Sorted By Test Name - Mayo Medical Laboratories

LIPA
81558
1996;276:544-548 4. Ridker PM, Hennekens CH, Stampfer MJ: A prospective study of lipoprotein(a) and
the risk of myocardial infarction. JAMA 1993;270:2195-2199 5. Tsimikas S, Brilakis ES, Miller ER, et al:
Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N Engl J Med 2005;353(1):46-57
Lipoprotein (a), Serum
Clinical Information: Lipoprotein (a) (Lp[a]), first reported in 1963 by the Norwegian
physician-investigator, Kare Berg, consists of an ordinary LDL particle combined with an additional
protein. As with LDL, the Lp(a) particle contains Apolipoprotein B100 (molecular weight=approximately
512,000 D), but additionally contains Apolipoprotein a (apo[a]) (molecular weight=275,000-800,000 D),
which is covalently linked through a disulfide bond to apolipoprotein B100. Apo(a) contains a series of
amino acid repeats known as "kringles" containing 3 intrastrand disulfide bonds that are highly
homologous to similar repeats found in plasminogen. There are a total of 11 apo(a) kringle sequences; 10
of them are present as single copies, but the remaining 1(K4 type 2) varies in copy number from 3 to 40.
The copy number of the K4 type 2 kringle is genetically determined and results in a high degree of
interindividual polymorphism in the molecular mass of apo(a), which can vary from 187 kDa to 662 kDa.
The size of the Lp(a) particle varies accordingly. To date, 34 different isoforms of apo(a) have been
identified. Because of its shared homologies with LDL and plasminogen, factors thought to participate
directly or indirectly in atherogenesis, Lp(a) has been the focus of numerous clinical and epidemiologic
studies attempting to establish increased serum Lp(a) concentration as a risk factor for coronary heart
disease (CHD) and stroke. Although results of studies to date are mixed, the preponderance of evidence
strongly suggests that Lp(a) is an independent risk factor for CHD and possibly stroke, and the Lp(a)
particle has been referred to as "the most atherogenic lipoprotein." Serum concentrations of Lp(a) appear
to be largely related to genetic factors, and unfortunately, diet and lipid-lowering pharmaceuticals do not
have a major impact on Lp(a) levels. Nevertheless, measurement of serum Lp(a) may contribute to a more
comprehensive risk assessment in high-risk patients. Concentrations of Lp(a) particles in the blood can be
expressed readily either as concentrations of Lp(a)-specific protein or as Lp(a) cholesterol. Cardiovascular
Laboratory Medicine measures and reports Lp(a) cholesterol individually (LPAWS/89005 Lipoprotein [a]
Cholesterol, Serum) and as a part of the lipoprotein profile (LMPP/83673 Lipoprotein Metabolism
Profile). The cholesterol content of Lp(a) particles varies little, and Lp(a) cholesterol can be quantified
readily. In many cases, we have observed Lp(a) cholesterol to be at levels of 25 mg/dL to 50 mg/dL, and
in some cases to be >100 mg/dL. Thus, Lp(a) can contain significant proportions of the serum cholesterol.
In such cases, knowledge of the concentration of Lp(a) and of the contribution of Lp(a) cholesterol to the
serum total cholesterol should be helpful to physicians in their evaluation of cardiovascular risk levels.
Unlike Lp(a) cholesterol, accurate immunochemical measurement of Lp(a)-specific protein, is
complicated by a number of factors. A significant problem is the issue of how to express the result of a
quantitative test for Lp(a)-specific protein in meaningful terms. Because the molecular size of
Lp(a)-specific protein varies over a broad range in the population (240,000-800,000 D), a test result
primarily related to the number of molecules of Lp(a)-specific protein in a specimen cannot be expressed
accurately or meaningfully in terms of mg protein/dL unless the molecular weight of the Lp(a)-specific
protein in that specimen has been determined. An additional related concern is that the degree of
atherogenicity of the Lp(a) particle in any specific case may depend on the molecular size of the
Lp(a)-specific protein. Alteration in serum Lp(a) concentration secondary to diet modification, exercise,
or drug therapy is minimal. Therefore, it is inappropriate to use Lp(a) as a general screening test in the
healthy population. However, in a patient with additional modifiable CHD risk factors, more aggressive
therapy to normalize these factors may be indicated if the Lp(a) value is also increased.
Useful For: Providing additional information on coronary heart disease (CHD) risk in patients known
or suspected to be at increased risk based on other factors, including family history of premature CHD or
stroke, hypertension, cigarette smoking, obesity, diabetes mellitus, increased concentration of LDL
cholesterol, and depressed concentration of HDL cholesterol.
Interpretation: The frequency distribution of serum lipoprotein (a) (Lp[a]) concentrations is markedly
skewed toward the low end, with approximately 85% of the population having concentrations 30 mg/dL have been associated with increased risk of coronary heart disease in
numerous studies. Observations over the last 3 decades have indicated that Lp(a) increases cardiovascular
risk 2 to 3-fold when its level in the blood plasma is >30 mg/dL (correspondingly, Lp[a] cholesterol
Current as of January 4, 2013 7:15 pm CST 800-533-1710 or 507-266-5700 or MayoMedicalLaboratories.com Page 1115