Alterations in biomarkers of cardiovascular disease (CVD) in active acromegaly
L Boero1, M Manavela, L Gómez Rosso
1Department of Clinical Biochemistry, Faculty of Pharmacy and Biochemistry, CONICET, University of Buenos Aires, Buenos Aires, Argentina. lauraboero@fibertel.com.ar
Insights
Active acromegaly patients exhibit an atherogenic lipoprotein profile, including elevated triglycerides and apolipoprotein B. These lipid alterations, along with increased cholesteryl ester transfer protein and endothelin-1, suggest a heightened risk for atherosclerotic cardiovascular disease.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Metabolic Disorders
Background:
- Acromegaly is associated with increased mortality due to cardiovascular and metabolic comorbidities.
- The lipoprotein profile in acromegaly patients is not well-established, with conflicting data.
- Understanding these profiles is crucial for managing cardiovascular risk in acromegaly.
Purpose of the Study:
- To characterize the lipoprotein profile in active acromegaly patients.
- To identify emergent biomarkers of cardiovascular disease in acromegaly.
- To compare these profiles with sex- and age-matched healthy controls.
Main Methods:
- Studied 18 active acromegaly patients and 18 healthy controls.
- Assessed glucose, hormonal status, lipoprotein profile, and C-reactive protein (CRP).
- Measured cholesteryl ester transfer protein (CETP), lipoprotein-associated phospholipase A2 (Lp-PLA2), endothelin-1, vascular cell adhesion molecule-1 (VCAM-1), and leukocyte markers (CD18, CD49d, CD54).
Main Results:
- Acromegalic patients showed a more atherogenic lipoprotein profile after BMI adjustment, with higher triglycerides and apolipoprotein B.
- Increased cholesteryl ester transfer protein (CETP) activity and endothelin-1 levels were observed in acromegaly patients.
- Elevated CD49d content on lymphocytes and correlations between endothelin-1 with GH, IGF-1, and IGFBP-3 were noted.
Conclusions:
- Lipoprotein profile alterations in acromegaly contribute to an increased propensity for atherosclerotic cardiovascular disease.
- These findings add to the known specific cardiomyopathy in acromegaly.
- Further research is warranted to explore therapeutic strategies targeting these metabolic and cardiovascular risks.
Objectives:
In acromegalic patients, cardiovascular and metabolic comorbidities contribute to enhance mortality. Available data on the lipoprotein profile of these patients are controversial. Our aim was to characterize the lipoprotein profile and emergent biomarkers of cardiovascular disease in active acromegalic patients in comparison with sex- and age-matched healthy controls.
Patients:
Eighteen patients with active acromegaly and 18 controls were studied.
Measurements:
Glucose levels, hormonal status, lipoprotein profile and C reactive protein (CRP) were evaluated by standardized methods. Cholesteryl ester transfer protein (CETP) and lipoprotein-associated phospholipase A(2 )(Lp-PLA(2)) were measured by radiometric techniques, endothelin-1 and vascular cell adhesion molecule (VCAM)-1 by enzyme-linked immunosorbent assay, and leucocytes CD18, CD49d and CD54 by flow cytometry.
Results:
After adjusting for body mass index (BMI), acromegalic patients presented a more atherogenic lipoprotein profile, consisting of higher levels of triglycerides and apolipoprotein B and alterations in the ratios which estimate insulin resistance and atherogenic risk. CETP activity was significantly increased in acromegalic patients as compared to controls (168 +/- 17 vs. 141 +/- 30% per ml h, respectively; P < 0.05). Endothelin-1 levels evidenced an increase in the patients' group (0.9 +/- 0.2 vs. 0.7 +/- 0.2 ng/l, respectively; P < 0.01) and showed positive and significant correlations with GH, IGF-1 and IGFBP-3 (r = 0.45, 0.42 and 0.44, respectively; P < 0.01 for all of them; with BMI as a fixed variable). Lymphocytes from acromegalic patients showed increased CD49d content (282 +/- 59 vs. 246 +/- 48 arbitrary units, respectively; P < 0.05).
Conclusions:
Taken together, the alterations described seem to contribute to constituting a state of higher propensity for the development of atherosclerotic cardiovascular disease, which adds to the presence of specific cardiomyopathy.
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