Articles |
From the Departments of Medicine (C.H.T., L.B.) and Pediatrics (S.H.), Columbia University, New York, NY.
Correspondence to Lars Berglund, MD, PhD, Division of Preventive Medicine and Nutrition, Department of Medicine, Columbia University College of Physicians and Surgeons, P&S 9510, 630 West 168th Street, New York, NY 10032. E-mail berglun{at}cudept.cis.columbia.edu
Abstract Estrogen lowers lipoprotein(a) [Lp(a)] levels, but
the mechanisms involved have not been clarified. To address the
relationship between estrogenic effects on Lp(a) and serum lipids, and
on other plasma proteins of hepatic origin, 15 healthy postmenopausal
women participated in a randomized, double-blinded, placebo-controlled,
crossover study with 4 weeks of oral conjugated estrogens (0.625 mg/d)
and placebo, separated by a 6-week period. Lp(a) levels decreased
during estrogen treatment in 14 of the 15 subjects (mean decrease,
23%; P<.001). In response to estrogen, apolipoprotein
A-I (apoA-I), HDL cholesterol, and triglyceride
levels increased by 12% (P=.001), 11%
(P<.001), and 10% (P=.02),
respectively. Apolipoprotein B (apoB) and LDL cholesterol
levels decreased by 7% (P=.01) and 12%
(P=.03), respectively. ApoB, LDL
cholesterol, and Lp(a) levels fell within 1 week of
treatment, whereas apoA-I and HDL cholesterol levels rose
more slowly. Levels of acid
1-glycoprotein
(AAG) and haptoglobin (HPT), two hepatically derived acute phase
proteins, also decreased during estrogen treatment by 18%
(P<.001) and 25% (P=.002),
respectively. Although the changes in AAG and HPT in response to
estrogen were highly correlated (r=.67,
P=.009), we were unable to detect a correlation between
change in either acute phase protein and change in Lp(a)
(r=-.14 and -.24, P=.64 and .41). The
lack of correlation between the changes in two acute phase reactants
and Lp(a) suggests different underlying mechanisms for the effects of
estrogen on these liver-derived proteins.
Key Words: apolipoprotein(a) hormone replacement therapy conjugated equine estrogens
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