Increased levels of pregnancy-associated plasma protein-A in patients with hypercholesterolemia: the effect of atorvastatin treatment
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
14661010
DOI
10.1016/s0002-8703(03)00446-0
PII: S0002870303004460
Knihovny.cz E-resources
- MeSH
- Anticholesteremic Agents therapeutic use MeSH
- Atorvastatin MeSH
- Biomarkers blood MeSH
- Hypercholesterolemia blood drug therapy MeSH
- Heptanoic Acids therapeutic use MeSH
- Middle Aged MeSH
- Humans MeSH
- Follow-Up Studies MeSH
- Pyrroles therapeutic use MeSH
- Case-Control Studies MeSH
- Pregnancy-Associated Plasma Protein-A metabolism MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Anticholesteremic Agents MeSH
- Atorvastatin MeSH
- Biomarkers MeSH
- Heptanoic Acids MeSH
- Pyrroles MeSH
- Pregnancy-Associated Plasma Protein-A MeSH
BACKGROUND: Serum levels of pregnancy-associated plasma protein-A (PAPP-A) have recently been linked to plaque instability and are increased in acute coronary syndromes. The relation between PAPP-A levels and coronary risk factors, namely blood lipids, has not been studied to date. We have therefore investigated whether serum PAPP-A levels are increased in asymptomatic hypercholesterolemic subjects and whether PAPP-A levels are influenced by atorvastatin therapy. METHODS: We examined 27 subjects with isolated hypercholesterolemia free of manifest vascular disease and 29 age-matched healthy control subjects. Patients were examined at baseline and after 10 weeks of atorvastatin treatment (20 mg/d). RESULTS: In untreated hypercholesterolemic subjects, PAPP-A levels were significantly higher than in control subjects (8.02 +/- 1.86 mU/L vs 6.50 +/- 2.54 mU/L, P =.018). There was no correlation between PAPP-A levels and serum lipid levels. Atorvastatin treatment reduced total and LDL-cholesterol by 31% and 40%, respectively. Despite this profound lipid lowering, there was no significant change in the serum PAPP-A levels. CONCLUSIONS: PAPP-A levels are elevated in hypercholesterolemic subjects without clinical signs of atherosclerosis. PAPP-A may therefore not only reflect plaque instability but also serve as a marker of total atherosclerotic burden in asymptomatic subjects with hyperlipidemia. However, PAPP-A levels are not influenced by atorvastatin treatment.
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