Prevalence of avascular necrosis of femoral head in patients with cirrhosis of liver

  • Authors

    • Sanjeev Mahajan M S Ramaiah medical collegeM M institute of medical sciences and research
    • Daksh Gadi
    • Rahul Gupta
    • Anirudh Sharma
    • Premjeet Singh Thind
    • Som Gupta
    • Raminder Kaur
  • Avascular Necrosis, Liver Cirrhosis, Femur Head.
  • Background: Amongst the multiple etiologies implicated in the development of Avascular necrosis of the femoral head, literature regarding the association of cirrhosis of liver with osteonecrosis of femoral head is scanty and is correspondingly less studied. Considering a large number of patients with liver cirrhosis in this region of our country, this study was conducted to evaluate the association of cirrhosis as an independent risk factor in the development of osteonecrosis. To the best of our knowledge No such study has been done evaluating the same in this region.

    Methods: This prospective analysis aimed to determine the prevalence of osteonecrosis of femoral head in patients with cirrhosis of liver, patients presenting to the hospital with established cirrhosis, diagnosed with help of ultrasonography , were evaluated for the occurance of Avascular necrosis of the femoral head.

    Results: The prevalence of osteonecrosis of femoral head in patients with cirrhosis of liver was evaluated to be 1.2% in the present study. Amongst this cirrhotic subgroup, the prevalence of osteonecrosis of femoral head in cirrhotic patients due to excessive alcohol consumption was calculated to be 1.1% and that of the cirrhotic patients independent of alcohol consumption came out to be 1.4%.

    Conclusion: Analysis of the results of the present study establishes cirrhosis of liver, the cause of which could be independent or related to alcohol consumption, as a risk factor for the development of osteonecrosis of femoral head. Significance of alcohol related cirrhosis resulting in AVN of the femoral head, though, is challenged by the present study.

  • References

    1. [1] Aaron RK, Ciombor DM. Coagulopathies and osteonecrosis. Curr Opin Orthop 2001; 12:378-383.

      [2] Asano T, Takahashi KA, Fujioka M, Inoue S, Okamoto M, Sugioka N et al. A polymorphism decreased the risk for steroid-induced osteonecrosis of the femoral head after kidney transplantation. Pharmacogenetics 2003; 13:675-682.

      [3] Tektonidou MG, Moutsopoulos HM. Immunologic factors in the pathogenesis of osteonecrosis. Orthop Clin North Am 2004; 35:259-263.

      [4] Louis Solomon, David Warwick, Selvadurai Nayagam, 2010 Apley's System of Orthopaedics and Fractures, ninth edition, Hodder Arnold, London.

      [5] Calder JD, Buttery L, Revell PA, Pearse M, Polak JM. Apoptosis--a significant cause of bone cell death in osteonecrosis of the femoral head. J Bone Joint Surg Br. 2004; 86:1209–1213.

      [6] Weinstein RS, Nicholas RW, Manolagas SC. Apoptosis of osteocytes in glucocorticoid-induced osteonecrosis of the hip. J Clin Endocrinol Metab. 2000; 85:2907–2912.

      [7] Youm YS, Lee SY, Lee SH. Apoptosis in the osteonecrosis of the femoral head. Clin Orthop Surg. 2010; 2:250–255.

      [8] Schulte CM, Beelen DW: Avascular osteonecrosis after allogeneic hematopoietic stem-cell transplantation: diagnosis and gender matter. Transplantation 2004, 78:1055-1063.

      [9] Hung TH, Hsieh YH, Tsai CC, Tseng CW, Tseng KC, Tsai CC. Is liver cirrhosis a risk factor for osteonecrosis of the femoral head in adults? A population-based 3-year follow-up study. Intern Med. 2011; 50(21):2563-8.

      [10] Hirota Y, Hirohata T, Fukuda K, Mori M, Yanagawa H, Ohno Y et al. Association of alcohol intake, cigarette smoking, and occupational status with the risk of idiopathic osteonecrosis of the femoral head. Am J Epidemiol. 1993; 137 (5):530–538.

      [11] Fukushima W, Fujioka M, Kubo T, Tamakoshi A, Nagai M, Hirota Y. Nationwide epidemiologic survey of idiopathic osteonecrosis of the femoral head. Clin Orthop Relat Res. 2010; 468: 2715-2724.

      [12] Jones LC, Hungerford DS. Osteonecrosis: etiology, diagnosis, and treatment. Curr Opin Rheumatol. 2004; 16: 443-449.

      [13] Gallego-Rojo FJ, Gonzalez-Calvin JL, Muñoz-Torres M, Mundi JL, Fernandez-Perez R, Rodrigo-Moreno D. Bone mineral density, serum insulin-like growth factor I, and bone turnover markers in viral cirrhosis. Hepatology. 1998; 28:695–699.

      [14] Crosbie OM, Freaney R, McKenna MJ, Hegarty JE. Bone density, vitamin D status, and disordered bone remodeling in end-stage chronic liver disease. Calcif Tissue Int. 1999; 64:295–300.

      [15] Crawford BA, Labio ED, Strasser SI, McCaughan GW. Vitamin D replacement for cirrhosis-related bone disease. Nat Clin Pract Gastroenterol Hepatol. 2006; 3:689–699.

      [16] George J, Ganesh HK, Acharya S, Bandgar TR, Shivane V, Karvat A et al. Bone mineral density and disorders of mineral metabolism in chronic liver disease. World J Gastroenterol. 2009; 15:3516–3522.

      [17] Nishiguchi S, Shimoi S, Kurooka H, Tamori A, Habu D, Takeda T et al. Randomized pilot trial of vitamin K2 for bone loss in patients with primary biliary cirrhosis. J Hepatol. 2001; 35:543–545.

      [18] McInnes IB, Schett G. Cytokines in the pathogenesis of rheumatoid arthritis. Nat Rev Immunol 2007; 7: 429-442.

      [19] Smolen JS, Beaulieu A, Rubbert-Roth A, et al. Effect of interleukin-6 receptor inhibition with tocilizumab in patients with rheumatoid arthritis (OPTION study): a double-blind, placebocontrolled, randomised trial. Lancet 2008; 371: 987-997.

      [20] Wong PK, Quinn JM, Sims NA, van Nieuwenhuijze A, Campbell IK, Wicks IP. Interleukin-6 modulates production of T lymphocyte-derived cytokines in antigen-induced arthritis and drives inflammation-induced osteoclastogenesis. Arthritis Rheum 2006; 54: 158-168.

      [21] De Benedetti F, Rucci N, Del Fattore A, et al. Impaired skeletal development in interleukin-6-transgenic mice: a model for the impact of chronic inflammation on the growing skeletal system. Arthritis Rheum 2006; 54: 3551-3563.

      [22] Liu XH, Kirschenbaum A, Yao S, Levine AC. Cross-talk between the interleukin-6 and prostaglandin E(2) signaling systems results in enhancement of osteoclastogenesis through effects on the osteoprotegerin/ receptor activator of nuclear factor-{kappa}B (RANK) ligand/RANK system. Endocrinology 2005; 146: 1991-1998.

      [23] Moschen AR, Kaser A, Stadlmann S, Millonig G, Kaser S, Mühllechner P et al. The RANKL/OPG system and bone mineral density in patients with chronic liver disease. J Hepatol. 2005; 43:973–983.

      [24] González-Calvin JL, Mundi JL, Casado-Caballero FJ, Abadia AC, Martin-Ibañez JJ. Bone mineral density and serum levels of soluble tumor necrosis factors, estradiol, and osteoprotegerin in postmenopausal women with cirrhosis after viral hepatitis. J Clin Endocrinol Metab. 2009; 94:4844–4850.

      [25] Wiest R, Weigert J, Wanninger J, et al. Impaired hepatic removal of interleukin-6 in patients with liver cirrhosis. Cytokine 2011; 53:178-183.

  • Downloads

  • How to Cite

    Mahajan, S., Gadi, D., Gupta, R., Sharma, A., Thind, P. S., Gupta, S., & Kaur, R. (2016). Prevalence of avascular necrosis of femoral head in patients with cirrhosis of liver. International Journal of Medicine, 4(2), 74-78.