sodium-dodecyl-sulfate and Hypercholesterolemia

The intercellular lipids of stratum corneum are predominantly formed by cholesterol, ceramides and free fatty acids. Cholesterol synthesis is inhibited by statins, cholesterol-lowering drugs (lovastatin, pravastatin, simvastatin). The present study was undertaken to examine the effect of these drugs on skin barrier function. Knowledge about the effect on epidermis of systemic inhibition of cholesterol synthesis may improve our understanding of the skin barrier function. Seventeen statin-treated subjects were compared to controls. All were patch-tested with sodium lauryl sulphate (SLS), and the skin was evaluated after 24 h and after 7 days by measurement of transepidermal water loss (TEWL), erythema and visual scoring. After 24 h as well as after one week erythema was significantly less pronounced in the statin-treated group than in controls (p < 0.001). No significant differences in TEWL were found between the groups at any time. The results imply a decreased bioavailability of SLS in the statin-treated group, while no evidence for an altered permeability barrier to water was found.

Topics: Adult; Aged; Anticholesteremic Agents; Biological Availability; Cholesterol; Erythema; Female; Galvanic Skin Response; Humans; Hypercholesterolemia; Irritants; Lovastatin; Male; Middle Aged; Patch Tests; Permeability; Pravastatin; Simvastatin; Skin; Sodium Dodecyl Sulfate; Water Loss, Insensible

Low levels of high-density lipoproteins (HDLs) may constitute an independent risk factor that may be as important as elevated low-density lipoproteins (LDLs) in coronary artery disease (CAD). Concentrations and distributions of lipids, apolipoprotein (apo) B, and apoA-I in the plasma and lipoprotein subfractions of two groups of swine, one with familial hypercholesterolemia (FHC) and the other with diet-induced hypercholesterolemia (DHC), were examined. Normolipidemic (NL) animals served as controls. All pigs carried the Lpb5 apoB mutation, which is known to influence the formation of atherosclerotic lesions. Mean concentrations of serum total cholesterol in NL, DHC, and FHC were 80.0 +/- 9.3, 774.3 +/- 54.5, and 316.5 +/- 36.1 mg/dL, respectively; HDL cholesterol (HDL-C), 33.5 +/- 1.9, 137.0 +/- 9.9, and 22.3 +/- 2.2 mg/dL; triglycerides, 33.0 +/- 16.3, 40.3 +/- 11.7, and 56.8 +/- 7.2 mg/dL; apoB, 35.7 +/- 3.1, 142.0 +/- 4.8, and 169.3 +/- 13.9 mg/dL; and apoA-I, 62.4 +/- 9.3, 170.9 +/- 6.9, and 42.6 +/- 4.8 mg/dL. The distributions of total cholesterol, apoB, and apoA-I in plasma lipoprotein subfractions were also examined. Compared with NL, FHC had fourfold and 4.7-fold increases in total cholesterol and apoB, respectively, distributed in the lower densities (d < 1.043 g/mL), and low HDL-C and apoA-I levels, resulting in a high total cholesterol/HDL-C ratio (14.4:1) and elevated triglyceride levels. DHC was characterized by 10-fold and fourfold increases in total cholesterol and apoB, respectively, resulting in an LDL particle highly enriched in cholesterol, a fourfold increase of HDL-C, an almost threefold increase in apoA-I, and a normal triglyceride level.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Apolipoprotein A-I; Apolipoproteins B; Cholesterol; Diet; Disease Models, Animal; Electrophoresis, Polyacrylamide Gel; Gels; Hypercholesterolemia; Hyperlipoproteinemia Type II; Immunoelectrophoresis; Lipids; Lipoproteins; Male; Sepharose; Sodium Dodecyl Sulfate; Swine