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Review ofLiterature
increased risk for the development of CAD with a rate ofoccurrence
estimated to be 2-5 times greater than in normal controls (Loscalzo,
1990).
2. Renal system :
Diseases of the kidney and their accompanying signs (proteinuria
and nephrotic syndrome) as well as end-stage renal disease and their
treatment modalities (haemodialysis, peritoneal dialysis and kidney
transplantation) have all been found to increase Lp(a) plasma levels
substantially (Bartens an Wanner, 1994).
3. Liver:
To determine the influence of liver disease on Lp(a)
concentrations, Feely et al. (1992) compared its concentrations in
patients with varying degrees of severity ofhepatic cirrhosis and patients
with established coronary heart disease they found Lp(a) concentration to
be raised in patients with coronary heart diseas and reduced in those with
cirrhosis. Concentrations tended to be lower in those with more severe
diseases.
4. Hormones:
Fluctuations III Lp(a) seem to occur in states of hormonal changes
such as in diabetes mellitus, after estrogen treatment and during
pregnancy (Bartens and Wanner, 1994).
5. Smoking:
Wersch et al.(1994) compared 68 non-smoking and 118 smoking
pregnant women with a control group of 29 subjectively healthy, age
matched non-smoking non-pregnant females. This comparison showed
significantly higher Lp(a) values during the last trimester of gestation in
non-smokers. The higher Lp(a) concentration in the plasma ofnon­
smoking women during a normal pregnancy might be a physiologic
necessity for adequate fetal growth. Lower levels ofLp(a) were seen in
67