Corticosteroids and Cholelithiasis in Systemic Lupus Erythematosus
T. M. Reshetnyak
Research Institute of Rheumatology, Russian Academy of Medical Sciences, 115522 Moscow, Russia
Search for more papers by this authorG. V. Saparin
Department of Physics, Moscow State University, 119992 Moscow, Russia msu.ru
Search for more papers by this authorP. V. Ivannikov
Department of Physics, Moscow State University, 119992 Moscow, Russia msu.ru
Search for more papers by this authorCorresponding Author
V. I. Reshetnyak
The Research Institute of General Reanimatology, Russian Academy of Medical Sciences, 107031 Moscow, Russia
Search for more papers by this authorT. M. Reshetnyak
Research Institute of Rheumatology, Russian Academy of Medical Sciences, 115522 Moscow, Russia
Search for more papers by this authorG. V. Saparin
Department of Physics, Moscow State University, 119992 Moscow, Russia msu.ru
Search for more papers by this authorP. V. Ivannikov
Department of Physics, Moscow State University, 119992 Moscow, Russia msu.ru
Search for more papers by this authorCorresponding Author
V. I. Reshetnyak
The Research Institute of General Reanimatology, Russian Academy of Medical Sciences, 107031 Moscow, Russia
Search for more papers by this authorAbstract
The aim. To evaluate the frequency of gallstone formation and alteration of plasma lipid profiles in SLE patients long treated with prednisolone. Material and methods. Sixty patients with SLE were divided into 2 groups: (1) 38 SLE patients without gallstones; (2) 22 SLE patients with gallstones. Gallbladder ultrasonography was performed in all the patients, and the serum lipid profile was determined. To identify the composition and structure of gallstones obtained during cholecystectomy, color cathodoluminescence scanning electromicroscopy was used. Results. Gallstone disease was detected in 22 (36.7%) patients of the 60 examinees and in 22 (68.8%) of the 32 SLE patients receiving prednisolone therapy; whereas none of the 28 prednisolone-untreated patients was found to have the disease (P = .001). There were the most significant differences between the SLE patients with and without gallstones in the duration of administration of prednisolone and in its mean daily and mean monthly doses, and cumulative ones. Conclusion. Age at the onset of the disease, the mean daily dose of corticosteroids, and the duration of therapy with these agents are the most likely factors predisposing to gallstone disease in SLE patients. The CCL-SEM study identified predominantly the protein-cholesterol structure of gallstones.
References
- 1 Belmont H. M., Abramson S. B., and Lie J. T., Pathology and pathogenesis of vascular injury in systemic lupus erythematosus. Interactions of inflammatory cells and activated endothelium, Arthritis & Rheumatism. (1996) 39, no. 1, 9–22, https://doi.org/10.1002/art.1780390103.
- 2 Seleznick M. J. and Fries J. F., Variables associated with decreased survival in systemic lupus erythematosus, Seminars in Arthritis and Rheumatism. (1991) 21, no. 2, 73–80, https://doi.org/10.1016/0049-0172(91)90040-7.
- 3 Abu-Shakra M., Urowitz M. B., Gladman D. D., and Gough J., Mortality studies in systemic lupus erythematosus. Results from a single center. I. Causes of death, Journal of Rheumatology. (1995) 22, no. 7, 1259–1264.
- 4 Borba E. F. and Bonfá E., Dyslipoproteinemias in systemic lupus erythematosus: influence of disease, activity, and anticardiolipin antibodies, Lupus. (1997) 6, no. 6, 533–539, https://doi.org/10.1177/096120339700600610.
- 5 Petri M., Spence D., Bone L. R., and Hochberg M. C., Coronary artery disease risk factors in the Johns Hopkins Lupus Cohort: prevalence, recognition by patients, and preventive practices, Medicine. (1992) 71, no. 5, 291–302, https://doi.org/10.1097/00005792-199209000-00004.
- 6 Tan E. M., Cohen A. S., and Fries J. F., The 1982 revised criteria for the classification of systemic lupus erythematosus, Arthritis & Rheumatism. (1982) 25, no. 11, 1271–1277, https://doi.org/10.1002/art.1780251101.
- 7 Bombardier C., Gladman D. D., Urowitz M. B. et al., Derivation of the SLEDAI. A disease activity index for lupus patients, Arthritis & Rheumatism. (1992) 35, no. 6, 630–640, https://doi.org/10.1002/art.1780350606.
- 8 Assmann G., Schriewer H., Schmitz G., and Hägele E. O., Quantification of high-density-lipoprotein cholesterol by precipitation with phosphotungstic acid/MgCl2, Clinical Chemistry. (1983) 29, no. 12, 2026–2030.
- 9 Friedewald W. T., Levy R. I., and Fredrickson D. S., Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge, Clinical Chemistry. (1972) 18, no. 6, 499–502.
- 10 Saparin G. V., Cathodoluminescence: new methods in scanning electron microscopy, Biophysical Electron Microscopy, 1990, no. chapter 12, Academic Press, New York, NY, USA, 451–478.
- 11 Obyden S. K., Ivannikov P. V., and Saparin G. V., Color cathodoluminescence display in the scanning electron microscope of deep relief surfaces, Scanning. (1997) 19, no. 8, 533–540, https://doi.org/10.1002/sca.4950190802.
- 12 Loginov A. S., Chebanov S. M., Petrakov A. V., Saparin G. V., Obyden S. K., and Ivannikov P. V., Investigation of cholesterol, bilirubin, and protein distribution in human gallstones by color cathodoluminescence scanning electron microscopy and transmission electron microscopy, Scanning. (1998) 20, no. 1.
- 13 Reshetnyak V. I., Mechanisms of Bile Formation and Primary Biliary Cirrhosis, 2003, Red Square, Moscow, Russia.
- 14 EttingerW. H.Jr. and Hazzard W. R., Elevated apolipoprotein-B levels in corticosteroid-treated patients with systemic lupus erythematosus, The Journal of Clinical Endocrinology & Metabolism. (1988) 67, no. 3, 425–428.
- 15 Ettinberg W. H., Applebaum-Bowden D., and Hazzard W. R., Post heparin lipases in systemic lupus erythematosus; evidence for defect in triglyceride removal, Arthritis & Rheumatism. (1986) 29, no. supplement.
- 16 Ettinger W. H., Klinefelter H. F., and Kwiterovitch P. O., Effect of short-term, low-dose corticosteroids on plasma lipoprotein lipids, Atherosclerosis. (1987) 63, no. 2-3, 167–172, https://doi.org/10.1016/0021-9150(87)90117-1.
- 17 van Berge-Henegouwen G. P., [email protected], Venneman N. G., Portincasa P., Kosters A., van Erpecum K. J., and Groen A. K., Relevance of hereditary defects in lipid transport proteins for the pathogenesis of cholesterol gallstone disease, Scandinavian Journal of Gastroenterology. (2004) 39, no. 1, supplement 241, 60–69, https://doi.org/10.1080/00855920410011022.
- 18 Wang H. H. and Wang D. Q.-H., [email protected], Reduced susceptibility to cholesterol gallstone formation in mice that do not produce apolipoprotein B48 in the intestine, Hepatology. (2005) 42, no. 4, 894–904, https://doi.org/10.1002/hep.20867.
- 19 van Erpecum K. J., [email protected], Biliary lipids, water and cholesterol gallstones, Biology of the Cell. (2005) 97, no. 11, 815–822, https://doi.org/10.1042/BC20040088.
- 20 Portincasa P., Moschetta A., and Palasciano G., From lipid secretion to cholesterol crystallization in bile. Relevance in cholesterol gallstone disease, Annals of Hepatology. (2002) 1, no. 3, 121–128.
- 21 Jüngst D., [email protected], Gussmann E., Zündt B. et al., Solubility of cholesterol in the crystal-free gallbladder bile of gallstone patients, Journal of Laboratory and Clinical Medicine. (2004) 144, no. 3, 134–140, https://doi.org/10.1016/j.lab.2004.04.012.
- 22 Sherbakov V. M. and Tikhonov A. V., Isoforms of Human Liver Cytochrome P450, 1995, Press “Souzinformbiology KALINA” VINITI RAS, Moscow, Russia.
- 23 Wang H. H., Afdhal N. H., and Wang D. Q.-H., [email protected], Estrogen receptor α, but not β, plays a major role in 17β-estradiol-induced murine cholesterol gallstones, Gastroenterology. (2004) 127, no. 1, 239–249, https://doi.org/10.1053/j.gastro.2004.03.059.
- 24 Novacek G., [email protected], Gender and gallstone disease, Wiener Medizinische Wochenschrift. (2006) 156, no. 19-20, 527–533, https://doi.org/10.1007/s10354-006-0346-x.
- 25 Chijiiwa K., Hirota I., and Noshiro H., High vesicular cholesterol and protein in bile are associated with formation of cholesterol but not pigment gallstones, Digestive Diseases and Sciences. (1993) 38, no. 1, 161–166, https://doi.org/10.1007/BF01296790.
- 26 Strasberg S. M., Toth J. L., Gallinger S., and Harvey P. R. C., High protein and total lipid concentration are associated with reduced metastability of bile in an early stage of cholesterol gallstone formation, Gastroenterology. (1990) 98, no. 3, 739–746.
- 27 Zhou H., Chen B., Li R.-X. et al., Large-scale identification of human biliary proteins from a cholesterol stone patient using a proteomic approach, Rapid Communications in Mass Spectrometry. (2005) 19, no. 23, 3569–3578, https://doi.org/10.1002/rcm.2207.
- 28 Wilhelmi M., Jüngst C., Mock M. et al., Effect of gallbladder mucin on the crystallization of cholesterol in bile, European Journal of Gastroenterology and Hepatology. (2004) 16, no. 12, 1301–1307, https://doi.org/10.1097/00042737-200412000-00011.
- 29 Finzi L., Barbu V., Burgel P.-R. et al., MUC5AC, a gel-forming mucin accumulating in gallstone disease, is overproduced via an epidermal growth factor receptor pathway in the human gallbladder, American Journal of Pathology. (2006) 169, no. 6, 2031–2041, https://doi.org/10.2353/ajpath.2006.060146.
- 30 Sripa B., [email protected], Kanla P., Sinawat P., and Haswell-Elkins M. R., Opisthorchiasis-associated biliary stones: light and scanning electron microscopic study, World Journal of Gastroenterology. (2004) 10, no. 22, 3318–3321.
- 31 Kodaka T., [email protected], Sano T., Nakagawa K., Kakino J., and Mori R., Structural and analytical comparison of gallbladder stones collected from a single patient: studies of five cases, Medical Electron Microscopy. (2004) 37, no. 2, 130–140, https://doi.org/10.1007/s00795-003-0237-9.