, CPK levels and LFTs Adjust dose in those with Rl Caution with concomitant statin Often used in combination with a statin... 

Koh KK, Quon MJ, Han SH, et al. Additive beneficial effects of fenofibrate combined with atorvastatin in the treatment of combined hyperlipidemia. J Am Coll Cardiol 2005 45(10) 1649-1653. 

BARs are useful in treating primary hypercholesterolemia (familial hypercholesterolemia, familial combined hyperlipidemia, type Ila hyperlipoproteinemia). 

The principal use of niacin is for mixed hyperlipidemia or as a second-line agent in combination therapy for hypercholesterolemia. It is a first-line agent or alternative for the treatment of hypertriglyceridemia and diabetic dyslipidemia. 

Familial combined hyperlipidemia may respond better to a fibrate and a statin than to a fibrate and a BAR. 

F13. Fonda, M., DaCol, P. G., La Verde, R., Battello, C., Fisicaro, M., Tonizzo, M., and Cattin, L., Lipoprotein(a) serum concentration in familial combined hyperlipidemia. Clin. Chim. Acta 223, 121-127(1993). 

Hematologic Agranulocytosis nonthrombocytopenic or thrombocytopenic purpura bleeding thrombocytopenia eosinophilia leukopenia hyperlipidemia. Hypersensitivity Pharyngitis photosensitivity reaction erythematous rash fever combined with aching and sore throat laryngospasm respiratory distress angioedema anaphylaxis. 

The combination of amprenavir and low-dose ritonavir has been associated with elevations of cholesterol and triglycerides, AST, and ALT in some patients. Consider appropriate laboratory testing prior to initiating combination therapy with amprenavir and ritonavir and at periodic intervals, or if any clinical signs or symptoms of hyperlipidemia or elevated liver function tests occur during therapy. 

In 1995 the FDA approved saquinavir, the first protease inhibitor, for use in combination with other nucleoside analogue medications. In 1999 a soft gel capsule formulation of saquinavir with considerably improved absorption characteristics was developed. Ritonavir and indinavir have been approved for use alone or in combination with nucleoside analogue medications in people with advanced HIV disease. Nelfinavir is the first protease inhibitor labeled for use in children. Amprenavir is the newest of the protease inhibitors. Amprenavir can be taken with or without food, but it should not be taken with a high-fat meal because the fat content may decrease the absorption of the drug. The most disturbing adverse reactions to protease inhibitors consist of the lipodystrophy syndrome with severe hyperlipidemia and unpredictable fat redistributions over the body... 

Familial combined hyperlipidemia lib LDL, VLDL Chol,TG Increased VLDL production, increased conversion of VLDL to LDL. CHD, stroke... 

The bile acid sequestering resins lower elevated LDL cholesterol and therefore are useful in the treatment of type Ila hyperlipoproteinemia. However, because the resins can raise plasma VLDL in some patients, they are not recommended for treatment of combined hyperlipidemias (type Ilb) when both LDL cholesterol and VLDL triglycerides are high or in other conditions of elevated triglycerides. 

These drugs are used for treatment of hyperlipidemia. They lower the levels of lipoproteins and lipids in blood. The plasma lipids are present in lipoproteins after combining with apoproteins. They are high density lipoproteins (HDL), low density lipoproteins (LDL), very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL). 

Dietary measures are initiated first—unless the patient has evident coronary or peripheral vascular disease—and may obviate the need for drugs. Patients with familial hypercholesterolemia or familial combined hyperlipidemia always require drug therapy. Cholesterol and saturated and trans-fats are the principal factors that increase LDL, whereas total fat, alcohol, and excess calories increase triglycerides. 

Reductase inhibitors are useful alone or with resins, niacin, or ezetimibe in reducing levels of LDL. Women with hyperlipidemia who are pregnant, lactating, or likely to become pregnant should not be given these agents. Use in children is restricted to selected patients with familial hypercholesterolemia or familial combined hyperlipidemia. 

In combination with a resin or reductase inhibitor, niacin normalizes LDL in most patients with heterozygous familial hypercholesterolemia and other forms of hypercholesterolemia. These combinations are also indicated in some cases of nephrosis. In severe mixed lipemia that is incompletely responsive to diet, niacin often produces marked reduction of triglycerides, an effect enhanced by marine omega-3 fatty acids. It is useful in patients with combined hyperlipidemia and in those with dysbetalipoproteinemia. It is clearly the most effective agent for increasing HDL and the only agent that may reduce Lp(a). 

Combined drug therapy is useful (1) when VLDL levels are significantly increased during treatment of hypercholesterolemia with a resin (2) when LDL and VLDL levels are both elevated initially (3) when LDL or VLDL levels are not normalized with a single agent, or (4) when an elevated level of Lp(a) or an HDL deficiency coexists with other hyperlipidemias. 

This combination is sometimes useful in treating patients with familial combined hyperlipidemia who are intolerant of niacin or statins. However, it may increase the risk of cholelithiasis. 

Mixed hyperlipidemia is one of the most common lipid disorders, but only a minor fraction of the affected patients has a monogenic inherited disease. Most patients with mixed hyperlipidemia have a familial combined hyperlipidemia, a multifactorial disease for which the causative factors are not known. Patients have elevated remnant lipoproteins with elevated triglycerides > 3.0 mmol/1 and total cholesterol > 5.0 mmol/1. Two rare monogenic disorders lead to such a lipoprotein pattern,... 

Yeshurun D, Hamood H, Morad N, Naschitz J. [Acipimox (Olbetam) as a secondary hypolipemic agent in combined hypertriglyceridemia and hyperlipidemia.JHarefuah 2000 138(8) 650-3710. 

Athyros VG, Papageorgiou AA, Hatzikonstandinou HA, Didangelos TP, Carina MV, Kranitsas DF, Kontopoulos AG. Safety and efficacy of long-term statin-fibrate combinations in patients with refractory familial combined hyperlipidemia. Am J Cardiol 1997 80(5) 608-13. 

Spence JD, Huff MW, Heidenheim P, Viswanatha A, Munoz C, Lindsay R, Wolfe B, Mills D. Combination therapy with colestipol and psyllium mucilloid in patients with hyperlipidemia. Ann Intern Med 1995 123(7) 493—9. 

Acipimox had to be withdrawn in 10 of 32 patients with hypertriglyceridemia, excessive hypertriglyceridemia, and combined hyperlipidemia because of adverse effects or absence of clinical response (15). The other 22 completed... 

A 10-year-old child had status epilepticus controlled with a combination of valproate, oxcarbazepine, and 48 hours of propofol infusion in a dose of 5.5 mg/kg/ hour. After weaning from propofol, a classic ketogenic diet was instituted in an attempt to provide long-term control of the seizures. A day later status epilepticus recurred and propofol was restarted at a rate of 6-9 mg/ kg/hour to suppress seizure activity (the diet, valproate, and oxcarbazepine were also continued). Shortly thereafter, he developed the classical constellation of malignant ventricular arrhythmias, hyperlipidemia, rhabdomyolysis, lactic acidosis, and biventricular cardiac failure. He did not survive. 

Soon after the introduction of highly active antiretroviral combination treatments (HAART), lipodystrophy was associated with the use of protease inhibitors, and several reports have confirmed that a syndrome of peripheral lipodystrophy, central adiposity, breast hypertrophy in women, hyperlipidemia, and insulin resistance with hyperglycemia is an adverse event associated with the use of potent combination antiretroviral therapy, particularly including HIV-1 protease inhibitors (982-987). 

Hypertriglyceridemia due to sirolimus often does not respond to dosage reduction or hypolipidemic drugs. After liver transplantation (n — 6), significant hyperlipidemia improved after withdrawal of sirolimus (1070). The incidence of sirolimus-associated hyperlipidemia is up to 44%. After liver transplantation, there was hypercholesterolemia in 15% and hypertriglyceridemia in 10% of recipients. Sirolimus in combination with tacrolimus... 

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