High-density lipoprotein treatment

Systemic treatment of 13-cis retinoic acid frequently leads to cheilitis and eye irritations (e.g., unspecific cornea inflammation). Also other symptoms such as headache, pruritus, alopecia, pains of joints and bone, and exostosis formation have been reported. Notably, an increase of very low density lipoproteins and triglycerides accompanied by a decrease of the high density lipoproteins has been reported in 10-20% of treated patients. Transiently, liver function markers can increase during oral retinoid therapy. Etretinate causes the side effects of 13-cis retinoid acid at lower doses. In addition to this, generalized edema and centrilobulary toxic liver cell necrosis have been observed. 

Low high-density lipoprotein (HDL) cholesterol (less than 40 mg/dL or 1.04 mmol/L in males and less than 50 mg/dL or 1.3 mmol/L in females) or active treatment to raise HDL cholesterol. 

Chiesa G, Michelagnoli S, Cassinotti M, Gianfranceschi G, Werba JP, Paz-zucconi F, et al. Mechanisms of high-density lipoprotein reduction after probu-col treatment changes in plasma cholesterol esterification/transfer and lipase activities. Metabolism 1993 42 229-235. 

Pharmacology Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apo B, total triglycerides, and triglyceride rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high-density lipoprotein (HDL) and apoproteins apoAl and apoAII. 

Raloxifene (Evista) is a new SERM approved for use in the treatment and prevention of osteoporosis because it has estrogenic activity in bone. Raloxifene is an estrogen antagonist in both breast and endometrial tissues. The estrogenhke properties of raloxifene result in the maintenance of a favorable serum Upid profile (decreased low-density lipoprotein levels with no change in either high-density lipoproteins or triglycerides). Raloxifene is 95% bound to plasma proteins. Absorption of raloxifene is impaired by cholestyramine. 

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). 

In vivo studies were also conducted by several researchers. Anraku et al. (2009) examined the antioxidant effects of water-soluble chitosan in normal subjects by measuring the reduction of indices of oxidative stress. Treatment with chitosan for 4weeks produced a significant decrease in levels of plasma glucose and the atherogenic index, and led to an increase in high-density lipoprotein cholesterol (HDL-C). Chitosan treatment also lowered the ratio of oxidized to reduced albumin and increased total plasma antioxidant activity. Further, Anraku et al. (2011) proved the antioxidant effects of high MW chitosan in normal volunteers, and the obtained results were consistent with previous results observed by Anraku et al. (2009). 

Devroey D, Vantomme K, Betz W, Vandevoorde J, Kartounian J (2004) A review of the treatment guidelines on the management of low levels of high-density lipoprotein cholesterol. Cardiology 102 61-66... 

Hersberger M, Eckardstein A von (2003) Low high-density lipoprotein cholesterol physiological background, clinical importance and drug treatment. Drugs 63 1907-1945... 

A 64-year-old woman who had taken metformin for 3 years had a high-density lipoprotein concentration of 1.2 mmol/1, which fell to 0.26 mmol/1 when she took rosiglitazone. The HbAic fell from 10.1% to 7.9%. Fenofibrate was added and the HDL concentration fell further to 0.11 mmol/1. Triglycerides, 2.7 mmol/1 before treatment, increased to 4.7 mmol/1. Apolipoprotein A1 concentrations were low at 0.14 g/ 1 (reference range 1.1-2.05 g/1). On withdrawing both the rosiglitazone and the fenofibrate the HDL concentration rose to 0.95 mmol/1. 

Nicotinic acid is an antilipidemic agent that effectively reduces serum concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol, and triglycerides, and increases concentrations of high-density lipoprotein (HDL) cholesterol. It has been suggested that the marked lowering of serum cholesterol seen during treatment of dyslipidemia with nicotinic acid results from hepatotoxi-city (1). 

Major features of treatment guidelines and clinical trials. Abbreviations CRP, C-reactive protein HDL, high-density lipoprotein LDL, low-densty lipoprotein. 

A lipid profile (cholesterol, high-density lipoprotein, low-density lipoprotein, and triglycerides) and complete blood count were determined before and after four weeks of treatment for all patients. 

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