| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
,
and
WILLIAM R. HAZZARD
Department of Medicine, The Johns Hopkins Medical Institutions Baltimore, Maryland 21205
Address all correspondence and requests for reprints to: Walter H. Ettinger, Jr., M.D., Department of Medicine, 300 South Hawthorne Road, Winston-Salem, North Carolina 27103.
Patients treated with corticosteroids often have a dyslipoproteinemia characterized by elevated plasma levels of triglyceride and low density lipoprotein cholesterol and/or decreased levels of the high density lipoprotein2 fraction of high density lipoprotein cholesterol. This study was undertaken to determine if such patients also have elevated apolipoprotein-B (apoB) levels and/or abnormalties of the activities of the triglyceride Upases in postheparin plasma. Plasma lipoprotein levels and the postheparin activities of hepatic lipase and lipoprotein lipase were measured in 28 women with systemic lupus erythematosus (SLE) who were treated with prednisone, 10 women with SLE not treated with prednisone, and 15 normal women. The prednisone-treated group had higher mean plasma levels of triglyceride [2.06 ± 1.3 (±SD) vs. 1.15 ± 0.35 and 0.95 ± 0.46 mmol/L; P < 0.01], low density lipoprotein cholesterol [3.41 ± 1.4 (± SD) vs. 2.79 ± 0.67 and 2.84 ± 0.70 mmol/L; P < 0.01], and apoB [1.16 ± 0.35 (±SD) vs. 0.82 ± 0.13 and 0.76 ± 0.22 g/L] than the other 2 groups. Forty-three percent of the prednisone-treated group had apoB levels of 1.20 g/L or more compared to 1% of normal subjects and none of the untreated SLE group (P < 0.05). However, of the 12 prednisone-treated patients with elevated plasma apoB levels 5 had normal plasma lipid levels. There were no differences in the postheparin lipase activities among the 3 groups.
These data indicate that corticosteroid-treated patients have elevations in apoB as well as hyperlipidemia. The lipoprotein abnormalities may explain the increased risk of atherosclerosis reported in these patients.
* This work was supported in part by NIH Grant HL-38255.
Current address: Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.
Recipient of a Brookdale Foundation National Fellowship in Gerontology and Geriatric Medicine.
Received October 29, 1987.
This article has been cited by other articles:
![]() |
J.C. Sachet, E.F. Borba, E. Bonfa, C.G.C. Vinagre, V.M. Silva, and R.C. Maranhao Chloroquine increases low-density lipoprotein removal from plasma in systemic lupus patients Lupus, April 1, 2007; 16(4): 273 - 278. [Abstract] [PDF] |
||||
![]() |
J. P. Girod and D. J. Brotman Does altered glucocorticoid homeostasis increase cardiovascular risk? Cardiovasc Res, November 1, 2004; 64(2): 217 - 226. [Abstract] [Full Text] [PDF] |
||||
![]() |
F Formiga, J F Meco, X Pinto, J Jacob, I Moga, and R Pujol Lipid and lipoprotein levels in premenopausal systemic lupus erythematosus patients Lupus, May 1, 2001; 10(5): 359 - 363. [Abstract] [PDF] |
||||
![]() |
E. Borba and E. Bonfa Dyslipoproteinemias in systemic lupus erythematosus: influence of disease, activity, and anticardiolipin antibodies Lupus, January 1, 1997; 6(6): 533 - 539. [Abstract] [PDF] |
||||
![]() |
Y. Farhey and E.V. Hess Review : Grand Rounds from International Lupus Centres Accelerated atherosclerosis and coronary disease in SLE Lupus, January 1, 1997; 6(7): 572 - 577. [Abstract] [PDF] |
||||
![]() |
P. R.J. Ames Medical Perspective Antiphospholipid Antibodies, Thrombosis and Atherosclerosis in Systemic Lupus Erythematosus: a Unifying 'Membrane Stress Syndrome' Hypothesis Lupus, October 1, 1994; 3(5): 371 - 377. [PDF] |
||||
![]() |
J. H. Klippel Systemic Lupus Erythematosus: Treatment-Related Complications Superimposed on Chronic Disease JAMA, April 4, 1990; 263(13): 1812 - 1815. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |