Distribution of Low-Density Lipoprotein and High-Density Lipoprotein Subclasses in Patients With Sarcoidosis

Archives of Pathology and Laboratory Medicine - Tập 137 Số 12 - Trang 1780-1787 - 2013
Jelena Vekić1,2, Aleksandra Zeljković1,2, Zorana Jelić‐Ivanović1,2, Vesna Spasojević‐Kalimanovska1,2, Slavica Spasić1,2, Jelica Videnović-Ivanov1,2, Jasmina Ivanišević1,2, Violeta Vučinić-Mihailović1,2, Tamara Gojković1,2
1From the Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia (Drs Vekic, Zeljkovic, Jelic-Ivanovic, Spasojevic-Kalimanovska, and Spasic and Mses Ivanisevic and Gojkovic); and the Institute for Pulmonary Diseases and Tuberculosis, Clinical Centre of Serbia, Medical Faculty, University of Belgrade, Belgrade, Serbia (Drs Videnovic-Ivanov and Vucinic-Mihailovic).
2the Institute for Pulmonary Diseases and Tuberculosis, Clinical Centre of Serbia, Medical Faculty, University of Belgrade, Belgrade, Serbia (Drs Videnovic-Ivanov and Vucinic-Mihailovic).

Tóm tắt

Context.—Systemic inflammatory diseases are associated with proatherogenic lipoprotein profile, but there is a lack of information regarding overall distributions of lipoprotein subclasses in sarcoidosis. Objective.—To investigate whether patients with sarcoidosis have altered distributions of plasma low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particles. Design.—Seventy-seven patients with biopsy-proven sarcoidosis (29 with acute and 48 with chronic sarcoidosis) treated with corticosteroids and 77 age- and sex-matched controls were included in the study. Low-density lipoprotein and HDL subclasses were determined by gradient gel electrophoresis, while inflammatory markers and lipid parameters were measured by standard laboratory methods. Results.—Compared to controls, patients had fewer LDL I subclasses (P < .001), but more LDL II and III (P < .001) subclasses. This pattern was evident in both acute and chronic disease groups. Patients also had smaller HDL size (P < .001) and higher proportions of HDL 2a (P = .006) and 3a particles (P = .004). Patients with chronic sarcoidosis had smaller LDL size than those with acute disease (P = .02) and higher proportions of HDL 3a subclasses (P = .04) than controls. In acute sarcoidosis, relative proportions of LDL and HDL particles were associated with levels of inflammatory markers, whereas in chronic disease an association with concentrations of serum lipid parameters was found. Conclusions.—The obtained results demonstrate adverse lipoprotein subfraction profile in sarcoidosis with sustained alterations during disease course. Evaluation of LDL and HDL particles may be helpful in identifying patients with higher cardiovascular risk, at least for prolonged corticosteroid therapy due to chronic disease course.

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Archives of Pathology and Laboratory Medicine

Tập 137 Số 12

1780-1787

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