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Assessment of metabolic syndrome in patients with primary biliary cirrhosis

Erfassung des metabolischen Syndroms bei Patienten mit primär biliärer Leberzirrhose

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Summary

Background

Primary biliary cirrhosis (PBC) is a chronic, progressive liver disease with elevated serum lipids. It remains unclear if hyperlipidemia increases the risk for atherosclerosis in PBC patients. Metabolic syndrome (MS) promotes the development of atherosclerotic cardiovascular disease due to abdominal obesity and insulin resistance.

Aims

The aim of this study was to assess incidence and parameters of MS, as well as subcutaneous and visceral fat using noninvasive ultrasonographic measurement in patients with PBC in our population.

Methods

We included 55 patients with PBC and 44 age- and sex-matched healthy controls (CG-control group). Anthropometric measurements (weight, height, and waist circumference), age, sex, and body mass index were recorded for patients and controls. Laboratory tests for assessing MS and liver function tests were analyzed. We used ultrasonography to determine subcutaneous and visceral fat diameter and area (SF, VF and SA, VA, respectively), as well as perirenal fat diameter (PF).

Results

Patients with PBC had significantly higher levels of cholesterol and liver function tests. There were no statistically significant difference in serum insulin and HOMA levels, as well as incidence of MS was diagnosed in 30.9 % (17/55) PBC patients and 43.2 % (19/44) controls. We registered lower amount of VF (PBC:10.92 ± 3.63 mm, CG:16.84 ± 5.51 mm,p < 0.001), VA (PBC:403.64 ± 166.97 mm2, CG:720.57 ± 272.50 mm2,p < 0.001), and PF (PBC:7.03 ± 1.82 mm, CG 10.49 ± 2.70 mm,p < 0.001) in patients with PBC.

Conclusion

MS is not more frequent in patients with PBC compared with healthy volunteers in our population. Lower amount of VF could be related to lower risk for cardiovascular events in PBC patients.

Zusammenfassung

Hintergrund

Die primär biliäre Lebercirrhose (PBC) ist eine chronisch progressive Lebererkrankung mit Erhöhung der Lipide. Es besteht Unklarheit darüber, ob diese Hyperlipidämie das Risiko für eine Atherosklerose bei PBC Patienten erhöht. Das metabolische Syndrom (MS) begünstigt die Entwicklung einer kardiovaskulären Atherosklerose durch die dabei bestehende abdominale Obesitas und Insulinresistenz.

Ziel der Studie

war es, das Vorkommen eines MS, sowie Parameter desselben bei PBC Patienten im Vergleich mit der Normalbevölkerung zu erfassen, wobei das subkutane und viszerale Fett ultrasonographisch gemessen wurde.

Methodik

Wir schlossen 55 Patienten mit PBC und 44 gesunde – alters und geschlechts-gematchte – Kontrollen (CG-Kontrollgruppe) in die Studie ein. Anthropomorphometrische Messdaten (Gewicht, Körpergröße, Hüftumfang), Alter, Geschlecht und Body Mass Index wurden bei den Patienten und der Kontrollgruppe festgehalten. Laboruntersuchungen zur Erfassung des MS und Leberfunktionsproben wurden durchgeführt. Das subkutane (SF) und viszerale Fett (VF), deren Durchmesser und Fläche (SA, VA) sowie der Durchmesser des perirenalen Fettgewebes (PF) wurde ultrasonographisch erhoben.

Ergebnisse

Patienten mit PBC hatten signifikant erhöhte Cholesterin- und Leberfunktionsproben. Die Serum Insulin und HOMA Spiegel, sowie das Vorkommen eines MS (17 von 55 (30,9 %) PBC Patienten vs 19 von 44 (43,2 %) CG Kontrollen) unterschieden sich nicht signifikant in beiden Gruppen. Wir registrierten einen niedrigeren Gehalt von VF (PBC:10.92 ± 3.63 mm, CG:16.84 ± 5.51 mm,p < 0.001), VA (PBC:403.64 ± 166.97 mm2, CG:720.57 ± 272.50 mm2 p < 0.001), und PF (PBC:7.03 ± 1.82 mm, CG 10.49 ± 2.70 mm,p < 0.001) bei den PBC Patienten.

Schlussfolgerung

Das MS ist kommt bei Patienten mit PBC nicht häufiger als bei der Normalbevölkerung vor. Der von uns beobachtete niedrigere Anteil an viszeralem Fett könnte für ein niedrigeres Risiko kardiovaskulärer Ereignisse bei PBC Patienten sprechen.

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References

  1. Kaplan MM, Gershwin ME. Primary biliary cirrhosis. N Engl J Med. 2005;353:1261–73.

    Article  PubMed  CAS  Google Scholar 

  2. Van Dam GM, Gips CH. Primary biliary cirrhosis in The Netherlands. An analysis of associated diseases, cardiovascular risk, and malignancies on the basis of mortality figures. Scand J Gastroenterol. 1997;32:77–83.

    Article  PubMed  CAS  Google Scholar 

  3. Crippin JS, Lindor KD, Jorgensen R, et al. Hypercholesterolemia and atherosclerosis in primary biliary cirrhosis: what is the risk? Hepatology. 1992;15:858–62.

    Article  PubMed  CAS  Google Scholar 

  4. Cash WJ, McCance DR, Young IS, et al. Primary biliary cirrhosis is associated with oxidative stress and endothelial dysfunction but not increased cardiovascular risk. Hepatol Res. 2010;40(11):1098–106.

    Article  PubMed  CAS  Google Scholar 

  5. Sorokin A, Brown JL, Thompson PD. Primary biliary cirrhosis, hyperlipidemia, and atherosclerotic risk: a systematic review. Atherosclerosis. 2007;194:293–9.

    Article  PubMed  CAS  Google Scholar 

  6. Allocca M, Crosignani A, Gritti A, et al. Hypercholesterolaemia is not associated with early atherosclerotic lesions in primary biliary cirrhosis. Gut. 2006;55:1795–800.

    Article  PubMed  CAS  Google Scholar 

  7. Longo M, Crosignani A, Battezzati PM, et al. Hyperlipidaemic state and cardiovascular risk in primary biliary cirrhosis. Gut. 2002;51:265–9.

    Article  PubMed  CAS  Google Scholar 

  8. Stojakovic T, Putz-Bankuti C, Fauler G, et al. Atorvastatin in patients with primary biliary cirrhosis and incomplete biochemical response to ursodeoxycholic acid. Hepatology. 2007;46(3):776–84.

    Article  PubMed  CAS  Google Scholar 

  9. Stojakovic T, Claudel T, Putz-Bankuti C, et al. Low-dose atorvastatin improves dyslipidemia and vascular function in patients with primary biliary cirrhosis after one year of treatment. Atherosclerosis. 2010;209(1):178–83.

    Article  PubMed  CAS  Google Scholar 

  10. Grundy SM, Cleeman JI, Daniels SR, et al. American Heart Association; National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: an AmericanHeart Association/National Heart, Lung, and Blood Institute scientific statement. Circulation. 2005;112:2735–52.

    Article  PubMed  Google Scholar 

  11. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome—a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med. 2006;23:469–80.

    Article  PubMed  CAS  Google Scholar 

  12. Wang J. Waist circumference: a simple, inexpensive, and reliable tool that should be included as part of physical examinations in the doctor’s office. Am J Clin Nutr. 2003;78:902–3.

    PubMed  CAS  Google Scholar 

  13. Merino-Ibarra E, Artieda M, Cenarro A, et al. Ultrasonography for the evaluation of visceral fat and the metabolic syndrome. Metab Clin Exp. 2005;54:1230–5.

    Article  PubMed  CAS  Google Scholar 

  14. Hirooka M, Kumagi T, Kurose K, et al. A technique for the measurement of visceral fat by ultrasonography: comparison of measurements by ultrasonography and computed tomography. Intern Med. 2005;44(8):794–9.

    Article  PubMed  Google Scholar 

  15. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC, et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9.

    Article  PubMed  CAS  Google Scholar 

  16. Solaymani-Dodaran M, Aithal GP, Card T, West J. Risk of cardiovascular and cerebrovascular events in primary biliary cirrhosis: a population-based cohort study. Am J Gastroenterol. 2008;103(11):2784–8.

    Article  PubMed  Google Scholar 

  17. Floreani A, Variola A, Niro G, et al. Plasma adiponectin levels in primary biliary cirrhosis: a novel perspective for link between hypercholesterolemia and protection against atherosclerosis. Am J Gastroenterol. 2008;103(8):1959–65.

    Article  PubMed  CAS  Google Scholar 

  18. Despres JP, Cartier A, Côté M, Arsenault BJ. The concept of cardiometabolic risk: bridging the fields of diabetology and cardiology. Ann Med. 2008;40:514–23.

    Article  PubMed  CAS  Google Scholar 

  19. Allende-Vigo MZ. Pathophysiologic mechanisms linking adipose tissue and cardiometabolic risk. Endocr Pract. 2010;16:692–8.

    Article  PubMed  Google Scholar 

  20. Ahima RS, Flier JS. Adipose tissue as an endocrine organ. Trends Endocriol Metab. 2000;10:327–32.

    Article  Google Scholar 

  21. Gnacińska M, Małgorzewicz S, Guzek M, Lysiak-Szydłowska W, Sworczak K. Adipose tissue activity in relation to overweight or obesity. Endokrynol Pol. 2010;61:160–8.

    PubMed  Google Scholar 

  22. Duvnjak L, Duvnjak M. The metabolic syndrome—an ongoing story. J Physiol Pharmacol. 2009;60(7):19–24.

    PubMed  Google Scholar 

  23. Matsuzawa Y. The metabolic syndrome and adipocytokines. FEBS Lett. 2006;580:2917–21.

    Article  PubMed  CAS  Google Scholar 

  24. Balmer ML, Joneli J, Schoepfer A, Stickel F, Thormann W, Dufour JF. Significance of serum adiponectin levels in patients with chronic liver disease. Clin Sci (Lond). 2010;119:431–6.

    Article  CAS  Google Scholar 

  25. Tacke F, Wüstefeld T, Horn R, et al. High adiponectin in chronic liver disease and cholestasis suggests biliary route of adiponectin excretion in vivo. J Hepatol. 2005;42:666–73.

    Article  PubMed  CAS  Google Scholar 

  26. Xu A, Wang Y, Keshaw H, Xu LY, Lam KS, Cooper GJ. The fat-derived hormone adiponectin alleviates alcoholic and nonalcoholic fatty liver diseases in mice. J Clin Invest. 2003;112:91–100.

    PubMed  CAS  Google Scholar 

  27. Aygun C, Senturk O, Hulagu S, et al. Serum levels of hepatoprotective peptide adiponectin in non-alcoholic fatty liver disease. Eur J Gastroenterol Hepatol. 2006;18:175–80.

    Article  PubMed  CAS  Google Scholar 

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Conflict of interest

The authors declare that there is no actual or potential conflict of interest in relation to this article.

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Authors and Affiliations

  1. School of Medicine, University of Belgrade, Belgrade, Serbia

    Tamara Alempijevic, Aleksandra Sokic-Milutinovic, Aleksandra Pavlovic Markovic, Rada Jesic-Vukicevic, Djuro Macut, Dragan Popovic & Dragan Tomic

  2. Clinic for Gastroenterology, Clinical Centre of Serbia, 11000, Belgrade, 2 Dr. Koste Todorovica St., Serbia

    Tamara Alempijevic, Aleksandra Sokic-Milutinovic, Aleksandra Pavlovic Markovic, Rada Jesic-Vukicevic, Dragan Popovic & Dragan Tomic

  3. Institute for Medical Informatics, School of Dentistry, University of Belgrade, Belgrade, Serbia

    Biljana Milicic

  4. Clinic for Endocrinology, Diabetes and metabolic disorders, Clinical Centre of Serbia, Belgrade, Serbia

    Djuro Macut

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  1. Tamara Alempijevic
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  2. Aleksandra Sokic-Milutinovic
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Alempijevic, T., Sokic-Milutinovic, A., Pavlovic Markovic, A. et al. Assessment of metabolic syndrome in patients with primary biliary cirrhosis. Wien Klin Wochenschr 124, 251–255 (2012). https://doi.org/10.1007/s00508-012-0162-9

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  • DOI: https://doi.org/10.1007/s00508-012-0162-9

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