Lipoproteins are hydrophilic macromolecular complexes of lipids and proteins of spherical form and represent a transport form of lipids in the circulation. Proteins in lipids are called apoproteins. Using the ultra-centrifuge six fractions of lipoproteins can be separated, namely hilomicrons, lipoproteins of very low (VLDL), medium (IDL), low (LDL and high (HDL) density and Lp(a) lipoproteins. Among the conditions connected with the lipoproteins metabolism disorders, the most significant are arteriosclerosis, myocardial infarction and cerebral stroke as the most frequent complications.1,2 Along with the other risk factors (overweight, physical inactivity, male sex, cigarette smoking, positive familiar heredity for coronary disease, social and economic factors), high concentration of serum LDL-cholesterol along with low concentration of HDL-cholesterol and high concentration of glucose is of a particular importance.
Lp(a) lipoproteins show structural similarity with LDL unit. The thing that separates them from other lipoproteins is apo(a) glycoprotein, which is structurally similar and competing with plasminogene, the consequence of which is fibrinolisis inhibition. Lp(a) represents the main congenital risk factor for the development of arteriosclerosis. The value of 30mg/dl increases twice the risk of cardiovascular disease, independently from the level of other lipids and five times if, along with that, level of LDL-cholesterol is increased.3 It is not possible to influence concentration of Lp(a) by exogenous factors, although it has been observed that reduced values are found in liver disease and alcoholism.4
The genetic risk factors for development of arteriosclerosis should also be mentioned. In order for arteriosclerosis to be developed, the presence of surrounding factors is necessary along with the existing genetic factors. One of the most frequently mentioned risk genes for the development of arteriosclerosis is the gene for apolipoprotein (apo) E. Clinical expression of E2 izoform is dependent on surrounding factors, primarily excessive drinking of alcohol, excessive bodily mass and fatty food. There are only few studies published, which observed interaction between those two factors: gene for apolipoprotein E, as hereditary risk factor and excessive drinking as surrounding factor.5,6 Gueguen and al. also report about how alcohol dependency directly changes the effects of apo E polymorphism on apo B plane.7
Frohlich states that normal drinking of alcohol also leads to changes of lipoproteins metabolism.8 Various other studies also report that drinking of alcohol is connected with the increased levels of high density lipoproteins (HDL) and concentration of apolipoproteins (apo) A-I and A-II.9 Many biochemical mechanisms participate in this increasing hepatal as well as extrahepatal production of HDL.10-13 There is also reduced elimination of HDL from plasma.1415 However, alcohol has a reversed effect on the concentration of LDL-cholesterol and apoB concentration.1617 It has not been precisely determined how the reduction in concentration occurs, but some authors advocate the theory according to which alcoholics have accelerated elimination of LDL apo B or reduced conversion of VLDL into LDL apo B.18-20 In the phase of acute abstinence, with abstinence syndrome, an ease of Lp(a) concentration occurs, which can increase the risk of acute cardiac incident, in spite of the higher concentration of HDL.21 Upon the disappearance of abstinence syndrome, the values of serum lipids, apoproteins and lipoproteins reach the values of general population.16
The goal of this research was to examine the changes of concentrations of serum lipids and lipoproteins in long-time alcoholics at the beginning of treatment and after three weeks of abstinence from alcoholic beverages.
SUBJECTS AND METHODS
The study group consisted of 31 male patients with chronic alcohol dependence, aged between 19 and 59 years, mean±SD; 44. …